S aureus: eradicated in - Asociacion Medica de Puerto Rico

Transcription

JUNTA DE DIRECTORES
Dr. Rolance G. Chavier Roper
Presidente
Dra. Ilsa Figueroa
Presidente Distrito Este
Dr. Eduardo Rodríguez Vazquez
Presidente Saliente
Dr. Gustavo Cedeño Quintero
Presidente Distrito Noreste
Dr. Pedro Zayas Santos
Secretario
Dr. Roberto Perez Nieves
Presidente Distrito Sur
Dr. Benigno López López
Tesorero
Dra. Mildred R. Arché Matta
Presidente Distrito Central
Dra. Hilda Ocasio Maldonado
Vicepresidente
Dr. Raúl Castellanos Bran
Vicepresidente
Dra. Wanda G. Velez Andujar
Presidente Consejo de Educación Medica
Dr. Raúl A. Yordán Rivera
Vicepresidente
Dr. José C. Román de Jesus
Presidente Consejo Ético Judicial
Dr. Edgardo Rosario Burgos
Presidente Consejo Relaciones y Servicios Públicos
Dr. Arturo Arché Matta
Presidente Cámara Delegados
Dr. Modesto Gonzalez del Rosario
Presidente Consejo Servicios Médicos
Dr. Juan Rodríguez del Valle
Vicepresidente Cámara de Delegados
Dr. Jaime M. Diaz Hernandez
Presidente Consejo Salud Pública y Bienestar Social
Dr. Gonzalo González Liboy
Delegado AMA
Dr. Rafael Fernández Feliberti
Delegado Alterno AMA
Dr. Rafael Fernández Soltero
Presidente Consejo Política Pública y Legislación
Dr. Ricardo Marrero Santiago
Delegado Alterno AMA
Dr. Rafael Fernández Feliberti
Presidente Comité Asesor Presidente
Dr. Julio de la Cruz
Presidente Comite de Finanzas
JUNTA EDITORA
Humberto Lugo Vicente, MD
Presidente
Luis Izquierdo Mora, MD
Juan Aranda Ramírez, MD
Melvin Bonilla Félix, MD
Francisco J. Muñiz Vázquez, MD
Carlos González Oppenheimer, MD
Walter Frontera, MD
Eduardo Santiago Delpin, MD
Mario. R. García Palmieri, MD
Francisco Joglar Pesquera, MD
Raúl Armstrong Mayoral, MD
Yocasta Brugal, MD
José Ginel Rodríguez, MD
B LETÍN
Asociación Médica de Puerto Rico
CONTENIDO
44 Coexistent Asymptomatic Persistent Left Su-
2 Semblanzas
Dr. Ramón Suárez
3 Mensaje del Presidente / Message from President
Rolance G. Chavier Roper, MD
Editorial Article / Artículo Editorial
5 El XXII Congreso Interamericano De Cardiología En Puerto Rico
Mario R. García Palmieri, MD Historiador
Review Articles / Articulos de Reseña
9 Cardiovascular Services And Human Resources In Puerto Rico - 2008
Mario R. García Palmieri, MD
15 Cardiac Biomakers For The Evaluation Of
Acute Coronary Syndrome
Luis F. Rodriguez-Ospina MD; Claudia P. Rosales-Alvarez MD; Alejandro Lopez-Mas MD
23 Ventricular Septal Defects
Nelson E. Aguilar, MD; Jose Eugenio Lopez, MD
perior Vena Cava, Partial AnomalousVenous
Connection And Atrial Septal Defect: A Case
Report
Elías Bou Prieto MD, Alexis Canino Rodríguez MD,
José Martínez Toro MD
48 Spontaneous Coronary Artery Dissection: A
Rare Etiology Of St Elevation Myocardial Infarction
Hilton Franqui-Rivera MD, Ricardo G. ColacioppoSaavedra MD, José Martínez-Toro MD*
Challenging Educational Cases / Retos Educacionales.
es
51 Challenging Educational Electrocardiography
Cases
Charles D. Johnson, MD, FACC
57 Physicians And Pharmacists In Puerto Rico During The Wars Of Independence, 1810-1830
Ivette Perez Vega PhD, JD
65 ACKNOWLEDGMENTS
SEMBLANZAS
30 An Update To The National Cholesterol Edu-
cation Program: 2009 Suggested Changes
Arturo Medina-Ruíz, MD
34 The “Crush And Aspiration” Technique For
Debridement Of The Aortic Annulus Revisited
Héctor E. Marcano MD, Samuel Olmeda ORT,
Raúl García-Rinaldi MD
Dr. Ramón Suárez
Case Reports / Reporte de Casos
37 Giant Aneurysm Of The Non-Coronary Sinus
Catalogado en Cumulative Index e Index Medicus
Listed in Cumulative Index and Index Medicus No. ISSN-00044849
Registrado en Latindex -Sistema Regional de Información en
Línea para Revistas Científicas de América Latina, el Caribe,
España y Portugal
41 Giant Cardiac Myxoma In An Asymptomatic
BOLETIN - Asociación Médica de Puerto Rico
Ave. Fernández Juncos Núm. 1305
P.O.Box 9387 - SANTURCE, Puerto Rico 00908-9387
Tel.: (787) 721-6969 - Fax: (787) 724-5208
e-mail:pampr@asociacionmedicapr.org
Web site: www.asociacionmedicapr.org
Web site para el paciente: www.saludampr.org
Of Valsalva: A Case Report
Karen Rodríguez-Maldonado MD, José MartínezToro MD, José Pereyó-Díaz MD, Cid QuintanaRodríguez MD
57-Year-Old Women: A Case Report
Hilton Franqui-Rivera MD, Priscila HernándezVélez MD, Jorge Ortega-Gil MD, José MartínezToro MD, Iván González-Cancel MD, Carmen
Gurrea MD
Diseño Gráfico e Ilustración digital de cubierta realizados por
Juan Carlos Laborde
en el Departamento de Informática de la AMPR
E-mail: webmaster@asociacionmedicapr.org
Semblanzas
Dr. Ramón Suárez
Hematólogo y Cardiólogo
NN
Líder del sistema de salud, director de hospitales, investigador, continuador de la obra del Dr.
Ashford, tuvo a cargo el Tribunal Médico y fue
otro de los ilustres Presidentes de la Asociación
Médica de Puerto Rico.
acido en 1895 en Loiza Aldea, luego de
terminar la escuela en la Central High en Santurce
fue a estudiar Medicina a los Estados Unidos al
Medical College of Virginia donde se graduó en
1917.
En 1940 fue nombrado jefe de Medicina Interna de la Escuela de Medicina Tropical, hasta
1949.
Realizó estudios sobre hipertensión arterial, enfermedades cardiovasculares, e investiga
En 1920 regresó a Puerto Rico donde su ciones sobre la fiebre reumática. En 1945 publicó
actividad profesional fue mayormente con niños, los resultados del tratamiento de esprue tropical
con ácido fólico en una revista médica norteameal principio.
ricana. Estos y otros logros lo convirtieron en el
En el año 1928 fue designado director médi- primer hematólogo puertorriqueño y lo llevó a ser
co del Hospital Municipal de San Juan, nombrado nombrado a la Junta Editorial de la nueva revista
en la facultad de la Escuela de Medicina Tropical Blood.
y electo Presidente de la Asociación Médica de
Dedicado a la Cardiología, fundó en el HosPuerto Rico, cargo que desempeñó hasta 1930.
pital Mimiya un Centro de Investigaciones Clíni
Fundó su propio hospital, Mimiya (nombre cas. Tuvo una fructífera actividad, publicando 155
en memoria de su hija que había fallecido de leu- artículos en revistas médicas. Fue elegido como
miembro de un grupo de profesionales médicos
cemia a los 5 años de edad).
destacados, agrupados en la Association of Ame
En 1932, fue nombrado al Tribunal Exami- rican Physicians. Él fue el único puertorriqueño
nador de Médicos de Puerto Rico, posición que que perteneció a esta asociación hasta que, en
mantuvo por 14 años y del cual llegó a ser Presi- 1971, se incorporó al Dr. Mario Rubén García Palmieri.
dente.
El Centro Cardiovascular de Puerto Rico y
Trabajó junto al Dr. Ashford en la Escuela del
Caribe
lleva su nombre.
de Medicina Tropical, realizando trabajos de investigación en pacientes afectados por anemia y
La Asociación Médica le dedico la portada
esprue tropical.
de su Boletín en 1983 y hoy su pintura ocupa un
El Dr. Ashford, lo recomendó, en 1934, lugar destacado en el Salón de los Presidentes de
como Fellow del American College of Physicians nuestra Institución.
y fue el primer puertorriqueño en ser Gobernador
Al cumplir 107 años de historia, la Asociadel College of Physicians en la isla. Al fallecer el ción
Médica
de Puerto Rico se honra en dedicarle
Dr. Ashford, fue su sucesor en los trabajos de inesta
edición
al Dr. Ramón Suárez.
vestigación sobre anemia.
2
Boletín de la Asociación Médica de Puerto Rico - Volumen 101 Nro. 4 - Octubre - Diciembre 2009
Message from President
Rolance G.
Chavier Roper, MD
F
F
or the last 108 years, the Puerto Rico Medical Association (PRMA) has been serving
the doctors and patients of Puerto Rico. This institution has contributed enormously to the quality of medical education and has held the highest standards of our profession.
The PRMA has been the official representative of the American Medical Association
(AMA) and the Accreditation Council on Continuing Medical Education (ACCME), through its
Continuing Medical Education Council.
We are also the only professional organization in the field of medicine in Puerto Rico,
which is totally voluntary and represents more than 40 medical specialties. Throughout our
history, we have had the privilege of being led by some of the most prestigious physicians who
have practiced locally. We must mention doctors like Bailey K. Ashford, Agustin Stahl, Manuel
Pavia, Manuel de la Pila Iglesias, and Dr. Ramon Suarez, who we honor today by dedicating
this issue to him. Dr. Suarez has been an icon in the practice of cardiology and a great example
to Puerto Rican doctors. So many were his contributions in his specialty, that our Cardiovascular Center of Puerto Rico and the Caribbean bears his name.
Today, more than ever, we need more doctors like him.
We have been modernizing our institution and restoring the PRMA’s position and leadership in technology, communications, and public opinion in issues having to do with healthcare.
Health Information Technology is here to stay and will be the future of medicine. This publication is instrumental in the future of medical education and serves as a platform for the publication of peer reviewed articles necessary for residents and fellows to complete their research
work.
I want to thank the editorial board for their excellent work during this year and I must
especially mention Dr. Humberto Lugo Vicente, who has been instrumental in achieving the
level of quality of this publication. The PRMA counts on his leadership to continue publishing
this journal which has 107 years of uninterrupted history.
Dr. Rolance G. Chavier Roper
President, PRMA.
3
• Instrucciones para los Autores*
• Instructions to Authors*
El “Boletín” acepta para publicación artículos relativos a medicina, cirugía y las
ciencias afines. Igualmente acepta artículos especiales y correspondencia que
pudiera ser de interés general para la profesión médica. Se requiere que los autores
se esfuercen en perseguir claridad, brevedad, e ir a lo pertinente en sus manuscritos,
no importa el tema o formato del manuscrito.
El artículo, si se aceptara, será con la condición de que se publicara únicamente en
la revista. Para facilitar la labor de revisión de la junta Editora y la del impresor, se
requiere de los autores que sigan las siguientes instrucciones:
• Documento Digital
El documento completo, incluyendo las leyendas y referencias deberá estar escrito
en computadora (Word u OpenOffice) a simple espacio, letra Arial, tamaño 12
regular, justificado. Cada párrafo deberá separarse con un espacio doble. (DEBERÁ
SER GRABADO EN UN CD o DVD). Favor enviar ese material por correo a:
ASOCIACION MEDICA DE PUERTO RICO
Boletin
P. O. Box 9387
SAN JUAN, PR 00908-9387
PUERTO RICO
y por correo electrónico, con una carta de introducción dirigida al Editor, Dr.
Humberto Lugo-Vicente a: titolugo@coqui.net.
Deberá incluirse lo siguiente: título, nombre de autor(es) y su grado (ej.: MD, FACP),
ciudad donde se hizo el trabajo, el hospital o institución académica, patrocinadores
del estudio, y si un artículo ha sido leído en alguna reunión o congreso, así debe
hacerse constar como una nota al calce.
El articulo debe comenzar con una breve introducción en la cual se especifique el
propósito del mismo. Las secciones principales (como por ejemplo: materiales y
métodos) deben identificarse con un encabezamiento en letras mayuscula negritas
(bold).
Artículos referentes a resultados de estudios clínicos o investigaciones de laboratorio
deben organizarse bajo los siguientes encabezamientos: introducción, Materiales y
Métodos, Resultados, Discusión, Resumen (en español e inglés), Reconocimiento
y Referencias.
Artículos referentes a estudios de casos aislados deben organizarse en la siguiente
forma: Introducción, Materiales y Métodos si es aplicable,Observaciones del Caso,
Discusión, Resumen (en español e inglés), Reconocimientos y Referencias.
• Nomenclatura
Deben usarse los nombres genéricos de los medicamentos. Podrán usarse también
los nombres comerciales, entre paréntesis, si así se desea se usará con preferencia
el sistema métrico de pesos y medidas.
• Tablas
Las tablas deben aparecer en hojas separadas. En el documento original se debe
indicar los espacios donde se incluiran las tablas. Estas deben incluir el título, y
el número. Los símbolos de unidades deben limitarse al encabezamiento de las
columnas. Se usará en las tablas el mismo idioma en el cual está escrito el artículo.
Deben limitarse las tablas a solo aquellas que contribuyan al mejor entendimiento
del manuscrito. Deben ser confeccionadas en Word, OpenOffice o en archivo
de imagen jpg, pdf, png o tif (verificar que no se encuentra bloqueada ninguna
funcion)
• Ilustraciones y fotografías
Las fotografías se someterán en archivos de imagen pdf, jpg, tif o png (sin bloquear),
por separado, Se referenciarán de la misma forma que las tablas. En el documento
original se debe indicar los espacios donde van las fotografias e ilustraciones.
• Resumen
Un abstracto no mayor de 250 palabras en estudios clínicos y no mayor de 150
palabras en reporte de casos o reseña. Debe incluir los puntos principales que
ilustren la substancia del artículo y la exposición del problema, métodos, resultados
y conclusiones.
• Referencias
Las referencias deben ir numeradas sucesivamente de acuerdo a su aparición en el
texto. Los números deben aparecer en paréntesis al nivel de la línea u oración y no
como subindices ni ninguna otra forma de referencia. Al final de cada artículo
las referencias deben aparecer en el orden numérico en que se citan en el texto.
Deben utilizarse solamente las abreviaturas para títulos de revistas científicas según
indicadas en el “Cumulative Index Medicus" que publica la Asociación Médica
Americana.
Las referencias deben seguir el patrón que se describe a continuación.
1. Para artículos de revistas: Apellido(s) e iniciales del nombre del autor(es), título
del artículo, nombre de la revista, año, volumen, páginas. Por ejemplo: Villavicencio
R: Soplos inocentes en pediatría, Bol Asoc Méd P Rico 198 1; 73: 479-87. Si hay
más de 7 autores, incluir los primeros 3 y añadir et al.
2. Para citación de libros donde el autor(es) del capítulo citado es a su vez el (los)
editor(es): Apellido(s) e iniciales del autor(es), título del libro, número de edición,
ciudad, casa editora, año y página. Por ejemplo: Keith JD, Rowe RD, Vlad P: Heart
disease in infancy and childhood, 3d. Ed., New York, MacMillan, 1978: 789
3. Para citación de libros donde el editor(es) no es el autor(es) del capítulo citado
se añade el autor(es) del capítulo y el título del mismo. Por ejemplo: Olley PM:
Cardiac arrythmias; In: Keith ID, Rowe RD, Vlad P Eds. Heart disease in infancy
and childhood, 3d Ed., New York, MacMillan, 1978: 275-301
NO ENVIE PAPEL. ENVIE CD O DVD
B LETÍN
ASOCIACIÓN MÉDICA DE PUERTO RICO
Sólo serán considerados los artículos que cumplan estas instrucciones.
We will take only articles that follow this instructions.
The “Boletín” will accept for publication contributions relating to the various
areas of medicine, surgery and allied medical sciences. Special articles and
correspondence on subjects of general interest to physicians will also be accepted.
All material is accepted with the understanding that is to be published solely in
this journal.
All authors are urged to seek clarity, brevity, and pertinence in the manuscripts
regardless of subject or format.
In order to facilitate review of the article by the Editorial Board and the work of the
printer, the authors must conform with the following instructions:
• Digital Documents
The entire document, including legends and references should be typewritten in
computer (Word or OpenOffice) single spaced, Arial font, size 12 regular, justified.
Double spaced after each paragraph. (MUST BE SAVED IN A CD o DVD). Please
mail this material to:
ASOCIACION MEDICA DE PUERTO RICO
Boletin
P. O. Box 9387
SAN JUAN, PR 00908-9387
PUERTO RICO
and by email with an introductory letter to the Editor Humberto Lugo-Vicente, MD
at: titolugo@coqui.net
Should include the following: title, authors and their degrees (e.g. MD, FACP), city
where the work was done, hospital or academic institutions, acknowledgments of
financial sponsors, and if the paper has been at a meeting the place and date should
be given.
The article should start with a brief introductory paragraph or paragraphs which
should state its purpose. The main sections (for example, Materials and Methods)
should be identified by heading in bold capital letters.
Articles reporting the results of clinical studies or laboratory investigation should
be organized under the following headings: Introduction, Materials and Methods,
Result if indicated, Discussion, Summary in English and Spanish, Acknowledgments
if any, and References.
• Nomenclature
Generic names of drugs should be used; trade names my also be given in parenthesis,
if desired, metric units of measurement should be used preferentially.
• Tables
These should be typed on separate sheets with the title and table number centered.
The original document must show where the tables have to be placed. Symbol for
units should be confined lo the column headings. The language used in the tables
must be the same as that of the article. Include only those tables which will enhance
the understanding of the article. They should supplement, not duplicate the text.
Must be done in Word, OpenOffice or any image file like jpg, pdf, png or tif (verify
all functions are allowed)
• Illustrations and photos
Photographs must be sent in any image file like pdf, jpg, tif or png (not blocked),
by separate. They should be labeled in the same maner than tables. The original
document must show where ilustrations and photos have to be placed.
• Summary
An abstract not longer than 250 words for clinical studies and no longer than 150
words for case reports and reviews. It must include the main points that present
the core of the article and the exposition of the problem, method, results, and
conclusions.
• References
These should be numbered serially as they appear in the text. The number should be
enclosed in parenthesis on the line or writing and not as superscript or subscripts,
numbers. At the end of the article references should be listed in the numerical order
in which they are first cited in the text. The titles of journals should be abbreviated
according to the style used in the "Cumulative Index Medicus" published by the
American Medical Association. The correct forms of references are as given
below:
1. For periodicals: Surname and initials of author(s), title of article, name of journal,
year, volume, pages. For example: Villavicencio R.: Soplos inocentes en pediatría.
Bol Asoc Med P Rico 198 1; 73: 479 87. If there are more than 7 authors list only
3 and add et al.
2. For books when the authors of the cited chapter is at the same time the editor:
Surname and initials of author(s), title, edition, city, publishing house, ~ear and
page. For example: Keith JD, Rowe RD, Vlad P: Heart disease in infancy and
childhood, 3d Ed., New York, MacMillan, 1978: 789
3. For chapter in book when the author of the chapter is not one of the Olley PM:
Cardiac arrythmias: In: Keith JD, Rowe RD, Vlad P. Eds. Heart disease in infancy
and childhood, 3d Ed. New York, MacMillan, 1978, 275-301
DON’T SEND PAPERS. SEND CD’s OR DVD’s
D
Editorial Article / Articulo Editorial
D
esde la fundación de la Sociedad
Interamericana de Cardiología (SIAC) se han
celebrado 22 congresos interamericanos de
cardiología. En el pasado se celebraban cada
cuatro años y desde el 1995 se realizan cada
dos años. En la reunión de la asamblea de la
SIAC celebrada en Cancún en el año 2006 los
Dres. Luis Molinary y Wistremundo Dones solicitaron la sede para el 2009 para Puerto Rico,
la cual fue otorgada. El XXII Congreso Interamericano de Cardiología se celebró en el Hotel
El Conquistador en Fajardo, Puerto Rico, del 12
al 16 de junio del 2009 concurrentemente con
el XVI Congreso Puertorriqueño de Cardiología.
La planificación del congreso por delegación de
la Junta de Directores de la SIAC recayó sobre la Sociedad Puertorriqueña de Cardiología
(SPRC) presidida por el Dr. Héctor Delgado Mario R. García Palmieri
Osorio. La Junta de Directores de la SPRC de- Md Historiador
legó en un Comité Organizador compuesto por
nueve de los miembros de la Sociedad y presidido por el Dr. Luis Molinary con la responsabilidad de la organización del XXII Congreso
Interamericano. (Ver Foto 1)
El XXII
Congreso
Interamericano
De Cardiología
En Puerto Rico
Este comité fue aconsejado por un Comité Asesor Interamericano compuesto por 17
miembros, líderes en 15 sociedades nacionales
de cardiología de América (ver tabla 1).
Tabla 1
Comité Asesor Interamericano - Congreso 2009
Dr. Oscar Alvarado Contreras - Perú
Dr. Juventino Amaya Amaya - El Salvador
Dr. Pedro Diaz Ruis - Rep. Dominicana
Dr. Diego Delgado - Canadá
Dr. Edgardo Escobar - Chile
Dr. Horacio Faella - Argentina
Dr. Bartolomé Finizola - Venezuela
Dr. Valentin Fuster - Estados Unidos
Dr. Mario R. García Palmieri - Puerto Rico
Dr. Lorenzo Llerena Rojas - Cuba
Dr. Mario Lombana - Panamá
Dr. Fernando Manzur - Colombia
Dr. Marco Martínez Rios - México
Dr. Miguel Quiñones - Estados Unidos
Dr. Steve Niessen - Estados Unidos
Dr. José Ramíres - Brasil
Dr. Mauricio Varela - Honduras
Foto 1: Comité Organizador Dres. Wistremundo Dones, Luis Parés,
Carlos Girod, Héctor Delgado Osorio, Luis Molinary, Mario R. García
Palmieri, María L. Ríos, Esteban Linares y Francisco Meléndez. Todos
de Puerto Rico.
Por más de un año hubo múltiples comunicaciones
escritas a todas las sociedades nacionales de cardiología de América solicitando sugerencias y recomendaciones. Además se le envió material promocional en su idioma (español, inglés y portugués).
Se hizo promoción con folletos preliminares y blancos de inscripción. Hubo difusión por Internet.
Se hizo promoción en el XXI Congreso Interamericano de Cardiología en Lima, Perú (2007), en
el Congreso Mundial de Cardiología en Buenos AiEl Dr. Mario R. García Palmieri fue designado res (2008), en el Congreso Centroamericano y del
Presidente Honorario del Congreso Interameri- Caribe en Tegucigalpa (2008), además en la reunión
cano. La promoción del Congreso se comenzó anual del AHA y el ACC en el 2008 y 2009 respectidesde el 2007.
vamente.
5
La sesión inaugural del Congreso se llevó a
cabo el viernes 12 de junio de 2009 a las 7:00pm
en el salón principal del Hotel Conquistador con
la comparecencia de todos los congresistas. Se
dirigieron a los asistentes los componentes de la
mesa presidencial (ver Foto 2). Se dedicó un minuto de silencio en honor al Dr. Fause Attié Cury
recién fallecido. Una vez terminada la apertura se
pasó a unos salones adyacentes donde se ofreció
un cóctel buffet a los presentes incluyendo música
y comida típica puertorriqueña y una presentación
de bailes folklóricos. Ese mismo día en la mañana hubo una reunión del Comité Ejecutivo de la
SIAC de 7:00am 10:00am. La foto 3 ilustra los
presentes en la reunión.
Foto 2: Miembros de la Mesa Presidencial en Sesión Inaugural.
Dres. Carlos Girod (Moderador), Jaime Rivera Dueño (Secretario
de Salud de Puerto Rico, Wistremundo Dones (Pres. SIAC, 200920011), Oscar Alvarado (Pres. SIAC, 2007-2009), Héctor Delgado
Osorio (Presidente, Sociedad Puertorriqueña de Cardiología), Luis
Molinary (Presidente Comité Organizador del Congreso), Mario R.
García Palmieri (Presidente Honorario del Congreso)
El programa científico incluyó seis sesiones simultáneas diarias donde hubo 194 presentaciones científicas, incluyendo 8 sesiones plenarias. El Dr. Sidney Smith, Presidente Electo de la
Federación Mundial del Corazón, dictó la plenaria
de la Federación. El Dr. Valentín Fuster recibió el
premio al mérito en la investigación y dictó la conferencia que le corresponde al galardonado. (Ver
Foto 4) El Dr. Branco Mautner dictó la conferencia Mario R. García-Palmieri de la Sociedad Interamericana de Cardiología. Las otras 5 sesiones
plenarias fueron dictadas por los doctores Nanette
K. Wenger (Estados Unidos), Gianni Tognoni (Italia), Albert Waldo (Estados Unidos), Igor Palacios
(Venezuela y Estados Unidos) y James Willerson
(Estados Unidos).
Foto 4: Dres. Luis Molinary (Presidente Comité Organizador del
Congreso), Oscar Alvarado (Perú, Presidente 2007-2009), Esteban Linares (Puerto Rico, Comité Científico), Héctor Delgado Osorio (Puerto Rico, Presidente Sociedad Puertorriqueña de Cardiología 2007-2009), Valentín Fuster (Estados Unidos, Receptor Premio
al Mérito en la Investigación)
Para el Premio Dr. Ignacio Chávez al Investigador Jóven se hicieron presentaciones orales ante la audiencia, hubo un jurado y compitieron tres finalistas en español. El Dr. Oscar Andrés
Pinilla de Argentina obtuvo el primer premio, el Dr.
Sebastián Nani de Argentina recibió el segundo
premio y el Dr. Sebastián Ignacio Córdova Ortega
de Chile fue el receptor del tercer premio. Hubo
dos finalistas en el idioma inglés. El Dr. Jack Rubinstein de Estados Unidos obtuvo el primer premio y la Dra. Nitza Álvarez de Estados Unidos el
segundo premio.
Foto 3: Comité Ejecutivo de la Sociedad Interamericana de Cardiología (2007- 2009) Gustavo Restrepo (Colombia), Wistremundo Dones (Puerto Rico, Presidente Electo), Oscar Alvarado (Perú,
Presidente), Marco Martínez Ríos (México, Pasado Presidente),
Mario R. García Palmieri (Puerto Rico, Historiador), Jorge Lowenstein (Argentina, Invitado), Miguel Quiñones (Estados Unidos, VicePresidente), Diego Delgado (Canadá, Vice Presidente), Alfonso
Buendía (México, Secretario Tesorero)
6
El jurado para adjudicar los premios estuvo
compuesto por los doctores Marco Martínez Ríos
(México), Alfonso Buendía (México), Julio Pérez
(Estados Unidos) y Carlos Girod, Esteban Linares
y José Eugenio López de Puerto Rico.
Hubo un congreso de enfermería de dos
días con 20 presentaciones. En el congreso se
incluyó presentación de posters por dos días. Para
el programa científico se invitaron autoridades cardiológicas de reconocimiento internacional y participaron 105 conferenciantes del exterior y 53 de
Puerto Rico. Los temas que se discutieron cubrieron las ramas más importantes de la cardiología
incluyendo los últimos adelantos en la disciplina.
Hubo una sesión especial en el programa
para rendir un Homenaje Póstumo al Dr. Fause
Attié Cury, Ex Director del Instituto de Cardiología
Ignacio Chávez de México y Ex Presidente del XX
Congreso Interamericanote Cardiología celebrado
el Cancún en el 2006, que falleció en febrero del
2009. Hablaron en este acto el Dr. Mario R. García
Palmieri, Historiador de la SIAC, el Dr. Oscar Alvarado, Presidente y a nombre de la SIAC y el Dr.
Marco Martínez Ríos a nombre de los colegas de
México, de la Sociedad Mexicana y el Instituto de
Cardiología Ignacio Chávez.
Hubo múltiples simposios de 2½ horas de
duración organizados y patrocinados por diferentes organizaciones de cardiología de Norte, Centro
y Sur América. Entre éstas la Fundación García
Rinaldi, Cleveland Clinic, Baptist Health Center
of Miami, Sociedad Sudamericana de Cardiología, Sociedad Centroamericana y del Caribe de
Cardiología, Sociedad Interamericana de Ecocardiografía, Hospital Metodista de Houston, Texas;
American College of Cardiology de Estados Unidos, Instituto Nacional de Cardiología “Dr. Ignacio
Chávez” de México y el Texas Heart Institute / St.
Lucas Hospital de Houston. Hubo una sesión especial organizada por la Fundación Interamericana de Cardiología. (Ver Foto 6)
El programa otorgó 32 créditos de educación médica continuada a los profesionales de la
salud que asistieron. Concurrieron al congreso
cardiólogos de 31 países, incluyendo todos los países de Norte, Centro y Sur América. Hubo traducción simultánea en inglés y en español en 2 salas
de conferencias todos los días.
Entre los asistentes estuvieron presentes
los presidentes del “World Heart Federation”, del
“American College of Cardiology” y de la Fundación Interamericana de Cardiología. Participaron
9 presidentes de la SIAC (Ver Foto 5) y los presi- Foto 6: Dres. Eduardo Morales Briceño (Venezuela, Presidente
Fundación Interamericana de Cardiología), Mario R. Gardentes de las sociedades nacionales de Argentina, Electo
cía Palmieri (Puerto Rico), Pedro Colón Hernández (Puerto Rico),
Brasil, Canadá, Caribbean Society, Chile, Colom- Herman Shargrodsky (Argentina, Presidente Fundación Interamebia, El Salvador, Estados Unidos, Panamá, Para- ricana de Cardiología 2009-2011), Igor Palacios (Estados Unidos y
guay, Puerto Rico y Uruguay. Hubo delegados y Venezuela), Beatriz Champagne (Estados Unidos)
participación de todas las sociedades nacionales
A todos los asistentes del congreso se les
de cardiología de las Américas.
obsequió una copia del libro "Sociedad Interamericana de Cardiología: Historia Actualizada" escrito por el Dr. Mario R. García Palmieri. Este libro
contiene 488 fotos tomadas en 58 congresos y
reuniones científicas celebradas en 20 países de
América y el mundo que incluyen miles de cardiólogos junto a información nueva de la Sociedad
Interamericana del 1997 al 2009.
Foto 5: Presidentes de la SIAC que asistieron Dres. Bey Mario
Lombana (Panamá, 2002-2004), Bernardo Boskis (Argentina,
1985-1989), Mario Maranhao (Brasil, 1989-1993), Oscar Alvarado
(Perú, 2007-2009), Edgardo Escobar (Chile, 1996-1998), Mario
R. García Palmieri (1980-1985; 1998-2000), Wistremundo Dones
(2009-2011), Marco Martínez Ríos (México, 2006-2007). También
asistió Horacio Faella (Argentina, 2000-2002).
Sabemos que el éxito de los congresos nacionales e internacionales es en gran medida el
resultado del esfuerzo y dedicación de los compañeros que han dirigido nuestras sociedades y de
la facultad que ha participado en nuestros programas científicos. Un gran por ciento de las fotografías incluidas en el libro corresponde a nuestros
líderes y nuestros maestros
La Asamblea General se llevó a cabo el sábado 13 de junio de 2009 a las 7:00pm. Esta fue
presidida por el Dr. Oscar Alvarado y en la mesa
7
presidencial lo acompañaron el Dr. Wistremundo En la Asamblea se confirmó que el ConDones, Presidente Electo y el Dr. Alfonso Buen- greso Interamericano del 2011 será en Colombia.
día, Secretario Tesorero. (Ver Foto 7).
El Dr. Daniel Piñero de Argentina fue electo presidente de la SIAC para el periodo 2011 al 2013
(Ver Foto 10). La sede del congreso del 2013
está aún por decidirse. Se aprobó además, que
de haber fondos disponibles, la Junta de Directores de la SIAC patrocinará la participación de
conferenciantes visitantes de países de América
a algunos de los congresos nacionales de cardiología llevados a cabo por sociedades nacionales
pequeñas y de pocos recursos. Estas sociedades
deben comunicarse con la Junta de Directores de
la SIAC y solicitar la colaboración. Al final de la
reunión el Dr. Oscar Alvarado, Presidente de la
SIAC (2007-2009) transfirió el mallete de la presiFoto 7: Mesa Presidencial Asamblea SIAC 2009. Dr. Wistremun- dencia al Dr. Wistremundo Dones, Presidente de
do Dones (Presidente Electo 2009-2011), Dr. Oscar Alvarado (Pre- la SIAC (2009-2011).
sidente 2007-2009), Dr. Alfonso Buendía (Secretario Tesorero).
Hubo una asistencia espectacular con delegados y participación de todos los países llenando el salón. (ver Foto 8 y 9)
Foto 8: Participantes de la Asamblea de SIAC del 2009 con representantes y presidentes de las sociedades nacionales.
Foto 10: Dr. Oscar Alvarado (Presidente 2007-2009), Dr. Daniel
Piñero (Presidente Electo 2011-2013), (Presidente Dr. Wistremundo Dones (Presidente 2009-2011),
Foto 9: Dres. Mauricio Varela (Honduras), Luis Parés (Puerto
Rico), Jaime Goich (Chile), Fernando Lanas (Chile), Bey Mario
Lombana (Panamá), Mario Maranhao (Brasil), Antonio Palandri
Chagas (Brasil)
El Sábado, 13 de junio por la noche se celebró una cena baile de gala, En esta ocasión el
Dr. Oscar Alvarado se dirigió a los presentes. Durante el Congreso el Dr. Héctor Delgado Osorio,
Presidente de la Sociedad Puertorriqueña de Cardiología (SPRC) pasó el mallete de la presidencia
de la SPRC al Dr. Luis Parés Martínez.
En la reunión fueron electos los miembros
del Comité Ejecutivo de la SIAC
para el periodo
del 2009 a 2011.
Estos aparecen
en la Tabla 2.
8
Review Articles / Articulos de Reseña
Cardiovascular Services
And Human Resources
In Puerto Rico - 2008
Mario R. García-Palmieri MD
* From the Section of Cardiology, Department of Medicine UPR School of Medicine,
Puerto Rico Health Science Center, Rio Piedras, Puerto ico.
Presented at the XXII Interamerican Congress of Cardiology in Fajardo, Puerto Rico
on June 15, 2009.
Address for correspondence: Mario R. García-Palmieri, MD: University of Puerto
Rico School of Medicine; GPO Box 365067: San Juan, PR 00936-5067; Fax (787)
754-1739: e-mail: mario.garcia2@upr.edu
INTRODUCTION
ABSTRACT
Available information (2004-2008) concerning population statistics, the occurrence of
cardiovascular disease, cardiovascular services and human resources in Puerto Rico is presented. Relevant information concerning life
expectancy at birth, death by specific causes
in a recent four years period, the commonest
causes of death, and the related cardiovascular
risk factors prevalence data available is included. The surgical and medical interventional
services rendered to cardiovascular patients in
different institutions and their locations in Puerto Rico in the year 2008 is presented. Some remarks concerning the productivity of physicians
by our Schools of Medicine is included. Information about ACGME accredited postgraduate
cardiovascular training programs conducted in
Puerto Rico is presented. Data concerning the
prevalence of hypertension, diabetes mellitus,
overweight and obesity obtained by BRFSS in
presented.
Keywords: Life expectancy at birth, Death by specific causes, Invasive cardiology services, Cardiovascular postgraduate training,
Behavioral Risk Factor Surveillance Study, Medical Education.
C
ardiovascular disease remains the
leading cause of death in the US and Puerto Rico
(1,2). The modifiable risk factors of hypertension
and hypercholesterolemia in the general population, and the glycemic control of patients with diabetes, synergistically contribute to a patient’s risk
for cardiovascular events. Control of these risk
factors, in combination, substantially reduces a
patient’s risk for clinical events greater than any
single risk factor alone. Unfortunately the physicians practicing in Puerto Rico do not frequently
receive information about the prevalence of cardiovascular disease, risk factors, cardiovascular
services available and the involved human resources in our island. In this article we summarize
some of this information in order to help in orienting the medical profession. According to the census office of the Puerto Rico Planning Board the
population of Puerto Rico for the year 2005 was
3,912,054 with 52% due to the female population.
With 1,665,678 inhabitants aged 40 and above,
it is reasonable to expect a considerable number
of persons developing cardiovascular disease. In
1950, 3.9% of the population of Puerto Rico was
≥ 65 years of age. By 1990 this figure increased
to 9.7% and in the 2008 census data it was 15.3%
of the 3,954,307 inhabitants. The increase of the
number of elderly in Puerto Rico through the years
most likely is a reflection of the important economic, social and nutritional advances in association
to the new technology and discoveries in medicine
as well as the improvement in health care accessibility and quality offered to our population.
9
With the prolongation of life of the population more persons Unpublished data on 2005 from the stareach ages where cardiovascular disease is most frequently tistical Division of the Puerto Rico Health
encountered.
department is pending verification.
Also in the next 20 years it should be expected a
continuing increase in the population reaching 65 years of
age which usually is associated with a higher prevalence of
cardiovascular disease. The Puerto Rican health authorities
must give more attention now to the cardiovascular health
care of the elderly (3).
Relevant information concerning the status of cardiovascular services and the human medical resources is presented
for the benefit of the medical and public health personnel
involved.
Life Expectancy at Birth in Puerto Rico
The National Vital Statistics of the United States for
the year 2004 showed a life expectancy at birth in the United States for both sexes of 77.8 years and 75.2 for males
and 80.4 years for females (see Table 1). In Puerto Rico for
the year 2004 life expectancy was 77.16 for both sexes and
73.67 for males and 80.9 for females
Table 1. Life Expectancy at Birth (1950, 2004) United States and Puerto Rico.
(reference 4).
This table illustrates, besides the
data on heart disease, the deaths due to
cancer deaths, and other related vascular conditions such as cerebrovascular
diseases and hypertension from 2001 to
2004 (4).
In table 3 we present the leading
seven (7) causes of death in Puerto Rico
in 2004 (latest available) enumerating
the top seven causes. Heart disease
is number one, diabetes mellitus is the
third cause, Cerebrovascular disease is
the fourth and hypertension diseases in
the 7th demonstrating the prominence of
the cardiovascular illnesses as a health
care problem in Puerto Rico (4).
Table 3. Leading Causes of Death In Puerto Rico2004 (latest confirmed available)
Rate per 100,000 (Reference 4)
The 2004 figures for both sexes in U.S. and in Puerto
Among all the cardiovascular
Rico practically is identical, among the best figures in the deaths,
the most frequently encounworld and demonstrate a significant increase in Puerto Rico
tered
is
due to coronary artery diseaif compared to the figures of 1950.
se. Coronary artery disease and some
of its clinical manifestations, including
Deaths by Specific Causes
arrhythmias, is responsible for most of
Consistently, for the last years, diseases of the heart the cardiovascular services rendered in
has been the first cause of death in Puerto Rico as demons- Puerto Rico (1).
Behavioral Risk Factors Surveitrated by the 2001 to 2004 figures. Data on causes of dea- llance
study (BRFSS). Important Carth for the year 2004 (the only recent ones available identify heart disease as the first cause of death (see table 2). diovascular Data
Table 2. Deaths By Specific Causes, Puerto Rico, 2001-2004
10
Unfortunately the Department of Health of
Puerto Rico has for years discontinued the previously established policy of maintaining yearly
statistics of the prevalence of diseases. Nevertheless, the Department participates in the Behavioral Risk Factor Surveillance Study (BRFSS) since
1996. The Behavioral Risk Factor Surveillance
Study is a state-based telephone survey conducted by state health departments with assistance
from the Communicable Disease Center (CDC) in
Atlanta, Georgia. It is conducted in all 50 states,
the District of Columbia, Puerto Rico, Guam, and
Virgin Islands. It uses a representative sample of
non institutionalized civilian population ≥ 18 years
in each state territory (5).
Fig. 1 Prevalence of Diabetes Mellitus in Puerto Rico 1996-2007
(BRFSS) (Reference 5)
The BRFSS collects uniform, state specific data on preventive health practices and risk
factors and behaviors linked to chronic diseases
including the cardiovascular system. The data
collected yearly is compared with previous years
as well as with data collected nationally. Dr. Ruby
Serrano from the Department of Health of Puerto
Rico deserves recognition for the continuous participation of Puerto Rico in the BRFSS.
The information obtained by the BRFSS not
only presents data about the prevalence of different cardiovascular conditions, but it also provides
information concerning comorbidities or risk factors that influence, precipitate or leads to cardiovascular disease. Among these are hypertension,
smoking, cholesterol level, overweight and obesity
and the presence of diabetes.
The BRFSS 2008 collected data revealed
a prevalence of diabetes mellitus in Puerto Rico
of 12.3%, which is the highest in the United States where there is a mean prevalence of 8.2% see
Fig.1 (5). Since the middle sixties it has been reported that the prevalence of diabetes in Puerto
Rico is higher than any state in the United States.
The 2008 Study also revealed a 32.7% presence of high blood pressure (told by a health care
professional) see Fig 2. No information was obtained on the number of hypertensives that were
receiving therapy that was under medical control.
Fig. 2 Prevalence of Hypertension in Puerto Rico 1996-2007. BRFSS data. Ref. 5.
Fig 3. Prevalence of Overweight and Obesity in Puerto Rico by
Gender 1996-2007, (BRFSS) (Ref. 5)
Physical Inactivity as a Risk Factor
In the Puerto Rico Heart Health Program, a
prospective study of coronary heart disease inclu
The BFRSS also disclosed that overweight ding 9,136 rural and urban Puerto Rican men free
and obesity has a >60% prevalence in our adult of coronary heart disease aged 35-79 years fopopulation. In this study, in Puerto Rico, every llowed up for 8¼ and 15 years, multivariate analyyear since 1996, overweight and obesity has been sis revealed an independent inverse relationship of
most frequent in males than in females and around physical activity to the incidence of coronary heart
40% of hypertensives also have had overweight disease and that physical activity was a protective
and obesity ( see Fig 3). Myocardial infarction is factor against heart attacks. Sedentary subjects
had 38% more cardiovascular deaths (6-8).
more frequent in males (5).
11
Recognizing the global burden of chronic disease of which cardiovascular disease is the main
problem, at the Fifty-Third World Health Association Assembly held in 2000, physical inactivity was
affirmed as a key risk factor in the prevention and
control of chronic diseases (9).
In 2005, the World Health Organization
approved the statement “Increasing physical activity is now considered to be as important as tobacco
control, promoting a healthy diet and obesity prevention in minimizing the burden of non-communicable diseases on the world”. The performance
of physical activity is indicated for healthy persons
and for persons with cardiovascular disease.
There is a need for physicians to advocate
the performance of regular physical activity. The
high prevalence of obesity and the sedentary lifestyle that occurs in our society requires that priority
should be given by physicians to the prescription
of the performance of regular physical activity. For
this, physician-patient communication is essential.
Invasive Cardiovascular Services rendered in
2008 in Puerto Rico
In 2008, there are 18 institutions in Puerto
Rico distributed in the island in which heart catheterization studies are being performed (see table 4).
In 2006 a total of 17,855 catheterizations
were performed and in 2008 the figure reached
23,754 studies which is the highest figure of annual
catheterization ever performed in Puerto Rico. Fig
4 illustrates the location of the different catheterization centers through different towns. This helps
the practicing physician for the referral of their patients.
Catheterization Centers through the Island
(2008).
There are eight institutions in Puerto Rico
where cardiovascular patients can have both medical and surgical interventional procedures performed such as by-pass surgery, cardiac catheterization and angioplasties. These eight institutions,
as of 2008, are Auxilio Mutuo Hospital in Hato Rey,
Advance Cardiology Center in Mayagüez, Cardiovascular Center of Puerto Rico and the Caribbean
in Rio Piedras, Damas Hospital in Ponce, Pavia
Hospital in Santurce, San Pablo Hospital in Bayamón, San Lucas Hospital in Ponce and the Veterans Administration Hospital in San Juan.
Table 5 illustrates the total invasive procedures performed in Puerto Rico centers during the year
2008. Thirty-nine per cent of the patients submitted
to cardiac catheterization had an invasive procedure (by-pass surgery or angioplasty) performed.
Angioplasty was performed
more frequently than bypass surgery.
On the year 2008,
2,151 pacemakers and 621
defibrillators were installed
in Puerto Rico.
Table 4. Eighteen Centers of Cardiac Catheterization in Puerto Rico – 2008
Fig. 4. Distribution
12
At present pediatric
cardiac surgery is being performed only in the Puerto
Rico Cardiovascular Center. There are five pediatric
cardiovascular surgeons in
Puerto Rico with one of them
retired. Electrophysiological
Studies (EPS) and ablations
are done at the Cardiovascular Center, the Auxilio
Mutuo Hospital and a small
number at the Veterans
Hospital. Most of the Intravascular Ultrasonographic
Studies (IVUS) are done at
San Lucas Hospital in Ponce and a smaller number,
at the San Pablo Hospital,
Damas Hospital and Pavia
Heart Center.
A Heart Transplant Program is conducted
at the Cardiovascular Center of Puerto Rico, and
by July 2009, 117 heart transplants have been performed. Percutaneous valvuloplasty and percutaneous closure of septal defects are performed only
at the Cardiovascular Center. Percutaneous carotid interventional procedures are done at the Cardiovascular Center, Puerto Rico Medical Center, in
Manatí, Veteran’s Hospital and in Damas Hospital.
Percutaneous atherectomies for peripheral arterial
disease are performed at the Cardiovascular Center, Manatí, Damas Hospital and Menotita Hospital.
Medical Human Resources
The number of well trained cardiovascular
physicians practicing in Puerto Rico including all
the subdivisions of cardiology has increased significantly in our island mainly in the last 15 years.
These are four medical schools accredited
by the ACGME in Puerto Rico. Table 6 reveals
the number of medical graduates of each medical
school in Puerto Rico during the years 2008 and
2009. Besides these physicians there is an inflow
of Puerto Rican graduates mainly from Dominican
Republic, México and Spain.
In 2008 in Puerto Rico there are 19 cardiovascular surgeons; five (one retired) pediatric cardiovascular surgeons; 18 pediatric cardiologists,
three of which are interventional pediatric cardiologists; six electrophysiologists (four (4) Puerto Rican
electrophysiologists are in the Unites States); 16 interventional radiologists; and at least to 30 or more
cardiologists that do angioplasties. At least two (2)
interventional cardiologists and one electrophysiologists are expected to return to Puerto Rico on July
2009.
Cardiovascular Postgraduate Training
In the academic year 2008-2009 there are
only two ACGME accredited adult cardiovascular
postgraduate three years training programs in Puerto Rico. One at the Section of Cardiology of the
Department of Medicine of the University of Puerto
Rico (four (4) positions of fellows per year) and the
other accredited adult program is at the VA Hospital
(two positions per year). Two hundred and fifty eight
adult cardiologists have been trained in Puerto Rico
since 1954.
There are no accredited programs in Puerto Rico for training in cardiac surgery nor pediatric
cardiology. These are no programs for the added
competencies of electrophysiology and interventional cardiology. Three Puerto Rican cardiologists
have received additional training in heart failure and
heart transplantation in the Unites States. Our reality is that at present young physicians in Puerto Rico
interested in obtaining training in cardiac surgery,
Table 5. Invasive Cardiovascular Procedures performed in Puerto
Rico (2008)
Table 6. Medical Graduates from the LCME accredited Medical
Schools in Puerto Rico (2008 and 2009).
pediatric cardiology, electrophysiology, interventional cardiology and on congestive heart failure-heart
transplant programs must do so abroad principally in
the United States.
Continuing Cardiovascular Education
The availability of continuing cardiovascular
education is vital in order to insure that our local cardiac physicians are up to date with advances in the
cardiovascular field for the benefit of their patients.
Annual continuing cardiovascular medical
education programs are sponsored by the Puerto
Rico Society of Cardiology, the Puerto Rico Chapter
of the American College of Cardiology and the Section of Cardiology of the School of Medicine of the
University of Puerto Rico which help to keep our local
cardiac physicians ahead in the advances in the cardiovascular field. The fellows in tra ining frequently
present scientific papers in these meetings.
The cardiac fellows, receiving training in PR
every year, attend either the annual meeting of the
American Heart Association or the annual meeting of
the American College of Cardiology. Some of them
spend some elective time at well known academic
centers in the US.
13
DISCUSSION
The life expectancy at birth has consistently
increased in Puerto Rico in the last 60 years. In the
last 50 years there has been an increase in the number of persons suffering from cardiovascular disease and heart disease has been the main cause of
death for our population. In Puerto Rico there are 18
institutions in which heart catheterization studies are
performed Fig .4 illustrates the localization of these
centers in Puerto Rico.
There are eight institutions in which medical
and surgical interventional procedures such as cardiac surgery, cardiac catheterization and angioplasties are performed. We have presented the number
of invasive medical and surgical procedures carried
on in Puerto Rico during the year 2008. The institutions involved and their location have been included for the practicing physicians. The data presented was obtained from the staff and members of the
institutions concerned. The leading causes of death
in Puerto Rico in 2004 (latest data available) have
been included. Causes of death in 2005 are being
verified.
The cardiovascular medical resources available in Puerto Rico are listed.
Prevalence information data obtained by the
BRFSS in the last few years in Puerto Rico has been
included with tables provided by Dr. Ruby Serrano
from the Department of Health. The Cardiovascular
continuing medical education activities available in
Puerto Rico are presented.
The quality service rendered to cardiovascular patients in 2008 in Puerto Rico is possible due to
the presence of up to date well trained cardiovascular physicians. We feel confident in stating that today
our patients do not have to abandon Puerto Rico in
order to obtain excellent cardiovascular services as
practically all services are properly provided in our
island.
Salient findings concerning health practices,
risk factors and behaviors linked to cardiovascular disease in Puerto Rico obtained in the Behavioral Risk
Factor Surveillance Study are summarized. Information regarding adult postgraduate cardio vascular training opportunities in Puerto Rico as well as information concerning the number of cardiologists trained at
different local institutions have been presented.
REFERENCES
1.
García-Palmieri, MR. Status of Cardiovascular Disease in Puerto Rico. PR Health Sci J 2004; 23:35-38.
2.
García-Palmieri, MR. Evidence Based Secondary
Prevention of Coronary Artery Disease in the Elderly – 2006.
PR Health Sci J 2006; 25: 221-232.
3.
García Palmieri, MR. Update on Cardiovascular Disease in Puerto Rico in 2007. Bol Asoc Med PRico 2007;
99:199-204.
4.
Informe Anual de Estadísticas Vitales de Puerto
Rico 2005. Departamento de Salud, Secretaría Auxiliar de
Planificación y Desarrollo, San Juan, PR. Julio del 2008.
5.
Serrano R. Personal communication (2008) concerning official available BRFSS data from Puerto Rico.
6.
García-Palmieri MR, Costas R Jr, Schiffman J, Colón AA, Torres R, Nazario E. Interrelationship of serum lipids
with relative weight, blood glucose
and physical activity.
Circulation 1972; 5:829-836.
7.
García-Palmieri MR, Costas R Jr, Cruz-Vidal M,
Sorlie PD, Havlick RJ. Increased physical activity: a protective factor against heart attacks in Puerto Rico. Am J Cardiol
1982; 50:749-755.
8.
Crespo CJ, García-Palmieri MR, Pérez-Perdomo R,
McGee DL, Smit E,
Sempos CT, Lee IM, Sorlie PD.
The relationship of Physical Activity and
Body Weight
with all cause-mortality. Results from the Puerto Rico Heart
Program. Ann Epidemiol 2002; 12:543-552.
9.
World Health Report 2002: Reducing risks, promoting healtly life. Geneva. World Health Organization 2002.
Acknowledgement
Our gratitude is expressed to Dr. José Novoa Hernández,
from the Cardiovascular Center of Puerto Rico; to Dr. Orlando Rodríguez Vilá from the Auxilio Mutuo Hospital; Dr. Marcos Velázquez, from Mayagüez; Dr. Ernesto Soltero from
Damas Hospital; Dr. Rafael Rodríguez Servera, from Pavia
Hospital; Dr. Emilio del Toro, from San Lucas Hospital; Dr.
José Rivera del Rio, from San Pablo Hospital and Dr. Luís
Rodríguez-Ospina from the Veterans Administration for providing us the data from their institutions.
RESUMEN
Se presenta información reciente (2004-2008) sobre las estadísticas poblacionales y la ocurrencia de las enfermedades cardiovasculares en Puerto Rico. Se incluye información complementaria sobre la esperanza de vida al nacer, la muerte por causas especificas y las causas mas
frecuentes de muerte en Puerto Rico al 2004 que es la información más reciente disponible. Se
incluyen los centros de cateterismo en Puerto Rico más las instituciones donde se efectúan procedimientos médicos y quirúrgicos intervencionales y las cifras de estos procedimientos del año 2008.
Se presenta, información reciente sin publicar, sobre prevalencia de algunos factores de riesgo en
las enfermedades cardiovasculares, con datos obtenidos mediante el Estudio de Vigilancia de Factores de Riesgo, realizado por el Departamento de Salud junto al Communicable Disease Center
de Atlanta, Georgia conocido por el BRFSS. Se incluyen datos sobre los programas de educación
postgraduada cardiovascular acreditados disponibles en Puerto Rico, y las actividades de educación cardiovascular continuada que se celebran en Puerto Rico.
14
ABSTRACT
The traditional diagnosis of myocardial infarction relies primarily within the exhibited
patient’s clinical presentation, electrocardiographic changes, and elevation in cardiac
markers. Since the clinical presentation can
be highly variable and EKG changes are not
readily present for all patients, the use of markers of cardiac injury to support the diagnosis
of myocardial infarction has become a fundamental part of the evaluation of a patient with
suspected acute coronary syndrome. In 2007
the Joint European Society of Cardiology/
American College of Cardiology Committee
for the Redefinition of Myocardial Infarction
concluded that the main criteria for myocardial infarction should be a rise or fall of cardiac
biomarkers (namely cardiac troponins and
CK-MB) along with: (1) ischemic symptoms,
(2) ischemic changes in EKG, (3) Q waves in
EKG, or (4) imaging evidence of loss of myocardial viability or (5) wall motion abnormalities. These changes have increased search
interests for more sensitive and specific markers of acute myocardial injury; furthermore,
dedicated research has commenced in order
to specifically allocate markers that could even
predict myocardial ischemia. Therefore this
article will review traditional employment of
cardiac markers, providing current insight, information and experimental data with respect
to emerging markers of myocardial ischemia.
Index words: cardiac, biomarkers, acute, coronary syndrome
Cardiac
Biomakers For
The Evaluation
Of Acute
Coronary
Syndrome
Luis F. Rodriguez-Ospina MD*
Claudia P. Rosales-Alvarez MD*
Alejandro Lopez-Mas MD*
From the *Cardiology Section, Department of Medicine, VA Caribbean Healthcare System, Puerto Rico.
Address correspondence to: Luis F. Rodriguez-Ospina,
MD FACC; Cardiology Section, VA Caribbean Healthcare System, One Veterans Plaza, #10 Casia Street,
00927-3201. E-mail address: Luis.F.Rodriguez-Ospina@med.va.gov
W
w
INTRODUCTION
ithin the United States alone, more
than eight million patients are evaluated at numerous emergency departments each year having
chest pain complaints, with over one third of these
patients being admitted and diagnosed with Acute Coronary Syndrome (ACS) (1). The traditional
diagnosis of myocardial infarction relies primarily
within the exhibited patient’s clinical presentation,
electrocardiographic changes, and elevation in
cardiac markers. The clinical presentation can be
highly variable as EKG changes are not readily
present for all patients; therefore, there is an increased tendency to rely primarily with the employment of markers of cardiac injury to support the
diagnosis of myocardial infarction. This approach
was best manifested within the Universal definition of myocardial infarction (2), when in 2007 a
task force of ESC/ACCF/AHA/WHF members met
to undertake the task of redefining the terminology
associated with myocardial infarction.
15
In accordance with new definitions, the
main criteria for myocardial infarction were constituted as a detected rise or fall of cardiac biomarkers (namely cardiac Troponin and CK-MB).
It was defined that at least one value above the
99th percentile of the upper reference limit met the
criteria, along with displaying at least one of the
following events, described as (1) ischemic symptoms, (2) ischemic changes in EKG, (3) Q waves
in EKG, or (4) imaging evidence of loss of myocardial viability or (5) wall motion abnormalities.
Subsequent definitions divided myocardial infarction in different types, dictated primarily by noted
precipitating events. Accordingly, these changes
have increased search interests for more sensitive
and specific markers of acute myocardial injury;
furthermore, dedicated research has commenced
in order to specifically allocate markers that could
even predict myocardial ischemia.
When adjusted to relative risk regardless of CPK
value, elevated CK-MB was associated with a
25% to 49% increased relative risk of primary endpoints.
Cardiac troponins:
The troponin complex consists of three
subunits that serves to regulate the calcium mediated contractile process of striated muscle. The
complex includes troponin C, which binds Ca2+;
then, troponin I (TnI), which binds to actin and inhibits actin-myosin interactions; and finally, troponin T (TnT), which binds to tropomyosin, thereby
attaching the troponin complex to the thin filament
(6). The cardiac complex configuration of these
proteins are products of specific genes, therefore,
their constitution are unique for the heart (7). The
cardiac isoforms of cTnI and cTnT have additional
unique N-terminal amino acid sequences, allowing
This article will review traditional employ- for specific antibody and assay development and
ment of cardiac markers, providing current insight, detection of each component within the bloodsinformation and experimental data with respect to tream. The diagnostic utilities of cTnI and cTnT
emerging markers of myocardial ischemia.
are comparable (8).
CK-MB:
Troponins usually begin to rise within a period of two to three hours after the onset of MI, and
Creatine kinase is the enzyme that cataly- remain elevated for up to ten days. Following the
zes conversion of creatine and ATP to phospho- two to three hours period after presentation, up to
creatine, subsequently acting as an energy reser- a total of 80 percent of patients with AMI will show
voir. Creatine kinase isoenzymes are dimers of these elevations (9). In addition to AMI, there are
M and B chains, and constituted by three combi- other conditions that may cause elevations in carnations: MM, MB, and BB. CK isoenzyme activity diac troponins, amongst those included one could
is distributed within a wide range of organ tissues find heart failure, pulmonary embolism, myocar(3). The amount of CK-MB fractional quantities ditis, trauma, or electrical cardioversion. These
found within the heart have been detected to be troponins may also be elevated in patients with
at higher percentages, once compared with most diagnosed renal failure. Accordingly, given the
other organ tissues. CK-MB has high specificity wide range of variants, the elevations in cardiac
for cardiac tissue, labeled as the preferred marker troponins will have to be evaluated in context with
of cardiac injury for many years (4). There is a no- other clinical findings displayed by the patient.
ted increase in CK-MB levels following a period of
two to three hours after a myocardial infarction, re- The Joint European Society of Cardiology/
maining at an elevated stage for up to 48 hours.
American College of Cardiology Committee for the
Redefinition of Myocardial Infarction recommen
The clinical utility as a prognostic tool for ded that an increased concentration of cardiac
this particular marker was evaluated in a research troponin be defined by means of a measurement.
study by Galla and colleagues, who employed It was determined that such measurement was exdata evaluated for 25,960 patients from the GUS- ceeding the 99th percentile of the distribution of
TO IIb, PARAGON A and B, and PURSUIT trials, cardiac troponin concentrations within the referenall of them combined (5). Patients evaluated ce group, and recommended a total imprecision
had a diagnosis of NSTEMI and Unstable angi- (coefficient of variation) at this decision limit of
na as primary diagnosis, presenting elevated CK- 10% (2). The coefficient of variation is a statistical
MB despite normal values of CPK. The primary measure of variations in results with data series
outcomes were 180 days myocardial infarction around the mean. Given that most normal subor death. The analysis showed that patients with jects have very low troponin levels, the value exnormal CK-MB, displaying either normal or ele- ceeding the 99th percentile will also be very low;
vated CPK had a 14.9% and 14.5% rate of pri- and at these levels, troponin assays are imprecimary end point respectively, versus patients with se, therefore, unable to meet both requirements.
elevated CK-MB with either normal or elevated Having a CV over the 10% value would mean
CPK, who had 20.8% and 18.2%, respectively. that results may be inaccurate by more than 10%
16
at very low troponin levels, making this measurement unreliable.
There are multiple cardiac troponin I assays
and only one troponin T assay, all of them with
different sensitivities, specificities and cut-off values. This occurs because there is no standardization. Variability results from the presence of modified cardiac troponins within the patient’s serum,
and variations in antibodies developed against
different products of cardiac troponin degradation
(10). Since most normal subjects have undetectable values of cardiac troponins, the value to meet
the requirements of the joint ESC/ACC committee
is very low and available assays are imprecise at
these low levels. The issue was addressed by a
research study performed by Panteghini, et al., in
2004, in which the majority of available assays were
compared (11). Pools of human serum containing
different cardiac troponin concentrations around
the MI decision limit were assessed to identify the
lowest concentration associated with a 10% CV.
Of the eleven assays that were compared in the
study none were able to meet with the 10% precision profile at the 99th percentile limit defined by
the manufacturer. In order to reach 10% precision
profile, the Tn levels considered abnormal would
have to be raised to a value slightly higher than
the 99th percentile at the expense of sensitivity of
the assays.
manufacturer, validation studies were warranted.
The prognostic value of troponin I assays has been
evaluated in multiple trials including the TIMI III-B
trial. The results measured the mortality rate at 42
days according to the baseline level of cardiac troponin I measured in patients with unstable angina
or non-Q wave myocardial infarction in over 1400
patients. There was a progressive risk increase
with higher troponin I levels (15).
Both clinicians and laboratory investigators
have supported that turnaround times for troponin
results should be less than 60 minutes, given the
fact that time to appropriate treatment strongly
affects the prognosis in patients with acute coronary syndromes (16). For this reason efforts are
being made to make the process of cardiac troponin measurement faster. This lead to the introduction of point of care troponin assays with which the
sample could be taken at bedside, with feasible
results available within minutes. A study published within the Journal of Academic Emergency
Medicine (17) compared the use of point of care
troponin I assay versus a central troponin I assay,
demonstrating a decreased time to anti-ischemic
therapy, although there was no difference in outcomes or length of stay. Efforts are being made to
include this modality of testing in chest pain center
protocols and some hospitals, including the SJVA
Medical Center, institution that implemented performance measures regarding time to report tro
There is currently only one troponin T as- ponin results. The goal is that over 90% of the
say available. A large multicenter study that in- patients evaluated at the ED have troponin results
volved 1105 patients, the third generation TnT as- within 60 minutes. Point of care Troponin may be
say showed both an improved imprecision profile the solution to meet these goals.
and a lower detection limit than previous generation troponin T assays. A detailed sensitivity for High sensitive CRP (hsCRP):
cTnT was examined using cut off values for cTnT
from 0.01–0.1 mg/l. Reduction in the cut off vaC-reactive protein (CRP) is the best chalue resulted in improvement in sensitivity but loss racterized
of the currently available inflammatory
of specificity, with optimal trade off in the range
biomarkers.
It is an acute phase reactant produof 0.04–0.06 mg/l (12). The prognostic value of
ced
in
smooth
muscle cells within human coronary
this assay has also been evaluated in several stuarteries
expressed
preferentially in diseased vesdies. One example is the GUSTO-IV trial, which
sels.
The
proposed
mechanism of the ability of
included 7,800 patients with unstable CAD from
CRP
to
predict
myocardial
damage is as a marker
458 centers in 24 countries during 1999 and 2000.
of
endothelial
dysfunction
(18).
CRP is responsible
An Increase in TnT levels was associated with inof
up-regulation
of
several
inflammatory
mediators
creased mortality, from 1.1% in patients with levels
such
as
tissue
factor,
complement
cascade,
and
inside the first quartile to 7.4% in patients with leexpression
of
adhesion
molecules.
Another
propovels in the fourth quartile at 30 days (13). Similar
results were shown in the FRISC study with over sed mechanism of action is down regulation of nitric oxide and angiogenesis mediators. More than
900 patients (14).
20 prospective epidemiologic studies demonstrate
In contrast, there is a large variety of tro- that hsCRP is an independent predictor of risk of
ponin I assays available in the market. All these myocardial infarction (MI), stroke, peripheral arteassays have proven sensitivity; however, they rial disease, and sudden cardiac death.
also have different cutoff values and imprecision
variables (11). Since most assays are not able There has been conflicting evidence reto meet the new definition of MI standards of CV garding the capacity of hsCRP to predict adver< 10% with the cutoff values assigned by the se outcomes in hospitalized patients with ACS.
17
A sub-study of the GUSTO IV trial with over 7000
patients had hsCRP measured at admission. Mortality and AMI at 30 days were measured on different quartile values of hsCRP. The study showed
that increasing levels of this marker had statistically significant correlation with mortality that was
2.0%, 3.3%, 3.9%, and 6.3% (p< 0.001). This
relationship was not observed with 30-day risk of
new MI (14). In contrast, the recent RISCA trial
enrolled 1210 patients and measured CRP on admission, at discharge and 30 days after admission
on patients with ACS to predict outcomes at one
year. Initial data evaluation showed statistically
significant relationship between CRP levels on
admission and death at one year, but this effect
disappeared after adjusting for common clinical
variables (19).
Myeloperoxidase:
Serum Amyloid A:
Most recent studies evaluating MPO as a
marker of cardiac injury evaluated its goal as a risk
assessment tool. The EPIC-Norfolk study evaluated baseline levels of MPO in over 3300 healthy
subjects after an eight-year follow up (27). The
study was designed to compare baseline MPO
levels in case subjects (n=1,138), which were
patient that developed ACS during the eight year
follow up period versus matched control subjects
(n=2,237) who were free of disease after follow up.
Results showed significantly higher levels of MPO
in control subjects. Risk of future CAD showed an
increasing trend toward higher quartiles of MPO
concentration with an odds ratio of 1.49, when
comparing the higher versus the lower quartile
(p<0.001). In the CAPTURE trial MPO concentration was measured in 1090 patients with ACS with
a six-month follow up period with primary end points of myocardial infarction and death (28). The
study showed that patients with MPO serum levels
above the cutoff value of 350 mcg/L had an increased cardiac risk (HR: 2.25, p=0.003). This study
was remarkable in that MPO was able to identify
at risk patients with negative troponin T (HR: 7.45,
p=0.001). After multivariate adjustment MPO was
an independent predictor of adverse outcomes at
a six month follow up (HR: 2.11, p=0.008).
Serum Amyloid A (SAA) is a family of proteins that is synthesized within the liver as a response to inflammation, stress or injury. They are
similar to CRP, forming part of the acute phase
reactants, in which its employment as a marker
of inflammation has been evaluated in several
studies (20-22). Serum amyloid A replaces apolipoprotein A1 in its relation with HDL, strongly
affecting cholesterol transport to cells (23). It has
been proposed that increased levels of SAA may
decrease the ability of HDL mediated cholesterol
efflux from cells, thereby promoting cholesterol accumulation (24). These observations have lead to
the hypothesis that elevated levels of SAA may be
a marker of atherosclerosis and acute myocardial
injury.
The ability of Serum amyloid A as a marker
of myocardial injury and extent of disease was evaluated by the WISE study (21),were plasma levels
of both SSA and CRP were taken from 705 women
referred for coronary angiography undergoing evaluation for myocardial ischemia. This study found
that both SAA and CRP were independently predictive of adverse cardiovascular outcomes, but
that SAA was also independently and moderately
associated with angiographic CAD with statistical
significance (p<0.001). This predictive outcome
was not observed with CRP. Another study performed in Japan (22) compared the ability of SAA v/s
CRP to predict adverse outcomes after a NSTEMI
or unstable angina in 277 patients. They measured both markers and divided the patients in four
groups: +CRP/-SAA, +CRP/+SAA, +SAA/-CRP
and –SAA/-CRP and primary end points were death, re-infarction or urgent revascularization at 30
days. The study showed that regardless of CRP
elevation, elevated SAA was associated with increased likelihood of adverse outcomes with statistical significance (p<0.05).
18
Myeloperoxidase (MPO) is an enzyme that
promotes oxidative reactions as well as activating
the inflammatory cascade. It is contained in macrophages and neutrophils, as these MPO rich
cells have been associated with atheromatous
plaque instability (25). Proposed mechanisms of
action include modulation of nitric oxide metabolism and metalloprotease activation (26). They
promote the generation of reactive nitrogen species and free radicals with resultant oxidative modification of LDL and destabilization of the atheromatous plaque. For these reasons interest has
emerged in exploring myeloperoxidase potential
as a marker of cardiac injury and for prognostic
considerations.
Brain Natriuretic Peptide
Brain natriuretic peptide (BNP) is a hormone
that is synthesized and released from the cardiac
ventricles in response to increased wall stress or
dilation (29). Some of the actions that have been
attributed to this hormone include inhibition of
sympathetic activity, inhibition of the RAAS axis,
and natriuresis (30). Patients with Heart failure
usually exhibit increasing levels of this hormone
according to the degree of ventricular dysfunction.
The original particle produced is called pro-BNP
and it is cleaved into BNP and amino terminal proBNP (NT-proBNP). Both of these products can
be measured by different assays; and their ability
as prognostic indicators after an acute coronary
event has been the subject of many clinical investigations.
One example is a sub study of the OPUS
TIMI-16 trial performed by De Lamos, et al. (31),
where BNP was measured from the samples taken
at a mean time of 40 hrs after onset of ischemic
symptoms for 2,525 patients with ACS. The levels of BNP were correlated with the risk of death,
heart failure and MI at 30 days and ten months.
Study results showed a proportional correlation
between risk of death and increasing quartile values of BNP (p<0.001). The association remained
when patients with U/A, NSTEMI or STEMI were
evaluated separately and after adjustment for independent predictors. This correlation was also
observed for the primary end points of myocardial
infarction and worsening CHF at ten months with
(p<0.01 and p<0.001 respectively). Similar results
were obtained when NT-proBNP was measured in
samples taken at a median of 9.5 hrs from onset of
symptoms in 6,809 patients with ACS in a sub study from the GUSTO-IV trial (32). Increasing quartiles NT-proBNP levels were related with increasing
risk of death with a mortality of 1.8%, 3.9%, 7.7%,
and 19.2% respectively at 1 year (p<0.001).
Ischemia Modified Albumin:
The N-terminal region of human albumin
is composed of an amino acid sequence that has
been showed to be the binding site of several transition metals (33). Changes in the albumin terminal region have been proven to alter binding of
these metals. This relation has been most extensively studied with cobalt (33-34) and an assay
measuring the albumin cobalt-binding (ACBTM)
test was developed (Ischemia Technologies, Inc.,
Denver, CO). It has been described that changes
immediately following myocardial ischemia, such
as tissue hypoxia, acidosis and free radical production affect albumin cobalt binding, reason for
which this assay has been proposed as a tool for
early detection of myocardial ischemia (34-36).
Christenson, et al., published a meta-analysis that involved all the publications regarding Ischemia Modified Albumin (IMA) on the American
Heart Journal in 2006 (37). Eight publications with
a total of over 1,800 patients met the inclusion
criteria. The results of this study suggested that
IMA had better sensitivity and negative predictive
value than TnT, EKG or the combination of these
two. They also evaluated a triple prediction test,
which was defined as no EKG changes, negative troponin T and negative IMA. Sensitivity and
NPV for acute ACS were 94.4% and 97.1% and,
for longer-term outcomes, were 89.2% and 94.5%,
respectively. This results lead to the conclusion
that the IMA may be used as a “rule out” tool for
earlier disposition of patients with ACS. A large
multicenter trial for validation of these findings was
being conducted, but it was suspended before
completion.
Lipoprotein Associated Phospholipase
A2:
Lipoprotein associated phospholipase A2
(Lp-PLA2) is an enzyme that hydrolizes phospholipids in LDL particles into fatty acids and lysophosphatidylcholine. These products in turn mediate the recruitment of inflammatory mediators
via stimulation of expression of adhesion molecules and cytokines (38). These mediators mature into apoptotic foam cells once in the intima
of affected vessels, perpetuating a self promoting
cycle of inflammation by producing more Lp-PLA2
(39). There has been work showing a relationship between coronary endothelial dysfunction and
increased levels of this particular enzyme, as well
as its presence in the fibrous thin cap of atherosclerotic plaques that are prone to rupture (39-40).
These observations have lead to increased interest in this enzyme as a potential marker for the
risk of myocardial ischemia and its main advantage would be that it may be able to identify the
potential patients before the acute coronary event
occurs.
The utility of Lp-PLA2 as a risk marker has
been evaluated in multiple published trials. A recent review from Marshal, et al. (41), evaluated
over 25 studies published between 2000 and 2007.
The evidence showed a consistent association of
increasing levels of Lp-PLA2 when comparing the
lower quartile levels versus the highest quartile;
with doubling the risk of cardiovascular disease.
These results were maintained after adjustment for
risk factors, lipids and high-sensitivity C-reactive
protein. These results support the addition of this
marker to traditional risk factor assessment. Patients presenting with elevation in this marker may
benefit further from more aggressive lipid lowering
therapy. Currently there are several ongoing trials
measuring LP-PLA2 levels after more aggressive
lipid lowering therapy, but the prognostic significance of this intervention is still unknown (41).
The multi-marker approach:
Coronary artery disease has a multifactorial
etiology. Attempts have been made to estimate
the risk of patients for developing an acute coronary event. The classically used risk scores have
depended on risk factors such as age, comorbid
conditions, smoking history and previous history
of CAD or its equivalents.
19
With the continuous emerging of new substances that may predict the likelihood of developing CAD or an ACS, there is increasing interest
in finding the perfect marker for cardiac injury. Recently, there have been multiple investigations regarding the validation of previously used and new
cardiac biomarkers as risk stratification tools and
as markers of acute ischemia. Since the perfect
cardiac marker has yet to be found, there are published and ongoing investigations evaluating the
use of combinations of several biomarkers for better prediction of cardiac risk (42).
The results showed that patients with elevated cardiac marker scores had an increased risk of
death, but when this was added to traditional risk
factor assessment there was no statistical significance. Shlipak, et al., obtained similar results in the
Cardiovascular Health Study where measurement
of six biomarkers failed to increase association with
the rate of cardiovascular death in the Cohort (46).
Conclusion:
The theme of cardiac biomarkers has been
extensively investigated and this trend will continue
Several studies have shown promising re- until better biomarkers or their combinations are
sults regarding the combination of several biomar- described. The data reviewed is only a small samkers for better prediction of cardiac risk. In a study ple of all available information regarding this theme
by Sabatine, et al., baseline levels of Troponin I, of discussion. The information has to be evaluaCRP and BNP were taken from 450 patients pre- ted thoroughly since there are several important disenting with ACS from the OPUS-TIMI 16 trial (43). fferences in the patient selection criteria, methods
Results showed that elevations in each of these and statistical analysis within the studies evaluated.
markers were independent predictors of the end More multi-center, randomized, prospective trials
points of death, MI or CHF. When the risk was ca- will be needed for employment of new tools to be
tegorized on the basis of elevated biomarkers, the considered for inclusion to guidelines for diagnosis
addition of each biomarker nearly doubled the risk or risk stratification of coronary artery disease. In
of each of the end points both at 30 days and 10 the meantime, this theme will continue to receive
months (p=0.01). A validation study using 1,635 much attention since it has shown promising data
patients from the TACTICS-TIMI 18 study showed and maybe a panel composed of multiple biomarthat patients with one, two or three elevated bio- kers may guide in the near future therapeutic opmarkers had a 2.1 (p=0.006), 3.1 (p=0.001) and tions. More will remain to be discovered with future
3.7 (p=0.001) fold increase in the risk of the same research and trials.
endpoints at six months. A recent study published in 2008 by Zethelius et al using data from the REFERENCES
ULSAM study, took baseline samples of Troponin
I, NT-proBNP, Cystatin c, and CRP from 1,135 1)
Storrow AB, Gibler WB. Chest pain centers: diagpatients (44). After adjustment for traditional risk nosis of acute coronary syndromes. Ann Emerg Med
factors, all of the measured biomarkers predicted 2000;35:449–61
Thygesen K, Alpert JS, White HD; Joint ESC/ACCF/
risk of death from cardiovascular causes. Hazard 2)
AHA/WHF Task Force for the Redefinition of Myocardial Inratios for different combinations of elevated bio- farction. Universal definition of myocardial infarction. Circumarkers in the whole cohort showed that partici- lation. 2007;116:2634–2653.
Roberts R, Gowda KS, Ludbrook PA, Sobel BE;
pants who had elevated levels of any two of the 3)
Specificity
of elevated serum MB creatine phosphokinase
biomarkers had a risk of death from cardiovascuactivity in the diagnosis of acute myocardial infarction. Am J
lar causes that was increased by a factor of more Cardiol 1975 Oct 6;36(4):433-7.
than 3 (P<0.001). When the patients had elevated 4)
Adams, JE 3rd, Abendschein, DR, Jaffe, AS. Biolevels of any of the three biomarkers or of the four chemical markers of myocardial injury. Is MB creatine kinase
biomarkers, the risk of death was increased by a the choice for the 1990s? Circulation 1993; 88:750.
Galla, JM, Mahaffey, KW, Sapp, SK, et al. Elevafactor of more than 7 and more than 16 respecti- 5)
ted creatine kinase-MB with normal creatine kinase predicts
vely (p<0.001).
worse outcomes in patients with acute coronary syndromes:
There have also been studies that show no
difference between using multiple biomarkers versus the traditional risk factors. A study published
by Wang, et al., measured the levels of ten biomarkers of 3,209 patients that attended an examination for the Framingham Heart Study (45).
The markers measured were: C-reactive protein,
B-type natriuretic peptide, N-terminal pro–atrial
natriuretic peptide, aldosterone, renin, fibrinogen,
D-dimer, plasminogen-activator inhibitor type 1,
homocysteine; and the urinary albumin-to-creatinine ratio.
20
results from 4 large clinical trials. Am Heart J 2006; 151:16.
6)
Cardiovascular Biomarkers: Pathophysiology and
Disease Management. Totowa, NJ, Humana Press, 2006, p
29.
7)
Allan S Jaffe, MD; Troponins, creatine kinase, and
CK isoforms as biomarkers of cardiac injury. www.uptodate.
com
8)
Melanson S, Tanasijevic M, Jarolim P; Cardiac Troponin Assays: A View From the Clinical Chemistry Laboratory: Circulation 2007;116;e501-e504
9)
Macrae, AR, Kavsak, PA, Lustig, V, et al. Assessing
the requirement for the 6-hour interval between specimens
in the American Heart Association Classification of Myocardial Infarction in Epidemiology and Clinical Research Studies. Clin Chem 2006; 52:812.
10)
Labugger, R, Organ, L, Collier, C, et al. Extensive ventricular remodelling. Eur Heart J 2003;24:2180–2185.
troponin I and T modification detected in serum from pa- 27)
Meuwese MC, Stroes ESG, Hazen SL, et al. Serum
tients with acute myocardial infarction. Circulation 2000; myeloperoxidase levels are associated with the future risk
102:1221.
of coronary artery disease in apparently healthy individuals.
11)
Panteghini, M, Pagani, F, Yeo, KT, et al. Evaluation The EPIC-Norfolk prospective population study. Journal of
of imprecision for cardiac
the American College of Cardiology. 2007;50(2):159–165.
troponin assays at low-range concentrations. Clin Chem 28)
Baldus S, Heeschen C, Meinertz T, et al. Myelope2004; 50:327.
roxidase serum levels predict risk in patients with acute co12)
P O Collinson, P J Stubbs, A-C Kessler, for the Mul- ronary syndromes. Circulation. 2003;108(12):1440–1445.
ticentre Evaluation of Routine Immunoassay of Troponin T 29)
Valli N, Gobinet A, Bordenave L. Review of 10 years
study (MERIT). Heart 2003;89:280–286.
of the clinical use of brain natriuretic peptide in cardiology. J
13)
James, SK, Armstrong, P, Barnathan, E, et al. Tro- Lab Clin Med. 1999;134:437–444.
ponin and C-reactive protein have different relations to sub- 30)
Stein BC, Levin RI. Natriuretic peptides: physiology,
sequent mortality and myocardial infarction after acute co- therapeutic potential, and risk stratification in ischemic heart
ronary syndrome: a GUSTO-IV substudy. J Am Coll Cardiol disease. Am Heart J 1998;135:914-23.
2003; 41:916.
31)
James A. de Lemos, David A. Morrow, Jane H. Bent14)
Lindahl, B, Venge, P, Wallentin, L. Relation between ley et al. The Prognostic Value of B-Type Natriuretic Peptide
troponin T and the risk of subsequent cardiac events in uns- in Patients with Acute Coronary Syndromes. N Engl J Med
table coronary artery disease. The FRISC study group. Cir- 2001;345(14):1014-1021.
culation 1996; 93:1651.
32)
James, Stefan K; Lindahl, Bertil; Siegbahn, Agne15)
Antman, EM, Tanasijevic, MJ, Thompson, B, et al. ta et al. N-Terminal Pro-Brain Natriuretic Peptide and Other
Cardiac-specific troponin I levels to predict the risk of morta- Risk Markers for the Separate Prediction of Mortality and
lity in patients with acute coronary syndromes. N Engl J Med Subsequent Myocardial Infarction in Patients With Unstable
1996; 335:1342.
Coronary Artery Disease: A Global Utilization of Strategies
16)
Fred S. Apple, Robert L. Jesse, L. Kristin Newby, To Open occluded arteries (GUSTO)-IV Substudy. Circulaet al. National Academy of Clinical Biochemistry and IFCC tion 2003;108(3):275-281.
Committee for Standardization of Markers of Cardiac Da- 33)
Bar-Or D, Curtis G, Rao N, et al. Characterization
mage Laboratory Medicine Practice Guidelines: Analytical of the Co2+ and Ni2+ binding amino-acid residues of the NIssues for Biochemical Markers of Acute Coronary Syndro- terminus of human albumin. Eur J Biochem 2001;268:42–7.
mes. Circulation. 2007;115:e352-e355
34)
Bar-Or D, Lau E, Rao N, Bampos N, Winkler JV,
17)
Bertrand Renaud, Patrick Maison, Alfred Ngako et Curtis CG. Reduction in the cobalt binding capacity of hual. Impact of Point-of-care Testing in the Emergency De- man albumin with myocardial ischemia. Ann Emerg Med
partment Evaluation and Treatment of Patients with Sus- 1999;34:S56.
pected Acute Coronary Syndromes. Acad Emerg Medicine 35)
McCord J. Oxygen-derived free radicals in post is2008; 15:216–224.
chemic tissue injury. N Engl J Med 1985;312:159–63.
18)
Paul E. Szmitko, Chao-Hung Wang, Richard D. 36)
Cobbe SM, Poole-Wilson PA. The time of onset and
Weisel, John R. de Almeida, Todd J. Anderson, and Subodh severity of acidosis in the myocardial ischemia. J Mol Cell
Verma New Markers of Inflammation and Endothelial Cell Biol 1980;12:745–60.
Activation: Part I. Circulation. 2003;108:1917-1923
37)
Frank Peacock, Deborah L. Morris, Saif Anwaruddin
19)
Bogaty, P, Boyer, L, Serge Simard, et al. Clinical Uti- et al. Meta-analysis of ischemia modified albumin to rule out
lity of C-Reactive Protein Measured at Admission, Hospital acute coronary syndromes in the emergency department.
Discharge, and 1 Month Later to Predict Outcome in Patients American Heart Journal 2006;152(2):253-262.
With Acute Coronary Disease, The RISCA Study. J Am Coll 38)
Macphee CH, Moores KE, Boyd HF et al. LipoproCardiol, 2008; 51:2339-2346.
tein-associated phospholipase A2, platelet-activating factor
20)
Gabay C, Kushner I. Acute-phase proteins and acetylhydrolase, generates two bioactive products during
other systemic responses to inflammation. N Engl J Med. the oxidation of low-density lipoprotein: use of a novel inhibi1999;340:448–454.
tor. Biochem J 1999;338:479–487.
21)
B. Delia Johnson; Kevin E. Kip; Oscar C. Marroquin 39)
Lavi S, McConnell JP, Rihal CS et al. Local producet al. Serum Amyloid A as a Predictor of Coronary Artery Di- tion of lipoprotein-associated phospholipase A2 and lysosease and Cardiovascular Outcome in Women. Circulation. phosphatidylcholine in the coronary circulation: association
2004;109:726-732.
with early coronary atherosclerosis and endothelial dys22)
Masami Kosuge, Toshiaki Ebina, Toshiyuki Ishikawa function in humans. Circulation 2007;115:2715–2721.
et al. Serum Amyloid A is a Better Predictor of Clinical Outco- 40)
Vickers KC, Maguire C, Wolfert RL et al. Quantitames than C-Reactive Protein in Non-ST-Segment Elevation tion and distribution of lipoprotein-associated phospholipase
Acute Coronary Syndromes. Circ J 2007; 71: 186 –190
A2 and oxidized low-density lipoprotein in atherosclerotic le23)
Gunther Marsche, Sǎsa Frank, John G. Raynes et al. sions of carotid endarterectomy tissues. J Am Coll Cardiol
The lipidation status of acute-phase protein serum amyloid A 2006;(suppl A):346A.
determines cholesterol mobilization via scavenger receptor 41)
Marshall A. Corson, Peter H. Jones, and Michael H.
class B, type I. Biochem J. 2007 February 15; 402(Pt 1): Davidson. Review of the Evidence for the Clinical Utility of
117–124.
Lipoprotein-Associated Phospholipase A2 as a Cardiovas24)
Carole L. Banka, Ti Yuan, Maria C. de Beer et al. cular Risk Marker. Am J Cardiol 2008;101[suppl]:41F–50F.
Serum amyloid A (SAA): Influence on HDL-mediated cellu- 42)
James A. de Lemos, M.D., and Donald M. Lloydlar cholesterol efflux. Journal of Lipid Research, Volume 36, Jones, M.D., Multiple Biomarker Panels for Cardiovascular
1995.
Risk Assessment. NEJM 2008;358(20):2172-2174.
25)
Seigo Sugiyama, Yoshikatsu Okada, Galina K. 43)
Marc S. Sabatine, David A. Morrow, Eugene
Sukhova et al. Macrophage Myeloperoxidase Regulation Braunwald Et al. Multimarker Approach to Risk Stratification
by Granulocyte Macrophage Colony-Stimulating Factor in in Non-ST Elevation Acute Coronary Syndromes Circulation.
Human Atherosclerosis and Implications in Acute Coronary 2002;105:1760-1763.
Syndromes; Am J Pathol. 2001 March; 158(3): 879–891.
44)
Zethelius B, Berglund L, Sundström J, et al. Use of
26)
Kameda K, Matsunaga T, Abe N, et al. Correlation multiple biomarkers to improve the prediction of death from
of oxidative stress with activity of matrix metalloproteinase in cardiovascular causes. N Engl J Med 2008;358:2107-16.
patients with coronary artery disease. Possible role for left
45)
Wang TJ, Gona P, Larson MG, et al. Multiple biomarBoletín de la Asociación Médica de Puerto Rico - Volumen 101 Nro. 4 - Octubre - Diciembre 2009
21
kers for the prediction of first major cardiovascular events
and death. N Engl J Med 2006;355:2631-9.
46)
Shlipak MG, Fried LF, Cushman M, et al. Cardiovascular mortality risk in chronic kidney disease: comparison of
traditional and novel risk factors. JAMA 2005; 293:1737-45
RESUMEN
En los Estados Unidos más de 8 millones de personas al año se presentan a una
sala de emergencia con una queja principal
de dolor de pecho y una tercera parte de
esos pacientes son admitidos con un diagnostico final de síndrome coronariano agudo.
Históricamente, el diagnostico de infarto agudo al miocardio es guiado por la presentación
clínica, los cambios electrocardiográficos y la
elevación de marcadores cardiacos. Dado
que la presentación clínica es altamente variable y los cambios electrocardiográficos no
siempre están presentes, se está dando una
tendencia a utilizar marcadores cardiacos
como pieza clave para el diagnostico de infarto al miocardio. Entre los marcadores más
utilizados para evaluar isquemia cardiaca se
encuentran la creatine kinase, el CK-MB y
las troponinas cardiacas. Dado que la nueva definición de infarto al miocardio depende
grandemente de los niveles de las troponinas y/o el CK-MB, muchas investigaciones
tienen como meta encontrar nuevos marcadores noveles y más sensitivos para medir isquemia cardiaca. Este artículo de repaso de
literatura tiene como enfoque dar una idea al
lector sobre los marcadores que hay disponibles hasta el momento y la evidencia que los
respalda
For more information call:
Josephine Gerena or Jose Gerena, MD
(787) 307-3364
or download all forms and information from:
www.asociacionmedicapr.org
ABSTRACT
This is a review article that summarizes
updated information concerning isolated ventricular septal defects (VSD). VSD are one of the
most common congenital heart diseases. It includes anatomic consideration and classification
of the different types of VSD, pathophysiologic
categories, clinical features and diagnostic tools
such as electrocardiography, chest radiography,
echocardiography and cardiac catheterization.
We also reviewed the most important aspects
of the therapeutic management, including surgical indications for correction of ventricular septal
defects.
Key Words: Ventricular septal defects, Ventricular septum, Eisenmenger syndrome.
T
ANATOMIC CONSIDERATIONS
T
he ventricular septum is a complex nonplanar structure that is composed of two main anatomic components, 1- The membranous septum, a
small portion located just beneath the aortic valve
and behind the septal leaflet of the tricuspid valve, and 2- The muscular septum which extends out
from the membranous septum and includes the inlet, trabecular and infundibular or outlet portions.
VSD may occur at various locations in any of these
components (3).
Membranous defects are the most common
variety of VSD, accounting for 75 to 80% of all cases. Rarely limited to the membranous septum,
and more often extending into one of the adjacent
portions of the muscular septum. Membranous
VSD can undergo partial or complete spontaneous
closure by apposition of the septal leaflet of the tricuspid valve, which is seldom accompanied by tricuspid regurgitation, or formation of an aneurysm
of the ventricular septum (4), and less commonly,
by prolapse of an aortic cusp into the defect (5).
Defects in this region are also called paramembranous, perimembranous, subaortic or infracristal.
Ventricular
Septal Defects
Nelson E. Aguilar, MD*
Jose Eugenio Lopez, MD*
*From the Section of Cardiology, Department of Medicine,
University of Puerto Rico School of Medicine and the Cardiovascular Center of Puerto Rico and the Caribbean.
Address reprints requests to: Nelson Aguilar MD, Section of
Cardiology, Department of Medicine, UPR School of Medicine, Puerto Rico Health Science Center, Rio Piedras, PR
00936.
Ventricular septal defects (VSD) are the
second most common morphologic
congenital malformations of the heart
encountered in the pediatric population,
accounting for approximately 20% of all
patients with congenital heart diseases
(1). Prevalence is reported as high as
3.3 to 3.8 per 1,000 life births (2).
ciated with an atrial septal defect as part of a complete AV-canal. They do not close spontaneously.
The infundibular septum is represented by
a small portion of muscle interposed between the
outflow tracts of the left ventricle (LV) and right ventricle (RV). VSD in the infundibular septum account
for approximately 5% of defects in North America,
but are more common (approximately 30%) in Asia
(1). These defects are also called subpulmonic, supracristal or doubly committed defects (when there
is no muscle interposed between the outflow components of the ventricles) (6, 8). Doubly committed
defects are commonly associated with prolapse of
the left and right coronary cusp of the aortic valve
into the RV, with or without aortic regurgitation (8).
Outlet defects rarely close spontaneously.
Muscular defects — The most common type
of muscular defects are within the trabecular septum (10 to 15% of all cases)(6), and vary from small
to large, from single to multiple, to a honeycombed
“Swiss cheese” structure which has the same net
functional effect as a single large defect (1) . Small
muscular defects are prevalent in neonates with
estimates as high as 53/1000 life births, more common in premature infants. Approximately 90% close spontaneously within 1 to 10 months of age (7).
The incidence of spontaneous closure of
VSD varies according to the type of the defect, size
of the defect and whether the defect is solitary or
multiple (9). Multiple VSDs have a strong tendency
to close, but Swiss cheese fenestrations do not close spontaneously. The incidence of closure is estimated at 50 to 75% for restrictive perimembranous
and trabecular VSD (10). Moderately restrictive and
nonrestrictive VSD can also close spontaneously
with an incidence of 10 to 15% (1). Spontaneous
closures occurs most commonly in the first year
Around 5 to 8% of VSD are inlet type. Inlet of life, but has been reported in older children and
defects are seldom isolated, more commonly asso- young adults (11).
23
PATHOPHYSIOLOGY
NATURAL HISTORY
The presence of a VSD in utero has minimal or no effect on the normal cardiac physiology,
the resistances downstream from each ventricle
are equal and there is minimal shunting of blood.
Once the infant is delivered, there is a fall in pulmonary vascular resistance (PVR), while the systemic vascular resistance (SVR) remains high.
This results in a left-to-right shunt.
The natural history of untreated VSD is related to the size of the defect.
·Small VSD: Seventy-five percent undergo spontaneous closure within the first two years
of life. Small VSD that persist into adulthood are
usually benign; most of the patients remain symptom free and have normal life expectancy (14, 15).
Possible complications are bacterial endocarditis
The physiologic effects of VSDs depend (1 to 3%) and aortic regurgitation (2 to 5%) (14,
upon the size of the defect and the PVR (12). 16). Features predictive of a benign course are: - a
These variables change over time and the clini- left-to-right shunt less than 33% (Qp/Qs <1.5), - no
cal manifestations may change accordingly. The- evidence of LV volume overload, - normal PA pressure, - no VSD-related aortic regurgitation (14).
re are four physiologic categories:
·Small (restrictive) defects with high resistance to flow permit only a small left-to-right
shunt. RV pressure remains normal or only minimally elevated; pulmonary artery (PA) pressure
and resistance are normal and there is little increase in LV stroke work.
·Moderate (moderately restrictive) defects
offer resistance to pressure but little resistance
to flow. The RV pressure, PVR, and PA pressure
may remain low or be moderately elevated, the
magnitude of the left-to-right shunt depends primarily upon the size of the defect. This can result
in volume overload of the left chambers, and signs and symptoms of heart failure.
·Large (nonrestrictive) defects offer little
resistance to flow and pressure, the pressures in
the ventricles are equal and they function as a
common pumping chamber with two outlets. The
magnitude of the left-to-right shunt depends on
the relative pulmonary and systemic vascular resistance. As PVR declines, there is a large left-toright shunt that generates increased pulmonary
blood flow, increased pulmonary venous return,
and increased volume load to the LV that culminates in heart failure.
·Eisenmenger syndrome: nonrestrictive
defects with identical right and left ventricular
pressures and suprasystemic pulmonary vascular resistance, hence, predominantly right-to-left
shunt.
In patients with VSD and left-to-right shunt,
LV output must increase to maintain systemic
blood flow at normal levels (13). By convention,
the magnitude of left-to-right shunting is designated by using the ratio of pulmonary to systemic
blood flow (Qp:Qs), a 50% shunt represents a 2:1
Qp:Qs.
24
·Moderate VSD: Usually not detected as
newborn due to the delayed fall in PVR, hence delayed onset of the shunt and murmur; heart failure
develop within the first few months of life. Spontaneous closure may occur, although less frequently
(17, 18). When PA and RV pressures are less than
50% of systemic pressure PVR usually does not
increase, the risk of irreversible pulmonary vascular obstructive disease increases when PA pressure is greater than 50% of systemic pressure (13).
·Large VSD: Infants with these defects
usually develop large left-to-right shunt in the first
few weeks of life, resulting in congestive heart
failure, frequent lower respiratory infections, and
failure to thrive. Unless surgery is performed in
the first year of life, there is increasing likelihood
that elevated PVR will become fixed, preventing
successful repair. When PVR exceeds SVR, the
shunting of blood reverses to a right-to-left shunt
causing cyanosis, a condition called Eisenmenger
syndrome (19), which is a serious and irreversible
medical problem that results in early death.
CLINICAL FEATURES
The clinical presentation may range from
an isolated murmur that is detected incidentally
to severe heart failure (20). The severity of symptoms varies according with the size of the shunt
and the ability of the LV to maintain systemic
output. Signs and symptoms develop when PVR
declines sufficiently to permit significant left-toright shunting.
The typical presentation of a small VSD
in a neonate involves the detection of a cardiac
murmur at four to ten days of life (21). The normal
decline in PVR can be delayed in infants with moderate and large VSD, thus, murmurs may not be
detected until several weeks postnatal (21); heart
failure develops by three to four weeks of age,
including tachypnea (from increased pulmonary
blood flow), tachycardia, poor feeding (appears
hungry but tires easily, sweats with feeds), poor
weight gain or failure to thrive, and diaphoresis,
particularly with feeding (13, 22). If Eisenmenger
syndrome develops, patient becomes cyanotic.
Arterial pulses
Vigorous LV contraction (to compensate for
the left-to-right shunt), is reflected in brisk arterial
pulses; the arterial pulse diminishes as PVR increases. If LV failure develops, the arterial pulse
diminishes and pulsus alternans may be present.
Bounding pulses suggest the development of aortic regurgitation. The arterial pulse in Eisenmenger
syndrome is normal.
Precordial palpation
Infants with small VSD and a large pressure gradient, have a palpable thrill; in moderate or
large defects there is a RV heave as PVR falls and
left-to-right shunt increases. The precordium becomes more active, with prominent apical impulse
as LV output increases to compensate for the leftto-right shunt; the cardiac apex is displaced outside the mid-clavicular line (22). In Eisenmenger
syndrome the hypertensive RV impulse displaces
the LV from the apex and the dilated pulmonary
trunk is palpable.
Auscultation
A well-split second sound (S2) suggests that
the PVR is not markedly increased, as pulmonary
resistance rises the degree of splitting decreases,
the S2 becomes loud and single in Eisenmenger
syndrome (23).
The character and duration of the systolic
murmur is helpful in evaluating the size of the defect (13). A very restrictive VSD is accompanied by
a soft and early systolic decrescendo murmur, since the defect decrease in size or obliterate in late
systole (24). The murmurs in larger defects are
classically 3 to 4/6 harsh, high frequency holosystolic, best heard at the left mid- to lower-sternal
border. During spontaneous closure the holosystolic murmur shortens, occurring only in early systole before disappearing (24). In infants who have
large VSD, as PVR approaches systemic levels,
the holosystolic murmur shortens and softens before disappearing. suggests the development of aortic regurgitation.
Patients with such murmurs require early surgery.
When PVR becomes suprasystemic, the left-toright shunt is abolished and the auscultatory findings are those of pure pulmonary hypertension,
the classic murmur of pulmonary regurgitation
(Graham Steell) becomes evident.
COMPLICATIONS
In addition to pulmonary vascular disease,
complications of VSD may include the development of endocarditis, aortic regurgitation, subaortic stenosis, and RV outflow obstruction.
·Infective endocarditis: Is uncommon, occurring 1 to 3% of patients (26). Surgical closure
reduces the risk, even in patients who have residual defects (27).
·Aortic valve prolapse and regurgitation:
May occur in subpulmonic and subaortic defects,
is more common in boys, has peak onset between
5 and 9 years of age and seldom occurs before 2
or after 10 years, and is associated with increased
risk of infective endocarditis (28).
·Subaortic stenosis: Patients with membranous VSDs can occasionally develop fibrous
or fibromuscular subaortic stenosis (29). The LV
outflow tract obstruction generally is progressive
and there is potential for damage to the aortic valve, recurrence after surgical resection is possible.
·RV outflow obstruction: Patients with
membranous defects may develop hypertrophy of
muscle in the RV infundibulum, which may result
in narrowing of the right ventricular outflow tract
(13). Double chambered RV (DCRV) results when
anomalous bands of muscle divide the RV cavity
into two chambers.
ELECTROCARDIOGRAM
The electrocardiogram (ECG) is influenced
by the size of the VSD, the size of the left-to-right
shunt and the PVR, it does not reflect the anatomic
location of the defect (13). The ECG is normal in
patients with restrictive VSD and normal PA pressure (30); in patients with moderate or large left-toright shunts the ECG shows left atrial enlargement
and LV hypertrophy, with usually normal QRS axis
(30). When the defect is large enough to maintain
elevated RV pressure, the ECG demonstrates bi
A diastolic rumble due to increased flow ventricular hypertrophy, with large equidiphasic RS
across the mitral valve may be heard at the apex complexes. In Eisenmenger syndrome the ECG
in infants with moderate to large VSD and Qp:Qs shows evidence of right atrial enlargement and RV
>2:1 (23, 25). A high-frequency decrescendo mur- hypertrophy. Patients who have undergone surgimur beginning with the first component of S2 and cal closure may develop right bundle branch block
best heard at the mid- to-lower left sternal border (complete or incomplete).
25
CHEST RADIOGRAPHY
The radiographic findings vary depending upon the size of the left-to-right shunt
and the state of the pulmonary vascular bed.
In small defects, the radiograph is usually
normal; in moderate to large defects with increased left-to-right shunts, the pulmonary
vascular markings are increased and the left
atrium, LV, and PA are enlarged. As PVR increases, RV enlargement becomes more
prominent and the LV decreases in size. In
Eisenmenger syndrome the lungs field are
oligemic, the left chambers are normal in size
and the hypertrophied RV occupies the apex,
the cardiac silhouette is unremarkable except
for enlargement of the pulmonary trunk.
ECHOCARDIOGRAPHY
Figure 1: Parasternal long axis view showing a ventricular septal
defect of the membranous septum
Two-dimensional and Doppler transthoracic and transesophageal echocardiography are useful to confirm the diagnosis, to
identify the location of the defect, to establish
the number of defects, to delineate associated anatomic features and to assess the size
and physiologic consequences of the shunt
(31). Three-dimensional echocardiography
enhances the assessment (32).
Membranous VSD are seen in the parasternal long axis view just below the aortic
valve (Figure 1), and beneath the septal leaflet of the tricuspid valve in short axis view
(Figure 2); VSD are usually not seen in the
four chamber view. In muscular defects (Figure 3), color flow mapping from the four
chamber view is crucial for detecting small
VSDs, which can be multiple. Subpulmonary
defects may be difficult to distinguish from
membranous defects in parasternal long axis
view, but they are easily identified beneath
the pulmonary valve in short axis images,
once detected, a careful interrogation of the
aortic valve is crucial to exclude cusp prolapse and aortic regurgitation. Inlet defects and
their characteristic relationship to the atrioventricular valves are best imaged in apical
four chamber view.
Figure 2: Short axis view showing a ventricular septal defect of the
membranous septum.
Shunt determination
The echocardiogram can give important qualitative information about the degree of the
shunt associated with the VSD. The magnitude of left-to-right shunting can be estimated using the ratio of pulmonary to systemic
blood flow (Qp/Qs), relying on measurements
of aortic and pulmonary velocity or velocity
time integrals (VTI), and corresponding lumi26
Figure 3:TEE. Four chamber view showing a ventricular septal
defect of the muscular septum.
nal diameters or cross-sectional areas (33). The
degree of shunting is influenced by the size of the
defect and by the balance of resistances in the
pulmonary and systemic circulations.
Assessment of RV and PA pressures
Using the modified Bernoulli equation (gradient
[mmHg] = 4 x [peak velocity] ²), the maximum velocity of flow across the VSD can be translated
into the pressure gradient between the LV and RV
(Figure 4). This value can then be subtracted from
the patient’s cuff systolic pressure to estimate the
systolic RV and PA pressures (in the absence of
RV outflow tract obstruction). Large gradients are
seen in patients with smaller defects, and small
gradients are seen in patients with elevated RV
and PA pressures (34). The common finding of tricuspid regurgitation also allows estimation of RV
and PA pressures. Right ventricular systolic pressure can be estimated using the sum of the estimated right atrial pressure and the gradient between the right atrium and RV, as derived from the
modified Bernoulli equation (35).
CARDIAC CATHETERIZATION
Cardiac catheterization, once commonly
performed in the evaluation of infants with VSD,
is now rarely performed. During the catheterization, the diagnosis of VSD is done by the finding
of a significant step-up in right ventricular oxygen
saturation. Once detected, the magnitude of the
left-to-right shunt can be estimated by the Qp:Qs
ratio which may help assess the need for closure
of the VSD or plan perioperative management (assessment of PVR, testing
of vasodilators) (13).
over time. If at the 12-month visit the murmur is
gone, repeat echocardiogram is not necessary;
children, in whom VSD closure is associated with
aneurysmal tissue, should be followed every two
to three years to monitor the possible development of obstruction to RV outflow (13). If the murmur persists at 12-month, an echocardiogram is
recommended to verify the diagnosis and to evaluate the presence of complications.
Surgical Management
Decisions regarding surgery must be made
on a case by case basis. Factors to consider include the severity of heart failure, likelihood of progression of pulmonary vascular disease or other
complications, likelihood of reduction in size or
spontaneous closure of the defect, and the morbidity and mortality of the procedure (13, 20).
Indications for surgical closure of VSD in
infants and young children include (13, 20):
·Infants less than 6 months of age who have
uncontrolled heart failure despite maximal medical
treatment or who have pulmonary hypertension.
·Children less than 12 months of age with
Qp:Qs >2:1, without elevated PVR.
·Subpulmonic and membranous defects
with aortic regurgitation, regardless of size (36).
Surgical closure of a VSD is contraindicated if PA pressure is suprasystemic or if PVR is
MANAGEMENT
The management of
VSD depends on the size
of the defect, the likelihood
of spontaneous closure,
the involvement of one or
more cardiac valves and
the anticipated complications and effectiveness of
surgical closure (13).
Infants with small
VSD are expected to remain asymptomatic and
to experience possible disappearance of the murmur
Figure 4: Doppler determination of pressure gradient across a membranous ventricular
septal defect. The velocity is 6.5 m/sec, which results in a gradient of 169 mmHg.
27
greater than 12 Wood units. Patients with PA pressure between 75 and 100% of arterial pressure or
PVR between 8 and 12 Wood units are considered
to be at high surgical risk, and additional information including the response of PVR to 100% oxygen and pulmonary vasodilators, should be considered.
16. Kidd L; Driscoll DJ; Gersony WM. Second natural history study of congenital heart defects. Results of treatment
of patients with ventricular septal defects. Circulation 1993;
87(2 Suppl):I38-51.
17. Van Hare GF; Soffer LJ; Sivakoff MC. Twenty-five-year
experience with ventricular septal defect in infants and children. Am Heart J. 1987; 114:606-614.
18. Onat T; Ahunbay G; Batmaz G; Celebi A. The natural
course of isolated ventricular septal defect during adolescence. Pediatr Cardiol. 1998; 19:230-234.
Transcatheter closure
19. Wood P. The Eisenmenger syndrome, or pulmonary
hypertension with reversed central shunt. Br Med J. 1958;
Transcatheter closure for muscular defects 2:701-708.
Frontera-Izquierdo P; Cabezuelo-Huerta G. Natural
has been achieved successfully when surgical 20.
and modified history of isolated ventricular septal defect: a
closure is difficult or unsuccessful (37). Ventricular 17-year study. Pediatr Cardiol 1992 Oct;13(4):193-197.
arrhythmia, heart block, considerable blood loss, 21. Van Praagh R; Geva T; Kreutzer J. Ventricular septal
and valvular damage are all potential complica- defects: how shall we describe, name and classify them? J
tions (13). Percutaneous closure of perimembra- Am Coll Cardiol. 1989; 14:1298-1299.
Alter BP; Czapek EE; Rowe RD. Sweating in congeninous defects is particularly associated with com- 22.
tal heart disease. Pediatrics 1968; 41:123-129.
plete heart block (38).
23. Leathan A; Segal B. Auscultatory and phono-cardiographic signs of ventricular septal defect with left-to-right shunt.
Circulation 1962; 25:318-27.
REFERENCES
24. Evans JR; Rowe RD; Keith JD. Spontaneous closure of
ventricular septal defects. Circulation 1960; 22:1044-1054.
1. Perloff, JK. Ventricular septal defect. In: The Clinical Re- 25. Nadas AS; Ellison RC. Phonocardiographic analysis of
cognition of Congenital Heart Disease, 5th ed, W.B. Saun- diastolic flow murmurs in secundum atrial septal defect and
ventricular septal defect. Br Heart J. 1967; 29:684-488.
ders Company, Philadelphia, 2003; 311-346.
2. Ferencz C; Rubin JD. Congenital Heart Disease: Preva- 26. Gersony WM; Hayes CJ; Driscoll DJ. Bacterial endocarditis in patients with aortic stenosis, pulmonary stelence at livebirth. Am. J. Epidemiol. 1985; 121:31-36.
3. Soto B; Becker AE; Moulaert AJ. Classification of ventri- nosis, or ventricular septal defect. Circulation 1993; 87(2
Suppl):I121-126.
cular septal defects. Br Heart J. 1980; 43:332-343.
4. Ramaciotti C; Keren A; Silverman NH. Importance of 27. Johnson DH; Rosenthal A; Nadas AS. A forty-year
(perimembranous) ventricular septal aneurysm in the natural review of bacterial endocarditis in infancy and childhood.
history of isolated perimembranous ventricular septal defect. Circulation 1975; 51:581-588.
28. Mori K; Matsuoka S; Tatara K. Echocardiographic
J Cardiol. 1986; 57:268-272.
5. Anderson RH; Lenox CC; Zuberbuhler JR. Mecha- evaluation of the development of aortic valve prolapse in
nisms of closure of perimembranous ventricular septal de- supracristal ventricular septal defect. Eur J Pediatr. 1995;
154:176-181.
fect. Am J Cardiol. 1983; 52:341-345.
6. Anderson RH; Wilcox BR. The surgical anatomy of ven- 29. Kitchiner D; Jackson M; Malaiya N. Morphology of left
ventricular outflow tract structures in patients with subaortic
tricular septal defect. J Cardiac Surg. 1992; 7:17-35.
7. Roguin N; Du ZD; Barak M; Nasser N. High prevalence stenosis and a ventricular septal defect. Br Heart J. 1994;
of muscular ventricular septal defect in neonates. Am Coll 72:251-260.
30. Papadopoulos C; Lee YC. Isolated ventricular septal
Cardiol. 1995; 26:1545-1548.
8. Griffin ML; Sullivan ID; Anderson RH. Doubly committed defect. Electrocardiography, vectocardiography and cathesubarterial ventricular septal defect: New morphological cri- terization data. Am J Cardiol. 1965; 16:359-368.
teria with echocardiographic and angiographic correlation. 31. Feigenbaum H; Armstrong WF; Ryan T. Ventricular
septal defect. In: Feigenbaum’s Echocardiography, 6th ed,
Br Heart J. 1988; 59:474-479.
9. Moe DG; Guntheroth WG. Spontaneous closure of un- Lippincott Williams-Wilkins, Philadelphia, 2005. 593-604.
complicated ventricular septal defect. Am J Cardiol. 1987; 32. Van den Bosch AE; Ten Harkel DJ. Feasibility and
accuracy of real-time 3-dimensional echocardiographic as60:674-678.
sessment of ventricular septal defects. J Am Soc Echocar10. Ahunbay G; Onat T. Regression of right ventricular diogr. 2006; 19:7-13.
pressure in ventricular septad defect in infancy. Pediatr Car- 33. Sanders SP; Yeager S; Williams RG. Measurement of
diol. 1999; 20:336-342.
systemic and pulmonary blood flow and QP/QS ratio using
11. Freedom RM; White RD; Pieroni DR. The natural his- Doppler and two-dimensional echocardiography. Am J Cartory of the so-called aneurysm of the membranous ventricu- diol. 1983; 51:952-956.
lar septum in childhood. Circulation 1974; 49:375-384.
34. Schamberger MS; Farrell AG; Darragh RK. Use of
12. Rudolph AM. The changes in the circulation after bir- peak Doppler gradient across ventricular septal defects
th: Their importance in congenital heart disease. Circulation leads to underestimation of right-sided pressures in patients
1970; 41:343-359.
with "sloped" Doppler signals. J Am Soc Echocardiogr. 2001;
13. Rudolph AM. Ventricular Septal Defect. In: Congenital 14:1197-1202.
Diseases of the Heart: Clinical-Physiological Considera- 35. Yock PG; Popp RL. Noninvasive estimation of right ventions, Rudolph, AM (Ed), Futura Publishing Company, New tricular systolic pressure by Doppler ultrasound in patients
York, 2001; 197-244.
with tricuspid regurgitation. Circulation 1984; 70:657-662.
14. Gabriel HM; Heger M; Innerhofer P. Long-term outco- 36. Ishikawa S; Morishita Y; Sato Y. Frequency and opeme of patients with ventricular septal defect considered not rative correction of aortic insufficiency associated with vento require surgical closure during childhood. J Am Coll Car- tricular septal defect. Ann Thorac Surg. 1994; 57:996-998.
diol. 2002; 39:1066-1071.
37. Knauth AL; Lock JE; Perry SB. Transcatheter device
15. Neumayer U; Stone S; Somerville J. Small ventricular closure of congenital and postoperative residual ventricular
septal defects in adults. Eur Heart J. 1998; 19:1573-1582.
septal defects. Circulation 2004; 110:501-507
28
38. Thanopoulos BD; Rigby ML. Outcome of transcatheter closure of muscular ventricular septal defects with the
Amplatzer ventricular septal defect occluder. Heart 2005;
91:513-516.
RESUMEN
Esta es una revisión bibliográfica que
resume una información actualizada en relación a la comunicación interventricular
(CIV) aislada. Es un tópico muy relevante
ya que la CIV es una de las cardiopatías
congénitas mas frecuentes. Se incluyen
consideraciones anatómicas y clasificación
de los diferentes tipos de CIA, categorías fisiopatológicas, aspectos clínicos y medios
diagnósticos como son: electrocardiografía,
radiografía de tórax, eco cardiografía y cateterismo cardiaco. También revisamos los
aspectos más importantes del manejo terapéutico, incluyendo las indicaciones quirúrgicas de la CIV.
Recomiéndelo
a sus pacientes
Inscríbase en el
buscador de
médicos
A
INTRODUCTION
A
fter the publication of NCEP-ATP III gui
delines in 2001, there have been multiple clinical
trials addressing issues not examined previously.
The new data favors lover cut-off points with aggressive use of cholesterol lowering statins therapy. I propose lowering LDL-C levels to around 70
mg/dL if we want to halt progression and induce
regression of the atheromatous plaque.
There has been three National Cholesterol
Education Programs. The Adult Treatment Panel I
(ATP I) was published in 1988, at that time statins
were not available and less effective medications
were recommended to lower cholesterol but “not
to low levels”.
The ATP II was published in 1993 and
again no clinical trials using statins were available then. Shortly after the publication of ATP II,
the Scandinavian Simvastatin Survival Study (4S)
was published in Lancet in 1994. It was a multicenter clinical trial to assess the effect of simvastatin on mortality and morbidity in 4,444 patients
with coronary artery disease aged between 35
and 70 years. The 4S study turned out to be a
milestone in cardiology and evidence-based medicine. It was clearly proven that treatment with
statins saved lives of patients with coronary artery
disease. A host of others multicentric clinical trials
followed paving the way for widespread use of this
class of drugs.
The West of Scotland Coronary Prevention Study (WOSCOPS) , published in The New
England Journals of Medicine in 1995 was the
first primary prevention clinical trial to assess the
effect of pravastatin on the prevention of coronary
events in males with high cholesterol without coronary heart disease. The study showed a reduction
of coronary heart disease deaths and of non-fatal
myocardial infarctions, and showed pravastatin
safety.
The ATP III published in 2001 included an
evidence-based set of guidelines on cholesterol
management. Since the publication of the ATP III,
five major clinical trials utilizing statin therapy and
clinical end points have been published. These
trials addressed issues not previously examined in
clinical trials of cholesterol-lowering therapy. The
objective of this update is to review the results of
these recent clinical trials and asses their implications for cholesterol management.
30
An Update To
The National
Cholesterol
Education
Program:
2009
Suggested
Changes
Arturo Medina-Ruíz, MD*
From the * Section of Cardiology, Department of Medicine, UPR School of Medicine, San Juan, Puerto Rico.
Address for correspondence: Arturo Medina-Ruíz, MD University of Puerto Rico School of Medicine; GPO Box
365067: San Juan, PR 00936-5067. E-mail: amrmd@
yahoo.com
ABSTRACT
In view of new, robust data published
after the publication of the NCEP-ATP III in
2001, I am proposing a more aggressive
management of cholesterol. Lower LDL-C
levels must be achieved to stop and regress
atherosclerosis and further reduce cardiovascular mortality.
Index words: update, national, cholesterol,
education, program
The Heart Protection Study (HPS) was
a secondary prevention study presented at the
November 13, 2001 American Heart Association
Scientific Session which included adults between
40 and 80 years of age from the United Kingdom
with stable coronary artery disease, and multiple
cardiovascular risk factors. The primary end points (all-causes mortality and deaths from heart
disease and related blood vessels disease) and
secondary end-points (effect on stroke, major cardiovascular events), favored Simvastatin 40mg
versus placebo with statistically significant p values. The authors concluded that the reduction of
LDL-Cholesterol (LDL-C) from any baseline level
further lowers risk of coronary events.
The Prospective Study of Pravastatin in
the Elderly at Risk (PROSPER) , presented at the
2002 American Heart Association Scientific Session was a primary and secondary prevention study in elderly patients between 70 to 82 years of
age with cardiovascular disease or at high risk of
developing cardiovascular disease and stroke. Elderly patients were randomized to receive Pravastatin 40mg or placebo. This study results showed
the benefits of statin therapy in older persons.
myocardial infarction and coronary heart disease
(CHD) death favoring the statin therapy. The results of ASCOT-LLA support the use of global risk
assessment in determining which patients may
receive benefits from lipid-lowering therapy. In
ASCOT, patients benefited regardless of baseline
cholesterol levels. Both, ASCOT and HPS achieved approximately a 35 to 40 mg/dL difference in
LDL-C between treatment and placebo groups and
showed significant event reduction. In contrast,
ALLHAT achieved only a modest LDL-C reduction
of 24mg/dL and did not show a significant event
reduction. The clinical implication of these data is
that high-risk patients with low LDL-C levels benefit from aggressive reductions of LDL-C with statin
therapy in primary prevention settings.
As a results of the previous clinical trials
it is now unethical to prescribe placebo drugs to
high-risk patients. Consequently, the last of the
five reviewed clinical trials compared treatment
with pravastatin 40mg daily (standard therapy, see
Table 1) with atorvastatin 80mg daily in patients
with an acute coronary syndrome. In The Pravastatin or Atorvastatin Evaluation and Infection
Therapy-Thrombolysis in Myocardial Infarction 22
(PROVE IT-TIMI 22) trial patients in the intensive
The third study reviewed in this paper is the therapy group with atorvastatin 80mg daily achieprimary prevention Antihypertensive and Lipid- ved approximately 50% reduction in LDL-C (down
Lowering Treatment to Prevent Heart Attacks Trial to approximately 62mg/dL), which is substantially
(ALLHAT) . ALLHAT at the time was the largest below current recommended levels of approxiantihypertensive trial and its lipid-lowering arm mately 100mg/dL. PROVE IT-TIMI 22 trial was
(ALLHAT-LLT) was the second largest lipid-lowe- stopped prematurely at 2.5 years because of the
ring trial and included large numbers of patients beneficial effects of intensive lipid-lowering theraover 65 years, women, African Americans, Latin- py appeared extremely rapid, as early as 30 days,
Americans, and patients with diabetes, treated lar- and continued throughout the follow-up period.
gely in community practice settings, randomized This trial confirmed the idea that aggressive lipidto Pravastatin 40mg versus usual care. Pravas- lowering is more beneficial, as first suggested by
tatin did not significantly reduce either all-cause the results of Dr. Nissen’s Reversing Atheroscleromortality or coronary heart disease when compa- sis with Aggressive Lipid Lowering (REVERSAL)
red with usual care. The results may have been trial . Taken together, the results of REVERSAL
due to the modest differential in total cholesterol and PROVE IT-TIMI 22 herald the beginning of a
(9.6%) and LDL-C (16.7%) between Pravastatin new era of intensive statin therapy.
and usual care compared with prior statin trials
favoring cardiovascular disease protection. The
no treatment benefits may have also been due to Drug
Dose (mg/dL) LDL-C Reduction (%)
high crossover of high risk hypertensive patients
in the usual care group to the active lipid-lowering
therapy group.
Atorvastatin
10
39
40
31
The Angloscandinavian Cardiac Outcomes Lovastatin
Trial-Lipid Lowering Arm (ASCOT-LLA) was a pri- Pravastatin
40
34
mary prevention study in high risk hypertensive
20-40
35-41
patients with three or more other cardiovascular Simvastatin
risk factors and total cholesterol ≤ 250mg/dL. In Fluvastatin
40-80
25-35
the lipid-lowering arm of ASCOT, 10,305 patients
5-10
39-45
were randomized to atorvastatin 10mg or place- Rosuvastatin
bo. Although the planned follow-up was five years,
the trial was stopped early at 3.3 years because of Table 1. Standard Doses: doses of statins required to attain
clear benefits in the primary end-points of nonfatal an approximately 30-40% reduction in LDL-C levels.
31
Since publication of the 4S study in 1994
there have been extensive publications of clinical
trials to lower LDL-C in both primary and secondary prevention showing the benefits of lowering
LDL-C in high-risk patients. The HPS and PROVE
IT demonstrated that there are additional benefits
in going from low to very low LDL-C, levels below
70 mg/dL in patients in the high risk category.
Based on these clinical trials the NCEP issued an update of the ATP III guidelines in 2004 .
The highlights of recommended changes are:
·In high-risk patients the recommended
LDL-C goal is <100 mg/dL, but when risk is very
high, and LDL-C goal of <70mg/dL is a therapeutic
option, including those patients at very high-risk
with baseline LDL-C < 100mg/dL. In those highrisk patients with high triglycerides or low HDL-C,
consideration can be given to combining a fibrate
or nicotinic acid with an LDL-C lowering drug.
·For moderately high-risk persons (2+
risk factors and a Framingham risk at 10 years
of 10% to 20%) the recommended LDL-C goal is
<130mg/dL, but an LDL-C goal of <100mg/dL is a
therapeutic option, including moderately high-risk
persons with baseline LDL-C of 100 to 129 mg/
dL.
·In both high-risk and moderately high-risk
persons the intensity of the drug therapy should
be of enough intensity to achieve at least a 30%
to 40% reduction in LDL-C levels.
·Any person at high risk or moderately high
risk who has lifestyle-related risk factors (obesity,
physical inactivity, high triglycerides, low HDL-C,
or metabolic syndrome) is a candidate for therapeutic lifestyle changes (TLC) to modify these
factors regardless of LDL-C levels.
·Last but not least, for persons in low-risk
categories recent clinical trials do not modify the
goals and cut-off points of therapy.
·Reductions of LDL-C from any baseline
further lower cardiovascular risk in high-risk patients (HPS, PROVE IT).
Increase levels of the inflammatory biomarker high sensitive C-reactive protein (hs-CRP)
predict cardiovascular events. Since statins lower
levels of hs-CRP (MIRACL trial, Aggrastad to Zocor trial, PROVE- IT trial)8 as well as cholesterol
the JUPITER trial hypothesis was that people with
hs-CRP, but without hyperlipidemia might benefit
from statin therapy. Apparently healthy men and
women without dyslipidemia, but with elevated levels of hs-CPR were randomized to receive rosuvastatin 20 mg versus placebo. The rates of a first
major cardiovascular event and death from any
cause were significantly reduced among the participants who received rosuvastatin as compare
with those who received placebo. The JUPITER
trial was stopped prematurely because of the robust data in favor of rosuvastatin versus placebo,
after a median follow-up of only 1.9 years of a five
years planned duration. How many physicians will
change their practice and prescribe rosuvastatin
to otherwise healthy persons?
Let me venture some predictions which
appear as recommnedations in the soon to come
NCEP-ATP IV:
·All patients with cardiovascular disease
should have an LDL-C goal of < 70mg/dL.
·All patients over age 40 years with Type
2 Diabetes, Framingham score over 20%, or hsCRP over 2 mg/liter should be on a statin to lower
LDL-C by 30-40%.
·Reemphasize the need to achieve nonHDL goals of <100mg/dL in patients with low HDLC and /or high triglycerides.
·Apo B will be an optional target of less that
80mg/dL in high-risk patients.
·Combination therapy will be advocated to
achieve the lipid goals.
These are the recommendations of the
ATP III 2004 update. Thus, NCEP ATP III 2004 ·Will probably include the recommend triple
update:10
goal therapy of: LDL-C < 70mg/dL, triglycerides
<150mg/dL and HDL-C > 40mg/dL.
·Confirm the benefit of lowering LDL-C to
< 100mg/dL in high-risk patients (HPS, ASCOT- CONCLUSION
LLA, PROVE IT).
There are abundant and robust clinical trials
·Support the inclusion of diabetic patients with clinical endpoints showing the benefits of agin the high-risk group (HPS).
gressive lowering of LDL-C levels to reduce cardiovascular events in both primary and secondary
·Confirm that older patients benefits from prevention. I propose an aggressive approach to
therapeutic lowering of LDL-C (PROSPER).
the management of cholesterol with an LDL-C.
32
• HPS-benefits in CVD patients and diabetes without CVD regardless of baseline
LDL-C (2002).
• PROSPER- benefits of lowering LDL-C is
extended to elderly patients (2002).
• ASCOT-LLA-benefits in high-risk hypertensive patients without CVD regardless of
baseline LDL-C (2003).
• PROVE IT-TIMI 22-early and late benefit
of intensive versus moderate lipid-lowering
in ACS (2004).
• JUPITER-healthy people without dyslipidemia, but with elevated hs-CRP levels who
receive rosuvastatin had lower rates of
major cardiovascular events.
Table 2. The Key Findings from the Recent Lipid-lowering
Trials
level around 70mg/dL to induce non-progression
(regression) of the atheromatous plaque. These
will reduce cardiovascular mortality, number one
killer.
9.
Nissen SE, Tuzeu EM, Schoenhagen P, et al. Effect
of intensive compared to moderate lipid-lowering therapy
on progression of coronary atherosclerosis: a randomized
controlled trial. JAMA. 2004 Mar 3; 291(9):1071-80.
10.
Grundy SM, Cleeman JI, Merz CN, Brewer HB Jr,
Clark LT, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel
III guidelines. Circulation. 2004 Aug 10;110(6): 227-239.
11.
Schwarts GG, Olsson Ag, Ezekowitz MD, et al. The
Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) trial: Effects of intensive atorvastatin
treatment on early recurrent events after an acute coronary
syndrome. Circulation 2000; 102: 2672-f.
12.
de Lemos JA, Blazing MA, Wiviott SD, et al. Early
intensive versus a delayed conservative simvastatin strategy in patients with acute coronary syndrome: Phase Z of the
A to Z Trail. JAMA 2004; 292: 619-623.
13.
Ridker PM, Danielson E, Fonseca FAH, Genest J,
et al. Rosuvastatin to prevent vascular events in men and
women with elevated C-reactive protein. N Engl J Med. 2008
Nov 20; 359(21):2195-2207. Epub 2008 Nov 9.
14.
Scharti M, Bocksch W, Koschyk DH, Voelker W.
Use of intravascular ultrasound to compare effects of different strategies of lipid-lowering therapy on plaque volume
and composition in patients with coronary artery disease.
Circulation. 2001 Jul 24; 104(4):387-92.
15.
Smilde TJ, van Wissen S, Wollersheim H, et al.
Effect of aggressive versus conventional lipid lowering on
atherosclerosis progression in familial hypercholesterolaemia (ASAP): a prospective, randomised, double-blind trial.
Lancet 2001; Feb 24; 357(9256):577-81.
16.
Taylor AJ, Kent SM, Flaherty PJ. ARBITER: Arterial
Biology for the Investigation of the Treatment Effects of Reducing Cholesterol: a randomized trial comparing the effects
of atorvastatin and pravastatin on carotid intima medial thickness. Circulation. 2002 Oct 15; 106(16):2055-60.
REFERENCES
1.
The Scandinavian Simvastatin Survival Group.
Randomized trial of cholesterol lowering in 4,444 patients
with coronary artery disease: The Scandinavian Simvastatin
Survival Study (4S). Lancet 1944; 344:1383-1389.
2.
Shepard J, Cobbe SM, Ford I, et al. For the West of
Scotland Coronary Prevention Study Group. Prevention of
coronary artery disease with pravastatin in men with hyperRESUMEN
cholesterolemia. N Engl J Med 1955; 333:1301-1307.
3.
NCEP ATP III Report. JAMA 2001; 285: 1711Debido a nuevos datos y abun
1718.
4.
MRC/BHF Heart Protection Study of cholesterol
dantes reportes luego de la publicación
lowering with simvastatin in 20,536 high risk individuals:
de las guías del NCEP-ATP III en el
Heart Protection Study of Collaborative Group. Lancet 2002;
2001, yo propongo un tratamiento más
360:7-22.
5.
Sherperd J, Blauw GJ, Murphy MB, Bollen EL, Bucagresivo del colesterol. Niveles más
kley BM, Cobbe SM, Ford I, et al. PROSPER Study Group.
bajos de LDL-C deben alcanzarse para
Prospective study of pravastatin in the elderly at risk. Lancet
2002; 360: 1623-1630.
parar el progreso e inducir regresión de
6.
The Antihypertensive and Lipid-lowering Treatment
la arterosclerosis y disminuir aún más
to Prevent Heart Attack Trial: ALLHAT Cooperative Research
las muertes cardiovasculares.
Group. JAMA 2002; 288:2998-3007.
7.
Sever PS, Dahlöf B, Poulter NR, Wedel H, Beevers G, et al. Prevention of coronary and stroke events with
atorvastatin in hypertensive patients who have average or
lower-than-average cholesterol concentration in the AngloScandinavian Cardiac Outcomes Trial-Lipid Lowering Arm
(ASCOT-LLA): a multicentric randomised controlled trial.
Lancet 2003 Apr 5; 361(9364):1149-58.
8.
Cannon CP, Braunwald E, McCabe CH, Rader DJ,
et al. Intensive versus moderate lipid lowering with statins
after acute coronary syndromes. N Engl J Med 2004 Feb 16;
350: 1495-1504.
33
The “Crush And
Aspiration”
Technique
For
Debridement
Of The Aortic
Annulus
Revisited
Héctor E. Marcano MD*
Samuel Olmeda ORT*
Raúl García-Rinaldi MD*§
From the * Cardiovascular Surgery Department, Advance
Cardiology Center, Mayaguez, Puerto Rico and the § Ponce
School of Medicine, Ponce, Puerto Rico.
Address reprint requests to: Raúl García-Rinaldi, MD, PhD
PO Box 6684 Marina Station, Mayaguez, PR, 00681-6684.
garciarinald@prtc.net
A
INTRODUCTION
A
ortic valve replacement is one of the
most effective operations in cardiovascular surgery. The type of prosthesis utilized remains the
choice of the surgeon and is based on the needs
and characteristics of the patient. Although the fundamental technique for aortic valve replacement is
standardized, various options for debridement and
decalcification of the annulus exist (1, 2, 3).
ABSTRACT
An effective technique for the
debridement of the aortic annulus
using a needle holder to crush the
calcify nodules, follow by the immediate aspiration of the pulverized material using a Yankauer suction device is reported.
Key words: aortic, valve, annulus,
debridement, replacement
Conservation of all decalcified fibrous tissue is a desirable option, and serves as a pliable
rim around the cuff of the prosthesis.
We employ a simple, yet very effective, technique for debridement of the aortic annulus. We
crush the calcific deposits and pulverize them with
a needle holder. The fragments are then rapidly
aspirated with the bare tip of a metal Yankauer
suction. The friction generated by the suction tip
helps to mobilize the pieces of calcium which are
immediately aspirated by the suction apparatus.
The connective tissue around the annulus remains
intact.
TECHNIQUE
Cardiac exposure, cardiopulmonary bypass,
left ventricular venting and cardiac protection are
established as by the choice of the surgeon. We
favor ample exposure of the aortic valve, using an
incision that can be extended into the non coronary sinus. We then proceed to methodically excise the calcified, deformed valve. The leaflets are
completely removed.
During debridement of the annulus we increase the volume of the cardioplegic solution, if
we are using retrograde coronary sinus perfusion
to avoid particle embolization into the left or right
main coronary arteries.
In order to remove the calcium nodules remaining on the annulus, we grasp the pieces of
One of the most important goals of annular calcium with a needle holder and gently crush
debridement is to remove the calcium deposits in them. In this manner we pulverize the nodules
order to improve the seating of the prosthesis and (see Figure 1).
to reduce the possibility of a paravalvular leak.
Khansari utilizes pituitary rongeurs (3). In contrast, The round cap of the Yankauer suction is
Doty does not use rongeurs but uses vascular for- removed leaving its bare tip. The edges of the tip
ceps to grasp and remove the pieces of calcium are firm and serve for further mobilize any remaiwith a twisting motion. He preserves all the con- ning calcium fragments on the annulus. These
nective tissue on the remaining rim of the excised fragments will be rapidly aspirated by the negative
valve (2).
force of the suction.
34
By using this technique we avoid inadvertent damage to the surrounding structures while
preserving all the annular fibrous tissue that will
help to anchor the valves sutures.
After debridement is completed, the area
of the annulus and left ventricle are irrigated with
cold saline. Insertion of the prosthetic valve is
continued according to the choice of the surgeon.
Figure 1: A needle holder is placed at a right angle
to the calcific nodules. The nodules are pulverized
by the crushing motion of the needle holder tip.
The pulverized tissue is immediately aspirated with
Yankauer suction.
This technique can be safely used when the
calcification extends to the anterior mitral leaflet. Crushing the nodules allow their removal without compromising the integrity of the
anterior mitral leaflet.
35
DISCUSSION
REFERENCES
The “crush and aspiration” technique of
debridement for the aortic annulus is very simple,
reliable and safe. After excision of the valve with
scalpel or scissors it facilitates debridement of the
heavily calcified aortic annulus avoiding damage
to surrounding tissues including the anterior mitral
leaflet and aorta.
1)
In: Edmunds LH (ed). Cardiac Surgery in the Adult.
New York: McGraw-Hill; 1997. p. 859-910
2)
In: Doty DB (ed). Cardiac Surgery Operative Technique. St. Louis:Mosby; 1997. p. 214-251
3)
Khansari S (ed). Cardiac Surgery, Safeguards and
Pitfalls in Operative Technique. Philadelphia: Lippincott-Raven; 1997. p. 47-85
Khansari have previously described crushing the calcified segments of the annulus with pituitary rongeurs (3). We on the other hand, avoid
rongeurs to crush the calcified deposits on the annulus and use a needle holder, which is safer and
more precise.
Our reluctance to use rongeurs is supported by Doty in his classical surgical textbook (2).
He warns against the use of rongeurs or other cutting instruments in the debridement of the aortic
annulus. He recommends that such instruments
must be used only with extreme caution (2). We
agree with his warning.
When we use a needle holder to pulverize
the calcified fragments, we avoid damage to surrounding structures and also preserve the annular
fibrous tissue, useful to anchor the valve sutures.
We have used this technique in over 250
patients and have never experienced a paravalvular leak.
RESUMEN
El reemplazo de válvula aortica (RVA)
es una operación efectiva en cirugía cardíaca.
Aunque la técnica fundamental para el RVA
esta estandarizada, existen varias opciones
para el debridamiento y decalcificación del
anulo. Es importante que al momento de debridar el anulo, se remuevan cuidadosamente los depositos de calcio. Esta maniobra no
sólo conserva el tejido fibroso anular que servirá de asiento para la prótesis valvular, sino
que también reduce las posibilidades de fuga
para-valvular. Nosotros utilizamos una técnica efectiva y segura para la debridación del
anulo, empleando un porta agujas para triturar
el tejido calcificado anular, seguido por la aspiración inmediata de este tejido pulverizado
usando un aspirador Yankauer. El tejido conectivo alrededor del anulo permanece intacto
y no se compromete la integridad de la valva
anterior del la válvula mitral. Hemos utilizado
esta técnica en más de 250 casos sin nunca
haber experimentado una fuga para-valvular.
Case Reports / Reporte de Casos
ABSTRACT
A 68 year old female patient with history of chronic lymphocytic leukemia, arterial
hypertension and dyslipidemia came for evaluation since she is constantly aware of the
beating of her heart. The echocardiogram
showed an aneurysm of the non coronary Sinus of Valsalva. Chest computer tomography
showed an aneurysm of the Sinus of Valsalva
measuring 5.5 cm of diameter. A sternotomy
was performed with resection of aneurysm
and replacement of the aortic valve. The
postoperative course was uneventful.
Index words: aneurysm, non-coronary, sinus,
valsalva
T
INTRODUCTION
T
he sinuses of Valsalva are three small
sacs in the aortic wall just above the attachment
to the aortic cusps. Sinus of Valsalva aneurysm
is a rare condition usually caused by a congenital
defect due to lack of fusion between the aortic media and the annulus fibrosus of the aortic valve.1
The prevalence is 0.09% and accounts for 1% of
all congenital anomalies of the heart. Sixty five to
85% originate in the right coronary sinus, 10-30%
in the non coronary sinus and less than 5% from
the left coronary sinus. It has been associated with
bacterial endocarditis, syphilis, Marfan’s syndrome
and inflammatory disease (such as Behçet’s disease) 2. Though it usually involves one sinus, there
are case reports of multiple congenital aneurysms
of the Sinuses of Valsalva.3
The diagnosis can be established by means
of a transthoracic echocardiogram. Transthoracic
color flow imaging and Doppler interrogation help
to distinguish between ruptured versus unruptured
aneurysm and to determine if there is occurrence of significant hemodynamic changes, such as
left to right shunt, significant valvular insufficiency secondary to volume overload after rupture or
the presence of a mass effect within intracardiac
chamber of unruptured ones. Rupture of the Sinus
of Valsalva aneurysm usually occurs in males after
puberty but before 30 years old 1.
Giant Aneurysm
Of The
Non-Coronary
Sinus Of
Valsalva:
A Case Report
Karen Rodríguez-Maldonado MD*
José Martínez-Toro MD*
José Pereyó-Díaz MD**
Cid Quintana-Rodríguez MD †
From the *University of Puerto Rico-Medical Science Campus, Internal Medicine Department-Cardiology Section, **
Department of Cardiology, and †Department of Surgery,
Cardiovascular Center of Puerto Rico and the Caribbean.
Address correspondence to: Karen Rodríguez Maldonado MD - PO Box 625, Mayagüez, P.R. 00681. Email:karenmariarm@hotmail.com
CASE REPORT
A 68 year old female patient with history
of chronic lymphocytic leukemia, arterial hypertension and dyslipidemia came to her cardiologist
complaining of constant awareness of her heart
beat. She denied chest pain, dyspnea upon exertion, shortness of breath either at rest or at supine position. No history of loss of consciousness.
Medications included atorvastatin and metoprolol.
She had no known drug allergies. She recently
had a partial colon resection due to diverticular disease. Her father suffered of brain aneurysm and
her mother of breast cancer.
The blood pressure was 115/64 mm Hg, pulse 84 beats per minute, respiratory rate 18 breaths/
minute, temperature 37.0 °C, weight 80 Kg, and
height 68 inches. The patient was an elderly female,
well- nourished, not acutely ill, and in no respiratory
distress while at rest. She was alert, awake and
oriented. There was no evidence of carotid bruit.
37
Normal jugular venous distention was present, and
the trachea was in the mid-lines. The heart rate
and rhythm were regular, no gallops or murmur.
Clear lung fields were encountered during anterior
and posterior auscultation. Bowel sounds were
normal and there were no palpable masses, either
hepatomegaly or splenomegaly. She had adequate radial, femoral, popliteal, dorsal pedis and tibialis posterior pulses. No focal motor deficit.
Hematological data showed a macrocytic and
hyperchromic anemia with hemoglobin level of 11.4
gm/dl and a mean corpuscular volume of 101.6. The
white blood cell counts were 28,300/ ml (NE% 7.3,
LY% 89.5, MO% 2.1, EO% 0.7, BA% 0.4). Biochemical data, liver function test and coagulation parameters were within normal range.
The patient brought an echocardiogram (Figures 2 and 3) which showed an aneurysm of the
An electrocardiogram (see Figure 1) showed non coronary Sinus of Valsalva with preserved left
a normal sinus rhythm with normal axis deviation. ventricular systolic function and aortic valve insufficiency. No evidence of aneurismal rupture.
Figure 1: Electrocardiogram with normal sinus rhythm.
Figure 2: Echocardiogram, parasternal -long axis view. Aneurysm of non coronary sinus of Valsalva
38
Figure 3: Continuous Doppler of aortic valve from apical view. Moderate to severe aortic valve insufficiency
Computer tomography of the chest showed a 6.5 cm
aneurysm of non coronary Sinus of Valsalva that increase
from 5.5 cm in six month (Figure 4).
Figure
4:
Chest
CT
s h o w i n g
aneurysm of
non coronary
Sinus of Valsalva
Figure 5: Left heart catheterization, right anterior oblique view. Sinus of Valsalva aneurysm
(arrow)
Left cardiac catheterization (Figures 5 and 6) showed
normal coronary arteries, preserved left ventricular systolic function, moderate aortic valve regurgitation with aneurysm of non coronary sinus of Valsalva, best seen in right
anterior oblique view.
Cardiovascular surgery was performed, the aneurysm at the non coronary Sinus of Valsalva was resected
and a hemashield graft was placed. The aortic valve was
excised and replaced with a 21 mm Carpentier-Edwards
Magna bio-prosthesis.
Figure 6: Left heart catheterization, left anterior oblique view. Sinus of Valsalva aneurysm
(arrow)
39
The postoperative course was uneventful REFERENCES
and the patient is doing well ten month after sur1. Perloff, J.K. Clinical recognition of congenital heart diseagery.
DISCUSSION
From five to 15 percent of aneurysm of sinus of Valsalva have their origin in the non coronary sinus. Those from non coronary sinus usually rupture within the right atrium. 4,5 The clinical
presentation of aneurysm of sinus of Valsalva varies depending on its origin, course and rupture
(acute versus chronic). There are reports of rupture within right atrium, right ventricle, interventicular septum, left ventricle, and left atrium. Reported complications include infective endocarditis,
atrioventricular conduction abnormalities, aortic
regurgitation from mild to severe6, distal emboli
(cerebrovascular, angina)7ventricular fibrillation8,
and heart failure.9,10 There is one case reported
with complete atrioventricular block during aneurysm extension into interventricular septum.11,12
The mechanism of heart failure is explained by
sudden hemodynamic changes during left to right
shunt, after rupture within the intra-cardiac chambers (reported at right side and left side chambers)
or due to obstruction of the ventricular outflow tract
by the aneurysm.10 The occurrence of ventricular
fibrillation had been documented during myocardial ischemia induced by direct coronary artery
compression (aneurysm of left coronary Sinus of
Valsalva with direct compression of left circumflex
coronary artery),8 with interventricular septum involvement and after rapid hemodynamic changes
during acute rupture of aneurysm.
Surgical repair of Sinus of Valsalva is usually recommended when it is associated with rupture in order to overcome the well-known complications of left to right shunt. In this case, the
patient was complaining of marked awareness of
her heart beat and there was no other complaint
suggestive of hemodynamic compromise. On physical exam a diastolic heart murmur, as expected
for moderate aortic regurgitation, was absent. The
decision to repair was made due to the increase
indiameter in less than 6 months from 5.5 cm to
6.5 cm by computer tomography associated with
moderate aortic valve regurgitation. From literature
review there is one large series study that showed
a 95% 20 year survival after surgical repair.13
The occurrence of the aneurysm of Sinus
of Valsalva is a rare condition with a wide range of presentations ranging from asymptomatic patients to cardiac arrhythmias, heart failure,
emboli or death. The diagnosis could be established with transthoracic echocardiogram. Surgical repair is recommended for all ruptured aneurysms and individualization of unruptured ones.
40
se. 2003: 457-470.
2. Koh, K.K., Lee, K.H., Kim, S.S., et al. Ruptured aneurysm
of the sinus of valsalva in a patient with Behçet’s disease. Int
JCardiol 1994;47:177–9.
3. Chamsi-Pasha,H., Musgrove, C. and Lorton, R. Echocardiographic diagnosis of multiple congenital aneurysms of the
sinus of Valsalva. Br Heart J. 59:724,1988.
4. Ritter, M., Oechslin, E., and Jenni, R. Giant congenital aneurysm of the non-coronary sinus of Valsalva. Heart
2002;88:243
5. Sakakibara,S., and Konno, S. Congenital aneurysm of
sinus of valsalva; anatomy and classification. Am. Heart J
1962; 63:405.
6. Moukarbel, G. V., and Abchee, A. B. Severe aortic insufficiency in a patient with sinus of Valsalva aneurysm invading
the interventricular septum. Heart 2004;90:1470
7. Shahrabani, R.M., Jairaj, P.S. Unruptured aneurysms of
the sinus of valsalva: a potential source of cerebrovascular
embolism. Br Heart J 1993;69:266–7.
8. Hoshino ,J., Naganuma, F., and Nagai, R. Ventricular fibrillation triggered by a ruptured sinus of Valsalva aneurysm.
Heart 1998;80:203-204 .
9. Glock, Y., Ferrarini JM, Puel J, et al. Isolated aneurysm
of the left sinus of Valsalva. Rupture into the left atrium, left
ventricle and dynamic coronary constriction. J Cardiovasc
Surg Torino 1990;31:235-238.
10. Tomita, T., Hanaoka,T., and Owa,M . Unruptured aneurysm of the sinus of Valsalva obstructing the right ventricular
outflow tract: magnetic resonance imaging findings. Heart
2002;88:42
11. Engel PJ, Held JS, Bel KJ, et al. Echocardiographic diagnosis of congenital sinus of Valsalva aneurysm with dissection of the interventricular septum. Circulation 1981;63:705711.
12. Walters, M. I., Ettles, D., Guvendik, L., and Kaye, GC.
Interventricular septal expansion of a sinus of Valsalva
aneurysm: a rare cause of complete heart block. Heart
1998;80:202-203
13. Van Son, J.A., Danielson, G.K., Schaff HV, et al. Long
term outcome of surgical repair of ruptured sinus of valsalva
aneurysm. Circulation 1994;90(5 pt 2):II20–9.
RESUMEN
Una mujer de 68 años de edad con historial de leucemia limfocitica crónica, presión
arterial alta y dislipidemia viene a su cardiólogo para evaluación. La paciente refiere sentir
constantemente las pulsaciones de su corazón. Un ecocardiograma muestra un aneurisma del Seno de Valsalva no coronariano.
Una tomografía computarizada de su pecho
muestra una aneurisma del Seno de Valsalva
no coronariano de 5.5 cm. Se realiza cirugía
cardiovascular para remover el aneurisma y
reemplazar la válvula aortica con una bioprotesis. El tiempo de recuperación fue sin ninguna
complicación.
Giant Cardiac
Myxoma In An
Asymptomatic
57-Year-Old
Women:
A Case Report
Hilton Franqui-Rivera MD†
Priscila Hernández-Vélez MD†
Jorge Ortega-Gil MD†
José Martínez-Toro MD†
Iván González-Cancel MD‡
Carmen Gurrea MD§
† From the University of Puerto Rico School of Medicine,
Department of Medicine, Cardiovascular Medicine Division
and ‡Department of Surgery and §Department of Pathology
and Laboratory Medicine, Cardiovascular Center of Puerto
Rico and the Caribbean.
Address reprints requests to: Hilton Franqui-Rivera, MD - 975
Gran Capitán, Palacios de Marbella, Toa Alta, PR 00953. Email: hiltonfranqui@gmail.com.
L
INTRODUCTION
L
eft atrial myxomas are the most common
primary cardiac neoplasms. Symptoms usually
arise when the size of the mass causes obstruction of blood flow. We present a case of an asymptomatic 57-year-old woman who was incidentally
found to have a large cardiac mass during echocardiography. The mass was removed and subsequently confirmed to be a benign cardiac myxoma
measuring 6.0 x 5.0 x 4.5 cm.
CASE REPORT
A 57-year-old woman with type-2 Diabetes Mellitus and arterial hypertension was seen
as an outpatient at the Cardiovascular Center of
Puerto Rico and the Caribbean. She had no complaints. On physical examination, she revealed an
irregularly irregular heart rhythm later confirmed
to be due to atrial fibrillation with appropriate ventricular response on 12-lead electrocardiogram.
ABSTRACT
Primary cardiac neoplasms are rare and
left atrial myxomas represent the most common
form of primary cardiac masses. We present
the case of a 57-year-old woman with Diabetes
Mellitus and arterial hypertension who was incidentally found to have a giant myxoma in the
left atrium. She was asymptomatic but given
the high risk of embolization and sudden cardiac death, surgical removal of the tumor was
performed. A 6.0 x 5.0 x 4.5 cm mass was recovered, confirmed to be a benign cardiac myxoma on microscopic examination. Symptoms associated with cardiac masses will depend upon
tumor location and size, usually related to flow
obstruction and embolization. An inflammatory
response due to secretion of cytokines may
also be observed. In this case, the patient had
no symptoms despite the size of the tumor that
occupied virtually 90% of the left atrial volume.
KEY WORDS: Cardiac tumors, Left atrial myxoma, Giant myxoma, Asymptomatic giant cardiac
myxoma
The remainder of the examination was within normal limits, without evidence of heart failure or cardiomegaly. Laboratory analyses, including complete blood counts, serum chemistry, and erythrocyte
sedimentation rate, were unremarkable, as well as
a chest x-ray. A two-dimensional echocardiogram
was obtained, demonstrating a 6-cm x 5-cm cardiac mass within the left atrium (Figure 1). Mild
aortic, pulmonary, and tricuspid valve regurgitation
were appreciated. There was mild left ventricular
dilation with normal systolic function and 61%
ejection fraction.
The patient was immediately evaluated for
prompt surgical removal of the mass due to high
risk of sudden cardiac death. A right and left-sided
cardiac catheterization was performed prior to surgery. Angiographic evaluation of the coronary arteries revealed normal anatomy without intraluminal plaque formation. Pulmonary artery angiogram
with delayed contrast to the left atrium confirmed
the presence of a large mass within the left atrium
(Figure 2). Intracardiac pressures and pulmonary
artery pressure were within limits.
The next day, the patient was submitted to
surgical removal of the mass. A 6.0 x 5.0 x 4.5
cm mass was removed from the left atrium (Figure 3). Microscopic examination of the specimen
revealed an abundant eosinophilic myxoid matrix
with stellar myxoma cells in small groups surrounding vascular vessels (Figure 4), consistent with
41
FIGURE 1: Transthoracic Echocardiogram. A, the parasternal long axis view
demonstrates a large
cardiac mass within
the left atrium; B, similarly, the mass is
also seen in the apical
four-chamber view.
*, cardiac mass; Ao,
aortic root; LA, left
atrium; LV, left ventricle; RA, right atrium;
RV, right ventricle.
FIGURE 2: Pulmonary Artery Angiography with Delayed Contrast of the Left
Atrium. A large mass occupies most of the left atrium
(arrowheads). *, cardiac
mass; LA, left atrium.
FIGURE 3: Gross
Specimen.
Large,
rubbery left atrial
mass measuring 6.0
x 5.0 x 4.5 cm.
benign left atrial myxoma. Microcalcifications
and hemosiderin collections were noted as
well. The patient had an uncomplicated recovery and was discharged home five days after
surgery. She has remained free of symptoms.
FIGURE 4: Hematoxylin & Eosin Stain
of the Specimen.
Abundant eosinophilic myxoid matrix
with stellar myxoma
cells in small groups
surrounding vascular vessels. Scattered
neutrophils,
microcalcifications,
and
hemosiderin
collections noted. A,
4x; B, 40x.
42
DISCUSSION
Though primary cardiac neoplasms are
rare, benign cardiac myxomas are the most common cardiac tumors arising in the left atrium (13). Because left atrial tumors tend to cause obstruction of blood flow or mitral regurgitation, these
usually produce symptoms that resemble heart
failure and/or mitral valve disease, including dyspnea, orthopnea, paroxysmal nocturnal dyspnea,
pulmonary edema, cough, hemoptysis, and fatigue (4-5). Systemic embolization may also occur
secondary to tumor fragmentation or thrombi formation (2).
Cardiac myxomas vary widely in size, most
commonly measure 1 to 3 cm in diameter though
tumors as large as 15 cm in diameter have been
reported (6). In general, the largest the tumor, the
most likely the patient is to present symptoms of
blood flow obstruction. Asymptomatic myxomas
have been found in less than 4% of cases (7).
In this case, our patient remained asymptomatic
despite the mass occupying most of the left atrial
volume.
Once the diagnosis of cardiac myxoma
is established, resection should be carried out
promptly due to high risk of embolization or other
complications, including sudden cardiac death (24). Operative mortality rate is less than 5% (2-3,
6-8). Close follow up is required due to the risk of
tumor recurrence seen in nearly 5% of patients (68).
RESUMEN
Los mixomas constituyen el tumor primario cardíaco más común. Éstos ocurren
con mayor frecuencia en la aurícula izquierda
y miden entre 1 a 3 centímetros de diámetro.
Los síntomas que producen se relacionan a
obstrucción del flujo sanguíneo, produciendo
síntomas de fallo cardíaco y síncope, o síntomas inflamatorios causados por liberación de
citoquinas y otras substancias. En este artículo hemos presentado un caso de una mujer asintomática de 57 años de edad en quien
incidentalmente se le encontró una masa de
6.0 x 5.0 x 4.5 cm en la aurícula izquierda.
La masa fue removida y se confirmó como un
mixoma benigno.
PRENSA MédicA
El periódico dirigido a
la comunidad médica y
el paciente puertorriqueño
REFERENCES
Núm. 2
nte, p.3
side
je del Pre
Mensa
s, p3
Noticia
Pu bli cac
la As
ión de
Mé dic
oci aci ón
ert o
a de Pu
Año 21
Ric o •
tor, p.4
del Edi
ritorio
Del Esc
nidad
er con dig ra, MD
Envejec
uierdo Mo
Luis Izq
ía, p12
pez león
zada del
a
La pun
p.14
evako Bav
Terry Ch de Emergencia,
na
Medici
d de
y la salu
bióticos
Los pre
D,
los niños ner Lugo, LN
Mi
Dennice
AMPR
Sería
idente,
tentes.
MD, Pres
s pre exis que exista la
Roper,
dicione
se
cual, aun
por con
G. Chavier
ima en el opción pública,
Rolance
oras
ión pres
un siste
ad de una
asegurad
o de la gest Asociación
posibilid “exchange” de onas puedan
la
comienz
un
do los
Desde el Barack Obama,
alda
crearía
de las pers se diluyan
resp
de
, en don
que
Rico ha
epto
dencial
privadas de tal manera
prima
de Puerto de salud y el conccomo
una
e
a
Médica
y
pars
eagru
d, tal
manteng
reforma
stra soci
os y se
planes de universal a la salu n actual.
s. En nue ncia es la
los riesg
todo
so
ració
para
inist
de acce
la compete
accesible
one la adm
ocrática
los prop
dad dem
crear un
basa en rimine
uesta se
disc
Esta prop el cual no se
en
sistema
Médicos
2
• Núm.
Geriatr
de
ncepto
do al co os federales
Respal
en fond icare para
ad
id
par
Med
icaid y
anos
de Med anos americ
ad
ico
los ciud s en Puerto R
te
residen
al proveer
la calidad so y
ntía de
e el acce La
mejor gara que garantic
s.
ma
paciente
un siste
ación
n de los
selecció enta la investig rrola libre
en el desa
ncia fom
compete y la innovación ología, de
a
tecn
y
tífic
s
cien
lemas
icamento
los prob
llo de med respondan a
que
6
manera
página
a en la
Continú
idos
Distingu
tores
s escri
Médico
nes
profesio
I. Mal
s; ambas
rvar a
Norman
n, escritore a médica de obsecomo un
tare
su profesió
ico es
raleza de una narrativa. La Un diagnóst ición y la
de
por la natu
ación.
cia, la intu
ente
una narr
icos son, la construcción
produce al unir la experien ado con su paci
Los méd
de
vínculo
historial
lucr
el
su
pleja
en
invo
com
pilar
tien
nte
ente y reco a se vuelve más r lo suficienteme
un paci
esta
la tram
de
debe
don
ico
méd
texto,
tación. El
interpre
, MD
donado
Médica
Prensa 9387
387
po Box n pr 00908-9
san JUa
Uested
e req
servIC
CHanGe
dard
t stan
presor
taGe
U.s. pos
paId
, p.r.
san JUan 3007
no.
perMIt
1.
Khandheria, BK, Seward, JB, Tajik, AJ. Transesophageal echocardiography. Mayo Clin Proc 1994; 69:856863.
2.
Lee, RJ, Bartzokis, T, Yeoh, TK, et al. Enhanced detection of intracardiac sources of cerebral emboli by transesophageal echocardiography. Stroke 1991; 22:734-739.
3.
Orsinelli DA, Pearson AC. Detection of prosthetic
valve strands by transesophageal echocardiography: Clinical significance in patients with suspected cardiac source of
embolism. J Am Coll Cardiol 1995; 26:1713-1718.
4.
Vasquez A, Sethi G, Maximov M, et al. Atrial myxomas in the elderly: a case report and review of the literature.
Am J Geriatr Cardiol 2004;13:39-44.
5.
Goswami KC, Shrivastava S, Bahl VK, et al. Cardiac
myxomas: clinical and echocardiographic profile. Int J Cardiol 1998;63:251-259.
6.
Meng Q, Lai H, Lima J, Tong W, Qian Y, Lai S. Echocardiographic and pathologic characteristics of primary cardiac tumors: a study of 149 cases. Int J Cardiol. 2002;84:69–
75.
7.
Dutta, T, Karas, MG, Segal, AZ, Kizer, JR. Yield of
transesophageal echocardiography for nonbacterial thrombotic endocarditis and other cardiac sources of embolism in
cancer patients with cerebral ischemia. Am J Cardiol 2006;
97:894-898.
8.
Wold, LE, Lie, JT. Cardiac myxomas: A clinicopathologic profile. Am J Pathol 1980; 101:219-240.
do
Conteni
Año 21
MBA
5
ón, p.1
Nutrici
o
o métod
mía com
La vasecto ación masculina
de esterilizuer-Merino, MD
Pedro Piq p.15
ía,
Urolog
es
La diabet tiago, MD
San
Luis A. p. 16
na,
Medici
y te
arazada
¡Estás emb un sonograma!
n,
ordenaron do-Encarnació
e, a la
ón. Deb
uier
compasi e para ser
Luis Izq
tenerle
ient
como parala distancia sufic el escritor,
6
MD
y
r
logía, p.1
vez, tene bos, el médico la vida de
Gineco
Am
osidad por y sus excrítico.
des
en la curi
de
ye un
compart por sus necesida
ser vicio
que inclu to
ás,
ctura al
los dem una curiosidad
Tan
ltado.
as;
La arquite : de París
ar su resu de un proceperienci
ina
comunic
n
dic
de
me
icipa
o
do
la
part
dese
ifica
n
o el otro
del sign as
sentido,
uno com
a San Jua uierdo, MD
entendid
ción de
Izq
y
so de crea cias que no son del caso,
Natalio na y las artes
rial
rien
dici
de expe
El histo
de
me
rtes
nte.
La
repo
ame
p. 19
complet te médico, los casos en
Letras,
de
todas
el expedien presentación
médicas,
, la
de
progreso y conferencias rias.
prolapso
ios
seminar de éstas son histo
iento del historia
Tratam
la
y cada una
litetravés de , MD,
stras de
recto a
que
obras mae
les de
Echeni
l que las diferentes nive
, Jessica
acio
Al igua
Ign
en
pretien
dades
inosa, MD
ratura, que , las enferme plejidades
Ángel Esp
sión
com
y
pren
.
MD
es
22
o,
com
ativa
p.
plicacion
ón narr
Marrer
dicina,
de
sentan com ejan a una ficci
a de me
n después un
Histori
que se asemter Percy, quie
irtió en
El Dr. Wal rculosis se convdecía que
tube
o,
complet compartían
contraer
s
a tiempo
novelista
escritor
to el
icos y los s idénticas. Tan
1
los méd
Médica
Prensa
s analítica
reza
4
dest
página
a en la
Continú
Anunciarse en Prensa Médica:
Publishing Resources, Inc.
Ron Chevako 787-647-9343
43
ABSTRACT
Congenital
structural
abnormalities not associated
with cyanosis may go undetected until late adulthood if
clinical symptoms are not evident. We report the case of a
17 year-old male, referred to
cardiology clinics for evaluation
of a murmur, which was found
to have asymptomatic severe
right heart chambers dilatation.
Right heart catheterization and
angiography revealed the diagnoses of partial anomalous pulmonary venous connection, an
atrial septal defect and persistent left superior vena cava.
Key Words: Atrial septal defect,
partial anomalous pulmonary
venous connection, persistent
left superior vena cava
C
INTRODUCTION
C
ongenital structural ab
normalities not associated with
cyanosis may be detected later
in adulthood due to a lack of clinical symptoms. Those causing enlargement of the right atrium and
ventricle include atrial septal defect, partial anomalous pulmonary
venous connections, coronary artery fistulas draining into the right
sided chambers, tricuspid valve
abnormalities including dysplasia
and Ebstein’s anomaly, pulmonary
valve insufficiency and arrhythmogenic right ventricular dysplasia/
cardiomyopathy (1). Other noncongenital causes of right heart
chambers dilatation are less likely
to be asymptomatic, and include
pulmonary embolism, pulmonary
hypertension and right ventricular
hypertrophy secondary to chronic pulmonary disease. Here, we
report a patient with an asymptomatic murmur and fixed splitting
of S2 in whom trans-thoracic and
trans-esophageal echocardiography showed right heart chambers
dilatation and enlarged coronary
sinus, but failed to show an atrial
44
Coexistent
Asymptomatic
Persistent Left
Superior Vena Cava,
Partial AnomalousVenous
Connection And
Atrial Septal Defect:
A Case Report
Elías Bou Prieto MD*
Alexis Canino Rodríguez MD*
José Martínez Toro MD*
* From the Section of Cardiology, Department of Medicine, University of Puerto
Rico School of Medicine
Address for correspondence: Elias Bou Prieto, M.D., Cardiology Section, Department of Medicine, UPR School of Medicine, PO Box 365067, San Juan,
Puerto Rico 00936-5067. E-mail: eliasbou@hotmail.com
septal defect or anomalous pulmonary venous connection. The
latter two diagnoses were found in subsequent right heart catheterization and angiography.
CASE REPORT
A 17-year-old male was referred for cardiology evaluation
due to a heart murmur found on routine physical examination. A
heart murmur had been pointed out when he was a child but no
further evaluation had been done. He had no complains throughout his life, denying ever feeling that he could not perform the
same physical activities and at the same performance as his
peers. His past medical history revealed no systemic illness. Family history was unremarkable for cardiac conditions or cases of
sudden cardiac death. On physical examination there was adequate blood pressure and heart rate. Upon cardiac auscultation
a grade 3/6 systolic murmur best heard in the left upper sternal
border, unchanged in quality throughout inspiration and a fixed
splitting of S2 were found. Unremarkable precordial palpation,
clear lungs and no clubbing or cyanosis were seen. Electrocardiogram showed normal sinus rhythm with normal QRS axis and
interventricular conduction. A transthoracic 2D echocardiogram
showed a prominent coronary sinus (Figure 1A),
enlargement of the right atrium and ventricle (Figure 1B and Figure 1C), and trans-pulmonic flows
by Doppler suggesting mild pulmonary stenosis
(Figure 1D). Mild tricuspid regurgitation was found,
providing an estimated right ventricular systolic
pressure of 45mmHg. A trans-esophageal echocardiogram was performed searching for congenital anomalies or shunting to explain previous findings. During injection of saline contrast through
the left antecubital vein, contrast was visualized in
the cononary sinus prior to the right chambers, demonstrating the presence of a persistent left superior vena cava. Injection of saline contrast through
the right antecubital vein failed to show the presence of an atrial septal defect. In view that there
1A: Long parasternal axis view showing prominent
was still no explanation for right chambers dilata- Figure
coronary sinus
tion, the patient was sent for left and right heart
catheterization. Hemodynamic data and oxygen
saturation measurements are shown in Table 1.
Table 1
Site IVC SVC RA RV PA PCW LV AO Sys Dias End Mean O2 Sat
-
-
-
-
83.8%
-
-
-
-
82.2%
-
-
-
10 87.9%
44 6 14 - 88.5%
35 16 - 26 87.1%
-
-
-
16 93.3%
152 -11 16 - 138 84 - 111 97.8%
Contrast injected in the pulmonary arteries
during right heart catheterization showed contrast
material simultaneously returning to both right
and left heart chambers, suggesting the presence
of an anomalous pulmonary venous connection.
Injection of contrast into the superior vena cava
showed contrast reflux through the anomalous
right pulmonary vein. Subsequently the right pulmonary vein was selectively canulated through its
drainage point into the superior vena cava, and
injected with contrast (Figure 2A). Injection of
contrast into the coronary sinus showed the presence of a persistent left superior vena cava (Figure 2B). Moreover, the catheter was advanced
through an atrial septal defect, reaching the left
atrium, through which the rest of the pulmonary
veins were canulated confirming their proper drainage to left atrium (Figure 2C). Qp/Qs calculation
was 1.5 : 1.0.
Figure 1B: Apical 4-chamber view showing right atrial and
ventricular enlargement
Figure 1C: Parasternal short axis view showing right ventricular enlargement
DISCUSSION
Anomalous pulmonary venous drainage is
a rare congenital lesion with an incidence of 0.4
– 0.7% (as seen in autopsy series) (2). If isolated,
45
Figure 2A: Anomalous right superior pulmonary
vein entering the right atrium
Figure 2B: Persistent left superior vena cava draining in the coronary sinus
it may be asymptomatic early in life. Symptoms
usually develop earlier in the presence of more
than one anomalous vein or in the presence of
other associated lesions (3) and are similar to
those occurring in patients with atrial septal defects. Although this patient had both conditions,
no symptoms were ever reported. Diagnostic
work-up is warranted in any patient with evidence of right heart chamber dilatation. Presence of
a dilated coronary sinus due to persistent left superior vena cava fails to explain right chambers
dilatation, reason for why further tests including
transesophageal echocardiogram and catheterization were performed. The determination of any
associated lesions and the degree of pulmonary
hypertension is essential, as well as the exclusion
of coexisting coronary artery disease, particularly
in patients older than 40 years of age (4). This patient was found to have a common form of partial
anomalous pulmonary venous drainage which is
an anomalous connection of the right pulmonary
vein into the superior vena cava. Drainage into the
right atrium is also common. A less common form
of partial anomalous pulmonary venous drainage
occurs from the left lung to the left brachicephalic
vein, or into the coronary sinus (5). Indications for
surgical correction include right heart dilatation,
irrespective of patient’s age, and/or the presence
of symptoms (3)
The most frequent lesion occurring in association to anomalous pulmonary venous drainage
is an atrial septal defect, of sinus venosus type
in the majority of cases, followed in incidence by
secundum defects. Secundum defects may be
suitable for transcatheter closure, whereas a surgical approach is used for closure of all other atrial
septal defects (4). A contraindication to closure is
severe pulmonary hypertension or Eisenmenger
physiology, both conditions were absent in this patient.
A persistent left superior vena cava is a
remnant of the embryonic left anterior cardinal
vein, which is expected to involute around the 8th
week of gestation (6). It drains via the coronary
sinus to the right atrium in more than 90% of patients. Rarely, it may drain directly into the left
atrium, this is usually in association to other congenital heart disease. Persistence of the left superior vena cava has a prevalence of 0.5% in the
general population. It usually produces no symptoms and therefore requires no treatment. Most of
the time it is incidentally detected on chest x-ray
after the placement of a pulmonary artery catheter
or pacemaker leads (7) or is suspected when there is difficulty performing these procedures.
Figure 2C: Pulmonary veins reached through an
atrial septal defect
Even though the patient described in this
report has not complained of any symptoms,
surgical correction of the partial anomalous pulmonary vein connection and the atrial septal defect are warranted due to the important degree of
left to right shunting evidenced by the marked dilatation of right heart chambers.
FOLLOW-UP
To this date the patient has received followup at cardiology clinics and remains asymptomatic. Although he has expressed unwillingness to
undergo surgical correction of his condition despite our medical advising, he has agreed to be seen
by a cardiothoracic surgeon for further discussion
of treatment options.
REFERENCES
1.
Satou Cook et al, Right Heart Dilatation in Adults:
Congenital Causes, AJR : 189, September 2007
2.
Healy, JE, An Anatomic survey of anomalous pulmonary veins; their clinical significance, J Thorac Surg 1952;
23:433
3.
Gatzoulis, M, Adult Congenital Heart Disease, A
Practical Guide, 1st ed., 2005
4.
Attie et al, Anatomical Closure for Secundum Atrial
Septal Defect in Patients Aged Over 40 Years. A Randomized Clinical Trial, JACC 2002 38(7), 2035-2042
5.
Dyme, JL, et al, Physiology of Isolated Anomalous
Pulmonary Venous Connection of a Single Pulmonary Vein
as Determined By Cardiac Magnetic Resonance imaging.
Am J Cardiol, 2006; 98:107
6.
Moore KL, Persaud, TVN, The Developing Human:
Clinically Oriented Embryology, The Cardiovascular System,
6th ed., 1998 pages 350-355
7.
Pahwah et al, Persistent left superior vena cava: an
intensivist's experience and review of the literature, South
Med J, 2003 May;96(5):528-9
OFICINAS ADMINISTRATIVAS
SUBSCRIPCIONES Y ANUNCIOS
Asociación Médica de Puerto Rico
PO Box 9387 • SANTURCE, Puerto Rico 00908-9387
Tel 787-721-6969 • Fax: 787- 724-5208
Email: mlaureano@asociacionmedicapr.org
ANUNCIOS EN BOLETIN Y WEB SITE
ralicea@asociacionmedicapr.org
Web Site: www.asociacionmedicapr.org
El “Boletín” se distribuye a los médicos y estudiantes de medicina de Puerto Rico y se publica en versión digital en www.
asociacionmedicapr.org.
Todo anuncio que se publique en el Boletín de la Asociación
Médica de Puerto Rico deberá cumplir con las normas establecidas por la Asociación Médica de Puerto Rico y la Asociación
Médica Americana.
La Asociación Médica de Puerto Rico no se hace responsable
por los productos o servicios anunciados.
La publicación de los mismos no necesariamente implica el endoso de la Asociación Médica de Puerto Rico.
Todo anuncio para ser publicado debe reunir las normas establecidas por la publicación. Todo material debe entregarse listo para
la imprenta y con sesenta días de anterioridad a su publicación.
RESUMEN
La AMPR no se hará responsable por material y/o artículos que
no cumplan con estos requisitos.
Los defectos estructurales congénitos en el corazón pueden pasar
desapercibidos durante la niñez si no
presentan a temprana edad con cianosis, arritmias o fallo cardiaco. Este
caso muestra la detección de varios
defectos congénitos en un paciente
asintomático que es referido a las clínicas de cardiología para evaluación de
un soplo. El hallazgo de cámaras derechas dilatadas por ecocardiografía
transtorácica levanta la sospecha de la
presencia de algún defecto congénito.
Mediante la evaluación con pruebas
más específicas se confirmó el diagnóstico propuesto de varios defectos
congénitos.
Todo artículo recibido y/o publicado está sujeto a las normas y
reglamentos de la Asociación Médica de Puerto Rico. Ningún
artículo que haya sido previamente publicado será aceptado para
esta publicación. La Asociación Médica de Puerto Rico no se
hace responsable por las opiniones expresadas o puntos de vista
vertidos por los autores, a menos que esta opinión esté claramente expresada y/o definida den tro del contexto del artículo.
Todos los derechos reservados. El Boletín está totalmente protegido por la ley de derechos del autor y ninguna persona o entidad
puede reproducir total o parcialmente el material que aparezca
publicado sin el permiso escrito de los autores.
"POSTMASTER"
If you do not receive this magazine in your desk or you changed
your address, send changes to our address.
47
W
INTRODUCTION
W
ith fewer than 300 cases reported
since first described in 1931, spontaneous coronary arteries dissection (SCAD) is an extremely
rare etiology of acute myocardial infarction1. We
illustrate a case of SCAD presenting as ST-segment elevation myocardial infarction in a premenopausal woman.
CASE REPORT
A 41-year-old woman with no systemic
illness presented sudden onset of severe, retrosternal chest pain. Associated symptoms
included diaphoresis, nausea, and vomiting of
gastric contents. The patient had no risk factors
for coronary artery disease other than cigarette
smoking. She was immediately taken to another
institution, where a 12-lead electrocardiogram
demonstrated ST segment elevations in leads
I, AVL, and V1 through V6. Within minutes, she
received intravenous fibrinolytic therapy with Tenecteplase. Shortly after receiving this therapy,
the patient collapsed and developed ventricular
fibrillation, requiring advanced cardiac life support (ACLS) measures, including orotracheal
intubation and mechanical ventilation.
The patient was transferred to our the
Cardiovascular Center of Puerto Rico and the
Caribbean, a specialized cardiovascular hospital with percutaneous coronary intervention
(PCI) capability. Upon arrival to our institution,
the patient was found unresponsive but with
spontaneous movements of the extremities.
Heart rate was 142 bpm and regular, respiratory rate was 24/min on mechanical ventilation
(set to 18/min), and blood pressure was 89/47
mmHg. Lung auscultation revealed diffuse inspiratory rales. The heart was tachycardiac with
a regular rhythm and free of murmurs or gallops.
The extremities were cold and clammy. Within minutes, the patient was taken to
the Invasive Laboratory Suite for emergency
PCI. Coronary angiography revealed an aneurysmatic dilation of the left main coronary (LMC)
artery as well as spiral dissection of the left anterior descending (LAD) artery extending from the
origin to the middle third of this artery with total
occlusion of the lumen at this point (Figure 1).
The Ramus branch also had signs of dissection;
the left circumflex artery and the right coronary
artery were intact. Left ventriculogram demonstrated anterior wall akinesia with 30% ejection
fraction (LVEF).
48
Spontaneous
Coronary Artery
Dissection:
A Rare Etiology
Of St Elevation
Myocardial
Infarction
Hilton Franqui-Rivera MD*
Ricardo G. Colacioppo-Saavedra MD*
José Martínez-Toro MD*
* From the University of Puerto Rico School of Medicine, Department of Medicine, Cardiovascular Medicine Division.
Presented at the 2009 Southern Regional Meeting of the
Southern Society for Clinical Investigation on February 13,
2009 in New Orleans, LA.
Address reprints requests to: Hilton Franqui-Rivera, MD 975 Gran Capitán, Palacios de Marbella, Toa Alta, PR 00953.
E-mail: hiltonfranqui@gmail.com
Following the coronary angiography findings,
the patient was immediately submitted to emergency
Coronary Artery Bypass Graft (CABG) surgery. She
had a left internal mammary artery (LIMA) graft placed to the LAD and a saphenous venous graft to the
Ramus branch. The patient recovered well and was
subsequently discharged home. A follow-up echocardiogram, obtained one month after this incident,
demonstrated mild improvement of cardiac function
with 40% LVEF.
DISCUSSION
Spontaneous coronary artery dissection
(SCAD) is a rare etiology of myocardial infarction.
Over 70% of cases occur in women who do not have
risks for coronary heart disease2 with a median age
of 39 years. Nearly 70% of cases are diagnosed during autopsy3 as sudden cardiac death is the most
common presentation4, though the full spectrum
of acute coronary syndromes and even congestive
heart failure may be observed.
The mechanism for this condition is unknown,
but multiple risk factors have been recriminated, including oral contraceptives, systolic arterial hypertension, rigorous physical exercise and cocaine5,6. Given the fact that over 30% of cases occur during the
peripartum period1, a hormonal etiology is considered
ABSTRACT
Spontaneous coronary artery dissection
(SCAD) is an extremely rare etiology of acute
myocardial infarction, most commonly seen in
pre-menopausal women with no risk factors
for atherosclerotic coronary artery disease
(CAD). We present the case of a 41-year-old
woman with no history of systemic illness who
presented severe, oppressive retrosternal pain
with ST-segment elevations in leads I, AVL, V1
through V6 in the absence of risk factors for
CAD. Emergency percutaneous coronary intervention (PCI) revealed an aneurysmatic dilatation of the left main coronary artery with complete dissection of the left anterior descending
artery and the ramus branch, causing distal
occlusion of the affected vessels. The patient
was submitted for emergency Coronary Artery
Bypass Graft (CABG) surgery. This is thought
to be caused by hormonal changes that cause weakness of the vasa vasorum and promote
hemorrhage into the media.
KEY WORDS: Spontaneous coronary artery
dissection, Pre-menopausal women, Coronary
dissection, ST elevation
likely. This coincides with studies suggesting that
oral contraceptives increase the risk of SCAD7.
Specifically, progesterone is believed to cause
weakening of the tunica media8, ultimately leading to dissection of the vessel. An inflammatory
reaction in the adventitia has been described by
histological examination, suggesting the possibility of periarteritis as an etiology4. However, this inflammatory response may be reactive rather than
causative.
In this case, we have presented SCAD in
a young woman without risk factors for coronary
artery disease except for cigarette smoking. History and laboratory testing, including toxicology
and drug screen, failed to illustrate possible causes for dissection. The patient was about three
weeks into her menstrual cycle, which coincides
with peak progesterone concentrations and the
above theories on the subject. Our patient had
received thrombolytics at another institution, and
even though this approach has been successful
in some cases, extension of the dissection is possible9,10. Once the diagnosis is established,
emergent PCI or CABG is likely to offer the most
survival benefit. In this case, CABG was our only
option because of the extension of the lesion, involvement of the left main coronary artery, and
total occlusion of the lumen distal to dissection.
FIGURE 1. Selective Angiography of the Left Coronary Artery, Anteroposterior (AP) View. Left coronary angiography
revealed an aneurysmatic dilation (white arrowheads) of the
left main coronary artery (LCM), spiral dissection of the left
anterior descending artery (LAD) and Ramus branch (black
arrowheads) with total occlusion of the lumen (arrows) distal to dissection. The left circumflex artery (LCfx) is shown
intact.
REFERENCES
1.
Leone, F, Macchiusi, A, Ricci, R, et al. Acute myocardial infarction from spontaneous coronary artery dissection a case report and review of the literature. Cardiol Rev
2004; 12:3-9.
2.
DeMaio, SJ, Kinsella, SH, Silverman, ME. Clinical
course and long-term prognosis of spontaneous coronary
artery dissection. Am J Cardiol 1989; 64:471-474.
3.
Jorgensen, MB, Aharonian, V, Mansukhani, P, Mahrer, PR. Spontaneous coronary dissection: a cluster of cases with this rare finding. Am Heart J 1994; 127:1382-1387.
4.
Basso, C, Morgagni, GL, Thiene, G. Spontaneous
coronary artery dissection: a neglected cause of acute myocardial ischaemia and sudden death. Heart 1996; 75:451454.
5.
Azam MN, Roberts DH, Logan WF. Spontaneous
coronary artery dissection associated with oral contraceptive use. Int J Cardiol 1995;48:195–198.
6.
Greenblatt JM, Kochar GS, Albornoz MA. Multivessel spontaneous coronary artery dissection in a patient with
severe systolic hypertension: A possible association. A case
report. Angiology 1999;50:509–513.
7.
Heefner WA. Dissecting hematoma of the coronary
artery. A possible complication of oral contraceptive therapy.
JAMA. 1973;223(5):550–551.
8.
Madu EC, Kosinski DJ, Wilson WR, Burket MW,
Fraker TD Jr, Ansel GM. Two-vessel coronary artery dissection in the peripartum period. Case report and literature review. Angiology. 1994;45(9):809–816.
9.
Buys, EM, Suttorp, MJ, Morshuis, WJ, Plokker, HW.
Extension of a spontaneous coronary artery dissection due
to thrombolytic therapy. Cathet Cardiovasc Diagn 1994;
33:157-160.
49
10.
Zupan, I, Noc, M, Trinkaus, D, Popovic, M. Double
vessel extension of spontaneous left main coronary artery
dissection in young women treated with thrombolytics. Catheter Cardiovasc Interv 2001; 52:230-232.
Pensando en el
paciente
Contenido
RESUMEN
Mensaje del Presidente, p.3
The Sword Way
Mondays thru Thursdays from 6 to 7:30 pm
Puerto Rico Medical Association
1305 Fernandez Juncos Ave., SANTURCE
For information visit yuyonkumdo.webs.com
or call (787) 238-6722
Rolance G. Chavier Roper, MD,
Presidente, AMPR
a la salud, tal y como los propone la
administración actual.
Desde el comienzo de la gestión
presidencial de Barack Obama, la
Asociación Médica de Puerto Rico ha
respaldado los planes de reforma de
salud y el concepto de acceso universal
Esta propuesta se basa en crear un
sistema en el cual no se discrimine
por condiciones pre existentes. Sería
un sistema en el cual, aunque exista la
posibilidad de una opción pública, se
crearía un “exchange” de aseguradoras
Los médicos son, por la naturaleza de su profesión, escritores; ambas profesiones
tienen el vínculo de la construcción de una narrativa. La tarea médica de observar a
un paciente y recopilar su historial produce una narración. Un diagnóstico es como un
texto, donde la trama se vuelve más compleja al unir la experiencia, la intuición y la
interpretación. El médico debe estar lo suficientemente involucrado con su paciente
Del Escritorio del Editor, p.4
Medicina, p.xx
¡Estás embarazada y te
ordenaron un sonograma!
Luis Izquierdo-Encarnación,
MD
Ginecología, p.xx
privadas, en donde las personas puedan
agruparse de tal manera que se diluyan
los riesgos y se mantenga una prima
accesible para todos. En nuestra sociedad democrática la competencia es la
mejor garantía de la calidad al proveer
un sistema que garantice el acceso y la
Continúa en la página 5
La punzada del pez león
Terry Chevako Bava
Medicina de Emergencia, p.xx
Envejecer con dignidad
Luis Izquierdo Mora, MD
Geriatría xx
Los prebióticos y la salud de
los niños
Dennice Miner Lugo, LND,
MBA
Médicos escritores
Norman I. Maldonado, MD
Noticias, p3
La diabetes
Luis A. Santiago, MD
Médicos Distinguidos
presort standard
U.s. postaGe
paId
san JUan, p.r.
perMIt no. 3007
Kum Do
Respaldo al concepto de
paridad en fondos federales
de Medicaid y Medicare para
los ciudadanos americanos
residentes en Puerto Rico
Prensa Médica
po Box 9387
san JUan pr 00908-9387
Con menos de 300 casos reportados en la
literatura desde que esta condición fue descrita por
primera vez en 1931, la disección espontánea de
las arterias coronarias (SCAD, por sus siglas en ingles) es una causa extremadamente rara de infarto agudo del miocardio. Presentamos a una mujer
de 41 años de edad sin historial de enfermedades
sistémicas que presenta dolor de pecho con elevaciones del segmento ST en las derivaciones I, aVL
y V1 a V6. Intervención percutánea de emergencia
demostró disección espiral que se extendía desde
el tronco principal izquierdo hacia la coronaria anterior descendiente izquierda, provocando oclusión
del lumen. La paciente fue sometida exitosamente
a una cirugía de puente aorto-coronariano. Aunque
la etiología de SCAD no es aún conocida, se cree
que niveles altos de progesterona debilita la túnica
media de los vasos sanguíneos, provocando así la
formación de la disección. Esto explica por qué la
mayoría de los casos ocurren durante el embarazo
y coincide con el hecho que nuestra paciente estuviese justo a mitad de su ciclo menstrual.
Publicación de la Asociación Médica de Puerto Rico • Año 21 • Núm. 1
CHanGe servICe reqUested
PRMA ACTIVITIES
Año 21 Núm. 2
Afiliado a la
Asociación Médica
Americana
como para tenerle compasión. Debe, a la
vez, tener la distancia suficiente para ser
crítico. Ambos, el médico y el escritor,
comparten la curiosidad por la vida de
los demás, por sus necesidades y sus experiencias; una curiosidad que incluye un
deseo de comunicar su resultado. Tanto
uno como el otro participan de un proceso de creación de sentido, del significado
de experiencias que no son entendidas
completamente. El historial del caso,
el expediente médico, los reportes de
progreso, la presentación de casos en
seminarios y conferencias médicas, todas
y cada una de éstas son historias.
Al igual que las obras maestras de literatura, que tienen diferentes niveles de
comprensión, las enfermedades presentan complicaciones y complejidades
que se asemejan a una ficción narrativa.
El Dr. Walter Percy, quien después de
contraer tuberculosis se convirtió en un
escritor a tiempo completo, decía que
los médicos y los novelistas compartían
destrezas analíticas idénticas. Tanto el
Nutrición, p.xx
La vasectomía como método
de esterilización masculina
Pedro Piquer-Merino, MD
Urología, p.xx
Tratamiento del prolapso de
recto a través de la historia
Ignacio Echenique, MD,
Ángel Espinosa, MD, Jessica
Marrero, MD
Historia de medicina, p.xx
La arquitectura al servicio de
la medicina: de París
a San Juan
Natalio Izquierdo, MD
La medicina y las artes y
Letras, p.xx
Continúa en la página 4
Prensa Médica 1
Challenging Educational Cases/Retos Educacionales
ABSTRACT
Three challenging educational electrocardiography
cases are presented and the
electrocardiographic findings
discussed.
Key Words : Electrocardiography, arrhythmias, cardiac
pacemakers
Challenging
Educational
Electrocardiography
Cases
Charles D. Johnson, MD, FACC
From the Section of Cardiology, University of Puerto Rico School of Medicine,
Puerto Rico Health Science Center, Rio Piedras, Puerto Rico.
Address reprints requests to: Charles D Johnson MD – PO Box 5067, University of Puerto Rico School of Medicine, Puerto Rico Health Science Center,
San Juan, Puerto Rico 00936.
CASE 1
This 51 year-old male has the following ECG: Figure 2 A.
• What is the ECG diagnosis?
• What is the electrophysiologic mechanism?
Make a Lewis laddergram.
Case 1.
3:2 Wenckebach block, at the mid AV node level.
Answer: Figure 2 B.
1:1 conduction at the lower AV node level.
Classic Type 1 (slow) Atrial Flutter (AFl),
with Multilevel atrioventricular (AV) conduction,
with alternating 2:1 and 4:1 conduction ratios, producing group bigeminal rhythm/paired QRS beats
at the ventricular level:
Some authors consider this as two tiers, rather than three, in the AV node - an upper AV node
level and a lower AV node level.
2:1 filtering, at the upper AV node.
Additionally, the paired beats show RBBB
alternating with incomplete RBBB of the beats
ending the shorter cycles-Ashman beats, phase
51
3 block, Schamroth's phasic aberrant ventricular basic beat to incomplete RBBB interval are visuaconduction.
lly the same, 520 ms.
The atrial flutter rate is near 250 beats per
minute. Left anterior hemiblock may also be present.
The basic beat to RBBB interval and the
CASE 2
The RBBB and the incomplete RBBB to
basic beat intervals are too, nearly the same,
although the latter may be about 10 ms longer; a
longer interval and longer RP then could explain
the subsequent greater degree of RBBB (1 - 4).
(LR)/ Base Rate is 60 ppm, the Upper Rate (UR) is
120 ppm and the AVD 150 ms. (Figure 4)
This 40-year-old male with the Sick Sinus
Syndrome (SSS) was implanted with a cardiac pa- • What is the diagnosis?
cemaker, VDD mode. The programmed Low Rate
52
Case 2.
Pacing ventricles only 21% of time (79%
sensing).
Answer:
Ventricular High Rate episodes - 636-745.
The VDD pacemaker is displaying single RV lead Impedance 150-183 ohms; Threschamber VVI mode pacing at the LR of 60 ppm. If the sinus P wave rate is slower than the program- hold 2 V at 0.4 ms. Programmed 2.5 V, 0.4 ms.
VEGM - VP VR
med LR, or if the sinus impulse is not sensed - that is, in the absence of a sensed atrial event the VDD
Pacemaker Clinic (8-26-08)
pacemaker then functions in the VVI mode pacing at the programmed LR. The third beat is a ventri
Figure 5 A ECG.
cular fusion beat.
The SSS is considered a contraindication • What is the diagnosis?
for implantation of a VDD pacing system! (5, 6).
• What would you do to fix it?
CASE 3
This 53 year-old male with congestive heart
failure, arterial hypertension, atrial fibrillation (AF)
and mitral valve replacement received Cardiac
Resynchronization Therapy (CRT)/ Biventricular
Pacing (BVP), implanted 8-16-07. Independent V
channels.
LR 80 ppm. Ventricular sensing 40% to 3%
of time (97% pac.)
RV lead: Impedance 171-185 ohms. Unipolar.
Threshold 3 V at 1.00 ms. Programmed 2.5
V, 0.5 ms.
Now V - V Interval is 28 ms, LV first.
Pacemaker Clinic (12-16-08).
The pacing system was programmed to the
VVI mode, with a LR of 50 ppm and a V-V interval Figure 5 B.
of 4 ms, left ventricle (LV) first. The initial right ventricular (RV) lead Impedance was 586 ohms.
• What is the diagnosis?
On 8-28-07, the RV lead showed a Lead
Warning!
Subsequent Pacemaker Clinic visits:
• What would you do to fix it?
The patient has not returned to the Pacemaker Clinic for a follow-up further evaluation.
53
Case 3.
Answer:
Figure 5 A.
Hayes et. al. note that the main interruptors of resynchronization are AF with rapid intrinsic conduction, which is sensed by the ventricles,
inappropriately programmed long AV intervals and
frequent premature ventricular contractions, (6).
Management of AF with less than 90% ven
BVP. AF. 40% sensing / only 60% V tricular pacing includes:
pacing.
RV lead Impedance 179 ohms.
•
Rate control or cardioversion.
Try to maintain sinus rhythm. Eliminate
The first two paced beats may be ventri- •
cular pseudofusion beats; the third paced beat is or decrease the AF. Pharmacologic suppression
a ventricular fusion beat, and the last two paced of AF. Treat AF aggressively to prevent spontabeats are possibly fully paced beats, although neously conducted QRS complexes. Control the
conducted ventricular response rate. AF Suppresmorphology differs slightly.'
sion algorithms.
Pharmacological agents - AV nodal bloc
The Golden Rule in CRT is to pace the ven- •
tricles as near to 100% of the time as possible, king drugs.
Consider AV node ablation for a fast venespecially to achieve over 90% ventricular pacing •
as a goal in order to obtain the benefits of the bi- tricular response unresponsive to B-blockers-drug
refractory rapid V rates.
ventricular pacing therapy.
54
•
Apply AF CRT algorithms, such as Ventri- Commonly there is a positive dominant pacular Rate Regulation- VRR (Boston Scientific) ced R wave in lead V1. But a negative QRS comand Conducted AF Response CAFR (Medtronic). plex, a lack of a dominant R wave, may occur in
lead V1- and this can be normal in BVP.
•
Increase and maintain a higher programmed Base Rate pacing, (5-8).
Lead 2 typical shows a negative complex;
the paced QRS complex may be negative in lead
Answer:
3 also.
Figure 5 B.
The ECG shows right axis deviation (RAD)axis in the right inferior quadrant. Broad paced
QRS complexes, 0.16-0.20 seconds wide. Broad
dominant R and Rs complexes occur in leads V1
to V3, with the R/S ratio greater than 1. Broad positive paced beats occur in lead 3.
qR, Qr, QR or QS complexes in leads 1,
aVL, V5; loss of these correlate highly with loss of
BVP-loss of LV capture.
The RV EGM shows BV VRs, compatible
with loss of RV pacing.
Lead 1: R/S < 1. Lead V1: R/S > 1.
The BVP VEGM displays a monophasic
pattern when there is intact capture of both the LV
and the RV.
LV Only Pacing/Isolated LV Pacing
VP VR indicates loss of capture in one of
the ventricular chambers, only single ventricular
capture.
Produces RAD, usually in the right inferior
quadrant; less commonly in the right superior quadrant.
Broad, positive, dominant paced R or R/s
complexes manifest in the precordial leads from
V1 to V4 or V5 (and in lead V6 if the pacing is basal LV); and also in leads 2, 3 and aVF particularly
in lead 3 there are broad positive R waves.
A notch after VP - two deflections.
Another ECG (2-3-09) shows dominant R
and R/S paced beats from Lead V1 through Lead
V5 and R/s complexes in Lead 2 and especially
Lead 3. The paced width is 0.17 second. Separate
LV and RV stimuli are visible.
This pattern may mimic the preexcited
rhythm of a left-sided accessory pathway, as seen
This CRT paced ECG suggests LV LEAD in this reported patient.
ONLY or ISOLATED LV PACING with loss of RV
Lead Capture.
The VEGM in loss of ventricular capture
of one of the ventricles shows a change from a
Reprogramming or revision of the device or monophasic complex to two discrete deflections,
including a late deflection, representing late actia new RV lead may be indicated.
vation of the RV in this case.- LV RV deflections.
(VP VR).
ECG Patterns:
Conventional Right Ventricular Apical Pacing
Produces in general a wide complex “LBBB”
type pattern, with a LBBB complex in lead VI and
a positive paced complex in lead V6, or QS complexes across the precordium; and negative paced
QRS complexes in leads 2, 3 and aVF. The mean
QRS axis is left and superior, usually in the left superior quadrant, but it may be in the right superior
quadrant.
BVP - Narrowing of the paced QRS complexes often occurs, so that the QRS width is less
than that of the native rhythm. RAD; typically the
axis is in the right superior quadrant toward the
right shoulder, but occasionally it is in the left superior quadrant.
Loss of capture in both ventricles revealing
a native wide LBBB complex also may show two
distinct deflections VP VR on RV and LV EGMs.
The benefits of LV only pacing may be similar to or better than BVP (5-8).
REFERENCES
1.
Marriott HJL. Practical Electrocardiography. 8th Edition. Baltimore, Williams & Wilkins, 1988, p 193-194, 374.
2.
Wang K, Asinger RW, Marriott HJL. Bigeminal
rhythms, common and uncommon mechanisms. J of Electrocardiology 2007; 40: 135-138.
3.
Schamroth L. The Disorders of Cardiac Rhythm.
2nd Edition. Vol 1. Oxford, Blackwell Scientific Publ, 1980, p
51-52, 184-185, 297, 585; 413 V 2.
4.
Kosowsky BD, Latif P, Radoff AM. Multilevel atrioventricular block. Circulation 1976; 54: 914-921.
55
5.
Besoain-Santander M, Pick A, Langendorf R. A-V
conduction in auricular flutter. Circulation 1950; 2: 604-616.
6.
Hayes DL, Friedman PA. Cardiac Pacing, Defibrillation and Resynchronization. A Clinical Approach. 2nd Edition. Hoboken, NJ, Wiley-Blackwell 2008, p123, 138, 241,
276-285, 373-374, 504-509.
7.
Barold SS, Stroobandt RX, Sinnaeve AF. Cardiac
Pacemakers Step by Step. An Illustrated Guide. Elmsford,
NY, Blackwell Publ, Futura 2004, p 246-254, 323-328.
8.
Stroobandt RX, Barold SS, Sinnaeve AF. Implantable Cardioverter- Defibrillators Step by Step. An Illustrated
Guide. Hoboken, NJ, Wiley-Blackwell, 2009, p 229-254,
388-399
RESUMEN
Se presentan y discuten tres casos electrocardiográficos educativos.
A
HEAVY
TOOL
FOR
A
FINE
ART
www.asociacionmedicapr.org
Historic Article/Articulo de Historia
ABSTRACT
At the beginning of the
19th Century, there was
a “chronic lack of physicians, medications, and
hospital facilities, easily
overwhelmed epidemics”
in Puerto Rico. But, the
arrival of newcomers
from various parts of the
world to the Island contributed to socio-economic
development and the improvement of health conditions and health care.
The Wars of Independence throughout Spanish American colonies
(1808-1826), resulted in
population movements
into the Island, particularly from Tierra Firme
(Venezuela), as well as
from Spain (1808-1814).
In 30 years the population doubled. Puerto
Rico had 44 physicians,
13 pharmacists, and 45
“curanderos” or “healers”; the municipality of
Ponce had 6 physicians
and 2 pharmacists. The
progress made by the
southern society was remarkable. Those arriving
from Venezuela were at
the time the most benefited of the Spanish emigrants. They were educated people mastering
languages, commerce,
agriculture, science and
medicine. This, in turn,
stimulated progress, and
economic and social wellbeing in Puerto Rico.
Index words: physicians,
pharmacists, war of independence, Puerto Rico
Physicians And
Pharmacists In Puerto
Rico During The Wars
Of Independence,
1810-1830
Ivette Perez Vega PhD, JD*
From the * Center of Historic Investigations, Department of History, Humanity Faculty,
University of Puerto Rico, Rio Piedras Campus.
Address reprints requests to: Dra. Ivette Pérez Vega - Centro de Investigaciones
Históricas, Universidad de Puerto Rico, Facultad de Humanidades, P.O. Box 22802,
San Juan, P.R. 00931-2802. Email: iperezvega@yahoo.com
D
INTRODUCTION
D
uring the 19th Century, newcomers from various parts of
the world to the Spanish island of Puerto Rico contributed to socioeconomic development and the improvement of health conditions and
health care.
Prior to the first decade of this century, Puerto Rico did not have
permanent settlements of immigrants. The commercial flow between
Spain and America was more fully developed in New Spain and Tierra
Firme (Venezuela). The under-population of Puerto Rico at the time,
which prevented agricultural, commercial, social, and health progress,
was redressed however, during the first decades of the century1. As
the Wars of Independence took place throughout the Spanish American colonies (1808-1826)2, there were new population movements into
the Island3, particularly from Tierra Firme. The main provisions of the
Royal Decree Cédula de Gracias in 1815 were to accelerate the slow
colonization pace of the Island by promoting the settlement of Spanish
and foreign immigrants4, while also providing asylum to refugees from
the Wars of Independence. It was hoped that the provisions would prevent the spreading of revolutionary ideas of political upheaval and the
abolition of slavery which were evident throughout the Americas, beginning with the Independence of the Thirteen North American Colonies
from England in 1776, the French Revolution in 1798, and the Haitian
Independence from France in 1804. The Royal Decree also promoted
slavery by allowing the entrance of blacks with the immigrants. With
the Royal Decree Cédula de Gracias5 , Spain encouraged a policy of
emigration among its citizens in the Continent, as well as in mainland
Spain in order to alleviate the precarious conditions during 1810-1830
resulting from its war with France (1808-1814). As an outcome, Puerto
Rico began experiencing economic growth that led to changes in the
country's economy from a subsistence agricultural one to a commercial one. This, in turn, was to have visible impact on all other aspects of
57
Puerto Rican life. It encouraged the entry of highly
trained and "well to do" groups, such as physicians
and pharmacists who created an efficient health
system. Also, of land owners and businessmen,
together with a slave labor force that helped to
transform Puerto Rican society and its economy
into a sugar plantation economy oriented to a world
market6. As the century progressed and laws passed to correct the health concerns, the death rates
of various illnesses began to drop and there were
far less instances of epidemic proportions, Puerto
Rico became a better place to live.
Physicians and pharmacists
At the beginning of the 19th Century, in Puerto Rico “there was a chronic lack of physicians,
medications, and hospital facilities, perhaps marginally compensated in normal periods, but easily
overwhelmed in epidemics”, as stated by the epidemiologist Dr. José Rigau-Pérez. Puerto Rico
was affected by epidemics of unspecified, but
lethal diseases, since the last two centuries, because plagues were very common in neighboring
countries7. Due to the poor environmental conditions, diseases in the earlier part of the period
ran rampant. There were two physicians in San
Juan, Emigdio Antique and Francisco Brignonis,
and one surgeon Louis Rayffer, who cared for
ordinary citizens; two regimental surgeons, José
Dorado and Juan Antonio Castella; a physiciansurgeon, Francisco Oller; and four practitioners,
Miguel Chavarría, Ambrosio Infante, Miguel Coto
and José María Rodríguez8. Most of them would
work at the Royal Military Hospital in San Juan
that was functioning since the 18th century with a
capacity of 500 beds.
During the decade of 1820 the physicians
practicing in the capital city San Juan were José
Espaillat, Francisco Oller, José María Vargas, and
Emigdio Antique. Afterwards, the physicians José
de Jesús Mirabal, José Rendón, Domingo Montes and José Calvo came to the city. In addition,
we found the pharmacists José Giusti, Alejandro
González, Antonio Balrells and Esteban de Coto.
In Ponce, the physicians who arrived were José
María Vargas, Domingo Arévalo, José de Tirado, José de Castro, José Domingo Díaz, Robert
Proust, and José Luveres9. Dr. Vargas moved
to San Juan in 1820 since Ponce did not have a
hospital, becoming one of the most prominent surgeons at the Military Hospital with Dr. José Espaillat, Dr. Francisco Oller and Dr. Emigdio Antique.
He was also professor of medicine and surgery
at the institution10. Besides, being a general surgeon, he was an ophthalmologist, obstetrician and
pathologist. He was also a member of the Economic Society of Puerto Rico, described as a person
of “outstanding character, socially and culturally”,
58
who “demonstrated an impeccable moral as well
as political conduct” in the Island11. He was responsible for re-introducing the smallpox vaccine
from Venezuela to Puerto Rico through Saint Thomas12. The pharmacists in Ponce were Gaspar
Duprel and Benito Paz Falcón, who possessed
a state license since 1813 to practice his profession13. Later, the physicians Honorato Bernal and
Isidoro Ávila arrived in Ponce. All these professionals were extremely respected and most of them
became very wealthy landlords and merchants,
belonging to the elite class of the society and holding high positions in the government and in the
military, as well as in health services.
In 30 years (1800-1830) the population of
the Island doubled and Ponce’s more than doubled. In 1830 there were 320,000 people in Puerto Rico and 15,000 in Ponce. Puerto Rico had 44
physicians, 13 pharmacists and 45 “curanderos”
or “healers”, and Ponce had 6 physicians and 2
pharmacists14. There were “curiosos” and quacks
or charlatans, particularly of French origin, who
were practicing medicine throughout the Island without permission of the Board of Health. In 1821,
the Board required all physicians and pharmacists
to present their state licenses to be able to practice their professions15.
Southern Coast of Puerto Rico
During the first decade of the 19th Century,
the town of Ponce was inhabited mostly by poor
people, with few establishments and houses surrounding the central plaza. Its population was
around 7,000 people and most of them lived in the
rural zone. Puerto Rico, at the time, had a total
population of around 160,000 persons16. There were no physicians or pharmacists in Ponce.
There were hardly any literate persons. This fact,
however, was a rather common one at the time
in the Caribbean Islands as well as in Europe itself. So, it was under these circumstances that the
economic, social, and health development of the
southern coast of Puerto Rico took place.
In 1810, the governor of the Island, Brigadier Salvador Meléndez Bruna, following the
policy established by the Spanish Crown, invited
Venezuelans to settle in Puerto Rico. Since Ponce had such an engaging conditions for the sugar
cane production and commerce, and its export
to different parts of the world, mainly the United
States, it attracted not only experienced people in
these areas, but also professional emigrants, as
physicians and pharmacists, who were interested
in those activities after 181017. The first ones to
arrive were Paz Falcón from Spain in 1813; Tirado
in 1816, Arévalo in 1817, and José María Vargas
in 1818 from Venezuela.
From 1809 to 1837, the Island was to be
governed by three officials who had resided in Venezuela: Meléndez Bruna (1809-1820), who had
strongly opposed the Venezuelan independence
cause; Francisco González de Linares (18221824), first civil governor of Puerto Rico, a rich
businessman who had lost his fortune during the
Venezuelan movement to overthrow the new government, Junta de Caracas18; and Miguel De La
Torre (1824-1837), the general who was defeated
by Simón Bolívar in the Battle of Carabobo in 1821,
the last battle fought in Venezuelan territory19.
the rest of the Caribbean and Europe. The immigrants, thus, established commercial connections
with the businessmen in Saint Thomas and with
the representatives of well-known American and
European firms. As an example we can cite the
Vargas Brothers, who became the agent in Ponce of Anduze and Gil, one of the most prestigious
commercial firms in St. Thomas24.
As the revolutions throughout the Latin American countries succeeded in the Wars of Independence from Spain, a notable flow of people mainly
from Tierra Firme entered the Island. The majority
was land-owners, who belonged to the Creole noble
class; also, bureaucrats, military officials, political
refugees, businessmen, clergymen and professionals, like physicians and pharmacists. They were
all running away from the uprisings that had onfurled on the mainland21. Many of the immigrants
established themselves in the center of Ponce,
together with the Spanish emigrants from the Península (Spain), mainly Catalonians, who wanted
to escape from the Napoleonic Wars and the poor
economic conditions in Spain at the time22. Also,
foreign immigrants (Europeans and North Americans) came from the neighboring islands, like
Saint Thomas, which served as a stopping point
prior to the entry in Puerto Rico23. The Danish Island of Saint Thomas became the most important
commercial center for Puerto Rico, as well as for
Migration from Tierra Firme continued well
into the 1820’s. As a result funds were needed;
donations from the general public were requested;
fixed taxes on municipalities were set; and bureaucratic, military and health positions were reserved
for the newcomers. The immigrants enjoyed employment and protection rights, unemployment benefits as well as pensions for widows and children.
A provision of the law of 181330 offered them free
grants of land; and other special concessions to
deal with their maintenance31. Many of them became employees of the central and the municipal
governments, as Benito Paz Falcón, who was named in 1813 a member of the Diputación Provincial, an elective parliamentary body, and in 1820
Provincial Deputy of Puerto Rico at the Spanish
Courts32.
The introduction of the macuquina in Puerto
Rico by the newcomers from Venezuela and its
acceptance as the monetary unit for the country
by the Spanish government contributed to the soIn 1821, Governor González de Linares lution of the money crisis which had assailed the
appointed the physicians José María Vargas, José Island at the turn of the 19th Century. This currenwas introduced in order to facilitate the emiRendón, Francisco Jiménez and Emigdio Antique cy
grants
from Venezuela25. But, later on, because
to the Board of Home Health Care in San Juan20, of its low value26, it was not accepted by many fofor the benefit of the sick people who could not vi- reign countries, such as the United States, France
sit a doctor. Next year, 1822, González de Linares and England. However, this monetary unit greatly
presented a complain against the Board of Health accelerated the emigrant flow from Venezuela to
in Ponce because it did not comply with its duties Puerto Rico and was used for many years, until
regarding the health services offered to the poor 185727.
people during the outbreak of diseases because
of their unsanitary living conditions. During the goThe majority of the emigrants from Tierra Firvernorship of De La Torre in 1825, he insisted on me brought along not only currency but also Afrithe requisite of a state license to be able to practi- can slaves, who were usually from the Caribbean
ce medicine in Puerto Rico. Then, in 1828, De La Islands (Guadeloupe and Martinique), and VeneTorre informed the Spanish Crown about the de- zuela. The owners preferred to transfer them to
crease and shortage of practicing physicians and Puerto Rico and sell them before they could espharmacists in the Island compared to the number cape back to the Continent and join the revoluof the ones that were present at the beginning of tionary forces. With the profits made from slave
the 1820s. Probably, many of them had died or had re-sales, and the currency they brought, the immoved to other countries; others could have been migrants became involved primarily in agriculture
busy working in the sugar production, commerce- and commerce. Dr. José de Castro followed this
slaves as soon as he arrived
export, and slave trade, instead of practicing their trend and sold his
28
,
bought a hacienda and other
from
Venezuela
professions full time.
properties in Ponce and entered the sugar production activity29.
Immigration Flow
Likewise, Dr. José Domingo Díaz, a surgeon
from Caracas, who before his arrival in 1822 with
his family, had been named in 1821 Head of the
Intendencia of Puerto Rico, in charge of the public
59
finances of the Island, at the same time that González de Linares was appointed governor of Puerto Rico. Both arrived in San Juan from Madrid with
their positions ordained by the Spanish Crown33.
Díaz was assigned in charge of a project for the
installation of a military hospital. This would be
supported by the affluent citizens of the southern
region, since the municipal funds of Ponce were
not enough to subsidize it34. Governor De La Torre
and Dr. José Domingo Díaz, designed in 1825 an
economy plan for the transfer of military employees from Tierra Firme and Santo Domingo to La
Habana35, since there must had been an excess
of militia in Puerto Rico. Díaz stayed as Intendente
of Puerto Rico until 1827, when he was discharged from his position, and later, in 1828, was designated Intendant of the Military Division of the
Island36; afterwards he went to Madrid to renew
his journalistic and politic work37.
Other physicians were nominated officials of
the health services. We can mention, Dr. Tirado,
who became Head of the Board of Health Services of Puerto Rico, and Dr. Arévalo who was, also,
a member of the Board. Newcomers who did not
fall into any of the previously mentioned categories
or professions, as physicians or pharmacists, nor
had a job at the Island would get half their former
salaries in bonus.
One of the most important functions of the
Board of Health was to inspect the ships and the
passengers that arrived at the ports of the Island,
mainly the slaves that were to be sold from Africa
and the Caribbean Islands because many could be
affected with contagious diseases, as smallpox38.
This was a widely feared disease. The Board was
concerned with various diseases, sometimes called by different names, such as typhoid fever or
typhus or “vómito negro” (black vomit). Besides,
it was interested in other serious conditions as
measles, dysentery, leprosy, and phthisis. A different problem that the Board had to control was the
introduction of illegal raw meats which were kept
in the ships in unsanitary conditions that affected
the health of the people39.
As late as 1821, a group of 800 refugees from
Venezuela and the Garrison of Cumaná, which had
been defeated in the revolutionary wars, arrived
at the Ponce harbor40. This people who had surrendered themselves during the war arrived from
Puerto Cabello in Costa Firme, like José de Castro, a 41 years old physician from Caracas, and
single41. Even though a majority of the refugees
brought money and slaves along in order to settle,
many could not contribute to their self-support or
to their families. It caused an overall discontent in
Ponce42. The native Puerto Ricans (criollos) and
the long-time residents (Spaniards and foreigners)
60
resented the arrival of the newly admitted refugees who rapidly obtained the best positions in
the Island with the same pay as they used to get
back in their country. Indeed, they constituted a
new source of competition. In effect, a "peaceful"
invasion of numerous emigrants and refugees was
taking place. Together with the established foreign
residents they soon assumed control of the sugar
production and export, the commercial loans and
the financing of plantations, the slave trade, and
the health services43.
We must mention the Frenchmen, who upon
their arrival in Puerto Rico acted very similar to the
Venezuelans in their economic interests, except in
the practice of their professions. As an example,
we can bring forward Dr. Robert Proust, who worked as a surgeon in Martinique and arrived from
Saint Thomas, and his associate the pharmacist
Gaspar Duprel, who came from Cumaná (Venezuela), but neither of them engaged in the practice
of their professions in Ponce. They participated in
the sugar production and the African slave trade
from the French Islands Martinique and Guadeloupe, and Saint Thomas. Furthermore they functioned as importers-exporters of goods and slaves,
and money-lenders. Also, they were in the specialized business of money exchange circulation in
the transfer of bills of exchange to foreign countries in the Caribbean region and Europe44. Proust
was related to J. Proust from Nantes, the captain
of a slave ship that travelled from Africa to Martinique. In 1827, Dr. Proust joined the prestigious
commercial German firm Overman and Voigt of
Ponce in the slaves business.
The wealthy and experienced immigrant
was the privileged one in commerce, thus becoming the loan center for all the needy, since there
was not a banking system in Puerto Rico45. An
example was the Venezuelan business firm the
Vargas Brothers (Joaquín, Miguel, Bernardino and
José María), previously mentioned, who in 1817,
with capital and slaves, immediately settled in
Ponce and became one of the wealthiest. Besides
being involved in commerce, they also devoted
themselves to the loan business.
We can, also, mention Dr. José de Tirado,
mentioned before, who had lived in Venezuela, became a wealthy businessman and planter in Ponce, and one of the 15 voters in the Island46. Due to
the revolutionary disruptions in Spain, as others,
he fled to Venezuela and finally went to Puerto
Rico with his family and slaves in 1811, settling in
Ponce in 1816. By 1820 he owned a sugar cane
hacienda. In like manner, Benito Paz Falcón from
Spain, previously mentioned, elected also one of
the 15 voters in the Island, became very active in
the sugar production. Only wealthy and important
people of Puerto Rico were elected to this group of
compromisarios who would represent the people
of the Island during public elections.
Guaira51. He arrived in San Juan also in 1817,
but moved to Ponce a year later in response to a
call to take care for the victims of a smallpox epidemic that was spreading in the district52. Both,
In general, the emigrant from Tierra Firme the Vargas Brothers and Arévalo were attracted by
would bring his personal effects, currency, slaves, the town’s economic development. The former befarming equipment and merchandise that prepared came prosperous businessmen and land-owners,
him to buy land and to enter into business transac- and Arévalo became an important planter, while
tions after arrival. Thus, it became rather easy for also, like one of the Vargas Brothers (José María),
him to settle without any difficulty. His economic continued practicing as a physician.
stability together with his advantages associated
The important group the Vargas Brothers,
with Spanish citizenship and the Spanish languapreviously
mentioned, had been persecuted, and
ge, helped him to immediately establish himself in
accused
of
conspiracy. They were captured by the
commerce, an activity that was prohibited to foroyalist
groups
(against the independence of Vereigners. The wealthy newcomers from Venezuenezuela)
in
Caracas,
who put them in prison. Afla had no interest in associating with the Spanish
ter
the
fall
of
the
first
Venezuelan
Republic (1812),
businessmen and landowners, long-time resi53
they
had
to
emigrate
.
Dr.
Vargas
went to Europe
dents of Ponce. As a result, the contacts between
54
to
continue
his
studies
in
medicine
, following his
members of these groups remained limited. The
liberation
during
Simón
Bolívar’s
occupation
of La
Vargas Brothers after they arrived as merchants
55
Guaira
.
As
a
result
of
the
vicissitudes
that
bein Ponce purchased a sugar cane hacienda, Caño
fell
in
Venezuela
with
the
fall
of
Bolívar
in
1814,
de los Jueyes. The commercial partnership with
Anduze & Gil Co. from Saint Thomas became an many civilian and military leaders were forced into
important enterprise as the company provided the exile. Paradoxically, Puerto Rico also had an imVargas with the capital for the development of the migration of Venezuelan patriots, as the Vargas
Brothers, who favored the independence of their
hacienda47.
country.
The majority of the new colonists moved
Neither, Dr. Vargas nor his brothers were seen
directly to buy land, such as the ones previously
as
subversive
the authorities of the Island. The
mentioned, Tirado, Castro, Arévalo, and Paz Fal- explanation forby
this would be the fact that the four
cón, after having evaluated the best properties or five years that Vargas spent in Europe could
and available lands with favorable production have helped him to conceal his true identity as
prospects. Finally, they purchased and easily de- a legitimate believer for the independence of his
veloped the promising capacity of the plantations. country, before the local authorities; or maybe for
This was possible because of the money they had his own benefit, he pretended to be a loyal subject
brought along, their commercial contacts in the to the Spanish Crown. In 1825, following the final
Caribbean, the American Continent, Spain, and victory of Ayacucho in 1824, and the complete lithe foreign countries, all of which facilitated them beration of the Venezuelan territory, he “escaped”
to obtain credit.
from Puerto Rico back to Caracas56, probably after been uncovered and denounced by Governor
The immigrants from Venezuela were ra- Miguel De La Torre. In 1830, Vargas became the
ther different from the Spaniards who had arri- first President of the Universidad Central de Veneved directly from Spain, like Benito Paz Falcón, zuela in Caracas; established the School of Mewho came from Valladolid. First, the former, like dicine at the University, and the public education
Dr. Arévalo and Dr. Vargas, were generally older. system for his country57. He is one of the greatest
Besides, they would come with their families and figures in the history of medicine in Latin America.
relatives. They obtained the best housing in Ponce, and bought big farms or haciendas, since they
Dr. José María Vargas was one of the two dehad economic resources, and a majority of them legates for the Constituent Congress that took plaor their families, had been planters in their native ce in Valencia (Venezuela) that opposed Bolívar’s
land. Many of them had been owners of impor- expulsion from his position as President of Venetant major or minor businesses and others were zuela. He became the executor of the will left by
professionals. As the Vargas Brothers48, who had the Liberator (Simón Bolívar) on his death in 1830.
been in La Guaira (Venezuela) but had fled the Five years afterwards, in 1835, Vargas was elecrevolution and arrived in Ponce in 181749. A simi- ted the first civilian President of the Republic of
lar case was that of the town physician Domingo Venezuela, following General José A. Páez’ admiArévalo from Caracas, known before50. In Vene- nistration58.
zuela he worked as the second ranking surgeon at
the Military Hospital of the Artillery Corps; in 1814 Miguel Vargas returned to La Guaira to setthe was the surgeon of the Second Battalion in La le as a businessman after 1821; Bernardino died
61
rather young in Ponce and, later, Joaquín in 1829.
The wife of the latter remarried59. This created family arguments over the Vargas’ hacienda inherited by the widow60. In that year, 1829, the French
emigré Agustín Lavarthé, the husband of the sole
daughter of Dr. Vargas arrived in Puerto Rico61.
He was named by Vargas, who was living in Caracas, to represent Mrs. Teresa Ponce and the
Vargas Brothers in this family dispute. She was
the elderly and wealthy mother of the Vargas Brothers, who was also living in Caracas. They were
claiming a fourth of the Vargas' hacienda which
had been taken over by the widow and her recent
husband62, and the other half that was taken by
Anduze y Gil. Lavarthé successfully won the dispute in 1831, and in 1838 became the administrator of the entire Vargas property63.
along with them basic changes for Puerto Rico
which provided for its overall development, and
Ponce became the most important commercial region of the Island. As a result, a new social and
economic life style was set by the newcomers who
became land owners, businessmen, and military
or government officials, as well as in health services positions, in the urban or in the rural sector.
Those arriving from Venezuela were at the
time the most benefited of the Spanish emigrants
that came to Puerto Rico. We find among them
first magistrates, a future president, clergymen,
high rank military officers, physicians and pharmacists; educated people mastering languages,
commerce, agriculture, science and medicine. As
it was expected, they participated in all the main
aspects of the economic, social, health, and politiWe have presented physicians and pharma- cal life of the region, belonging to the ruling class.
cists emigrants who came to Ponce during the time This in turn, stimulated progress, economic and
of their country's independence. In general, they social wellbeing in Puerto Rico.
kept contact with their congeners settled in San
Juan, whom they employed mainly as representatives of their important businesses in the Capital. Some of these personalities and slave traders REFERENCES
were: José Xavier de Aranzamendi, the Goenagas, the Carreras, Jaime Dalmau, Pedro Guarch, 1. Salvador Arana Soto, Historia de la Medicina en Puerto Rico hasta 1898. Madrid, Artes Gráficas Medinaceli,
Juan de Dios Conde64, and Juan de Dios Cuebas,
S.A., 1974.
attorney at law65. Those merchants in San Juan 2.
John Lynch, Las revoluciones hispanoamericanas,
became important sources of credit and slaves to
1808-1826, Barcelona, Editorial Ariel, 1985, pp. 213-54.
Caracciolo Parra Pérez, Historia de la Primera Repúblitheir counterparts in Ponce for their commercial
ca de Venezuela, Biblioteca de la Academia Nacional
and agricultural activities.
de la Historia, Madrid, Ediciones Guadarrama, 1960.
Héctor García Chuecos, Historia Colonial de Venezuela,
Economic profits
3 tomos, Caracas, Archivo General de la Nación, 1986.
Anuario del Instituto de Antropología e Historia, 2 tomos,
Vol. IV,V,VI, Caracas, Universidad Central de VenezueA considerable amount of the profits of those
la, 1969. Demetrio Ramos Pérez, La ideología de la remerchants, planters and professionals, physicians
volución española de la guerra de la independencia en
and pharmacists, emigrating from Venezuela and
la emancipación de Venezuela y en la organización de
Spain was invested in Puerto Rico in the purchase
su primera república, Madrid, Instituto de Estudios Poof other properties and businesses, slaves, and for
líticos, 1962.
sustaining families living abroad. It was also spent 3. Rosa Marazzi, ‘El impacto de la emigración a Puerto
Rico de 1800 a 1830: Análisis estadístico’, Revista de
in the construction and furnishing of expensive
Ciencias Sociales, Universidad de Puerto Rico, Vol. 18
houses. Furthermore, part of their gains was spent
No. 1-2 (June 1974), pp. 1-44.
in acquiring costly items and traveling abroad.
4. The foreign immigrants were mainly German, French,
English, Irish, Italians, Corsicans, and North American.
The progress made by the southern society 5. Cayetano Coll y Toste, Boletín Histórico de Puerto
Rico, 14 tomos, San Juan, Tip. Cantero y Fernández
was remarkable. As a result, there was a chanCía, 1914. Cédula de Gracias, Vol. 1, pp. 297-304; Esge in its economic priorities leading to a drive for
tablecimiento de colonos extranjeros, pp. 304-7; La Céluxurious and refined belongings. As described by
dula de Gracias y sus efectos, rectificaciones históricas,
the Spanish civil officer Pedro Tomás de Córdova
Vol. XIV, pp. 3-24.
in 1830: "This sector is already beyond the infant 6. Francisco A. Scarano, Sugar and Slavery in Puerto
Rico: The Plantation Economy of Ponce, 1800-1850,
agricultural stage. Those living here search for
University of Winsconsin, 1984.
commodities leading to rich owners. One can feel 7. Wisconsin,
José G. Rigau-Pérez, Smallpox Epidemics in Puerto
among them the restfulness and luxury provided
Rico during the Prevaccine Era, 1518-1803. Journal of
by wealth and generally the taste for comfort and
the History of Medicine and Allied Sciences. Vol. XXXVII, No. 4, October 1982, p. 436.
life's own pleasures”66.
8. José G. Rigau-Pérez, Surgery at the Service of Theology: Postmortem Cesarean Sections in Puerto Rico and
Conclusions
the Royal Cedula of 1804. Hispanic American Historical
Review, 1995, 75:3. pp. 396. Actas del Municipio de
The immigrants from 1810 to 1830 brought
San Juan, 1803-1809.
62
9. Arana Soto, op.cit. Arana Soto, Catálogo de Médicos 26.
Luis González Vales, Alejandro Ramírez y su tiemde Puerto Rico de siglos pasados. Burgos, Imprenta Al- po: ensayos de historia económica e institucional, San Juan,
decoa, 1966. Arana Soto, Catálogo de Farmaceúticos Puerto Rico, Editorial Universidad de Puerto Rico, 1978.
de Puerto Rico, 1512-1925. Burgos, Imprenta Aldecoa, Same author: ‘Alejandro Ramírez y la crisis del papel mone1966. On Dr. José Luveres: AGPR, FGE, Asuntos Polí- da: Apuntes para la historia económica de Puerto Rico en el
ticos y Civiles, c. No. 191, ent. 72.
siglo XIX’ (Conference at the Ateneo de Puerto Rico, 1974).
10. Ilia Del Toro, ed., Actas del Cabildo de Ponce, 1812- 27.
Luis González Vales, ibid, Alejandro Ramírez u su
1823, Ponce, Municipio de Ponce, 1993, No. 4, 6. tiempo. Same author: ibid, ‘Alejandro Ramírez y la crisis del
Antonio Cuesta Mendoza, Historia de la educación en papel moneda: Apuntes para la historia económica de PuerPuerto Rico colonial, 2 tomos, Vol. II (1821-1898), Santo to Rico.
Domingo, Imprenta Arte y Cine, 1948, pp. 118-20, 169. 28.
AGPR, PNP, fs. 151-2, 159-60, 252-3, 1818; 128-9,
Dr. Vargas had pursued his specialties in Edinburgh and 1819, 1era. pieza.
London.
29.
AGPR, PNP, fs. 265v, 431-432, 562v-563, 1828.
11. Actas del Cabildo de San Juan de Puerto Rico, 1817- 30.
Ley 1813: Cruz Monclova, op. cit., tomo I, p. 55.
1819, San Juan, Municipio, No. 118. Arana Soto, op. cit, 31.
AGPR, FGE, “Emigrados”, 1821-37, box 54.
Historia de la medicina, pp. 207-8, 212, 214, 236-7.
32.
Cruz Monclova, op. cit., pp. 118-119. Actas del Ca12. Ibid., Actas del Cabildo, No. 102, 109. Dr. Francisco bildo, op. cit. pp. 29, 64, 83, 84, 91, 132, 159, 295.
Oller was the first one to introduce the vaccine in P.R.
33.
Cruz Monclova, ibid, p. 137. AGI, Sec. 10, Ultra13. Arana Soto, op. cit, Catálogo de Farmaceúticos, p. mar, Legajo 441. AGI, Santo Domingo, leg. 2339. Rosario
114.
Rivera, op. cit.
14. Arana Soto, op. cit. Historia de la Medicina, p. 218.
34.
Arana Soto, op. cit., Historia de la Medicina, p.
15. Del Toro, p. 159.
213.
16. Eduardo Newmann Gandía, Verdadera y auténtica his- 35.
Cruz Monclova, op. cit, Vol. I, p. 192. La Habana,
toria de la ciudad de Ponce desde sus primitivos tiem- Cuba.
pos hasta la época contemporánea, San Juan, Imprenta 36.
Cruz Monclova, op. cit., p. 137, 178, 194. Arana
Burillo, 1913, pp. 65-66. Francisco Lluch Mora, Noticias Soto, ibid, p. 213. Rosario Rivera, op. cit.
referentes a Ponce en los siglos XVIII Y XIX en la 1itera- 37.
Navarro García, op. cit., pp. 114-115. Díaz’ book
tura de viajeros, crónicas e informes, Ponce, Centro de “Recuerdos sobre la rebelión de Caracas” was published in
Investigaciones Folklóricas de Ponce, 1986. Coll y Tos- Madrid in 1829.
te, op. cit, ‘Epistolario del Historiador’: Salvador Brau, 38.
José G. Rigau-Pérez, op. cit, Smallpox, pp. 423‘Carta a D. Pedro de Salazar sobre los orígenes de Pon- 438. Rigau-Pérez, “La Real Expedición Filantrópica de la
ce’, Vol. X, pp. 222-56.
Vacuna de la Viruela: Monarquía y Modernidad en 1803”.
17. Jesús Raúl Navarro García, Puerto Rico a la sombra Puerto Rico Health Sciences Journal, Vol. 24, No. 3, sept.
de la independencia continental, 1815-1840, San Juan, 2004, pp. 223-231. Arana Soto, La sanidad en Puerto Rico
Centro de Estudios Avanzados de Puerto Rico y el Cari- hasta 1898. San Juan, Academia Puertorriqueña de la Hisbe; Sevilla, Escuela de Estudios Hispano-Americanos, toria, 1978. Ilia del Toro, op. cit., pp.63-293. Arana Soto, op.
1999, p. 66-67.
cit., Historia de la Medicina, p. 227.
18. 0n Meléndez Bruna: Lidio Cruz Monclova, Historia de 39.
Ibid. Newmann Gandía, op. cit., p. 50.
Puerto Rico, Siglo XIX, 6 tomos, San Juan, Editorial 40.
Cifre de Loubriel, op. cit., La inmigración a Puerto
Univesidad de Puerto Rico, 1970, Vol. I (1808-68), pp. Rico, p. LXI.
18-102. On González de Linares: Cruz Monclova, Vol.. 41.
Raquel Rosario Rivera, Los emigrados llegados a
I, pp. 136-72. Linares was one of the fifty-two merchants Puerto Rico procedentes de Venezuela (1810-1848). San
established in Caracas in 1805: Mercedes M. Álvarez Juan, ESMACO Printers Corp., 1992.
F., Comercio y comerciantes y sus proyecciones en 42.
AGPR, PNP, Decreto orgánico, Elecciones, box 48,
la independencia venezolana, Caracas, Ministerio de leg. Donativos 1822.
Educación, Tip. Vargas, 1964, p. 59. Manuel Lucena 43.
Ivette Pérez-Vega, ‘Las oleadas de inmigracion
Salmoral, El comercio caraqueño a fines del período es- sobre el sur de Puerto Rico: El caso de las sociedades merpañol: Mercados, comerciantes e instrumentos de cam- cantiles de Ponce, 1816-30’, unpub. PhD diss., University of
bios, Caracas, Universidad de Santa María, 1984, pp. Valladolid, Spain, 1986.
27-28.
44.
AGPR, PNP, fs. 221, 1822; 175v-6v, 1820. AGPR,
19. On De Latorre: Cruz Monclova, op. cit., pp. 139, 175- FGE, Asuntos políticos y civiles, Pasaportes 1795-1819, Li222. Córdova, Memorias geográficas, históricas, econó- cencias 1819, c. 151, ent. 51. AGPR, FGE, Extranjeros, c.
micas y estadísticas de la Isla de Puerto Rico, Vol. IV, 96, ent. 28, 1er. doc. AGPR, PNP, fs. 139-41, 1818; 221,
pp. 159-69.
1822. AGPR, PNP, fs. 439-41v., 1827.
20. Cruz Monclova, ibid., p. 157.
45.
The first bank in Puerto Rico was established in
21. Coll y Toste, op. cit., ‘Socorro de los emigrados de Ve- 1890. Cruz Monclova, op. cit., Vol. III, third section, p. 238.
nezuela’, Vol. VI, p. 317; ‘Circular del gobernador Me- Ana Mercedes Santiago de Curet, Crédito, Moneda y Banléndez para proteger a los emigrados venezolanos’, Vol. cos en Puerto Rico durante el siglo XIX, Río Piedras, Puerto
XII, pp. 42-3.
Rico, Editorial Universidad de Puerto Rico, 1978.
22. Estela Cifre de Loubriel, La inmigración a Puerto Rico 46.
Ivette Pérez Vega, El cielo y la tierra en sus madurante el siglo XIX, San Juan, Puerto Rico, Instituto de nos: Los grandes propietarios de Ponce, Río Piedras, PuerCultura Puertorriqueña, 1964, pp. L, LXVII-III. Same au- to Rico, Editorial Huracán,1985, p. 73.
thor: La formación del pueblo puertorriqueño, La contri- 47.
Pérez Vega, op. cit., Las oleadas de inmigración,
bución de los catalanes, baleáricos y valencianos, San pp. 350-366.
Juan, Puerto Rico, Instituto de Cultura Puertorriqueña, 48.
AGPR, PNP, f. 190, 1821.
1975.
49.
AGPR, FGE, Emigrados, 1815-37, ‘Relación de los
23. Birgit Sonesson, ‘Puerto Rico y San Tomás en conflic- emigrados de Costa Firme establecidos en la jurisdicción de
to comercial, 1839-43’, unpubl. MA thesis, University of Coamo’, box 54, ent. 21; ‘Lista que..., tiendas de mercería y
Puerto Rico, 1973, first chapter.
pulpería’, 1816, Ponce, box 186, ent. 69.
24. AGPR, PNP, fs. 130-31v, 1830.
50.
Actas del Cabildo de San Juan de Puerto Rico,
25. Coll y Toste, Boletín, op. cit, ‘El papel moneda en Puer- 1817-1819. San Juan, Municipio, Acta No. 2, 12 May 1817.
to Rico’, Vol. III, p. 225.
63
51.
Francisco Alejandro Vargas, Médicos, cirujanos y
practicantes, Caracas, Academia Nacional de la Historia,
1960, núm. 45, p. 111.
52.
AGPR, FGE, ‘Lista de los vecinos blancos de Ponce’.
53.
0n José María Vargas and his family in Venezuela:
Blás Bruni Celli, Doctor José María Vargas, Obras Completas, 8 tomos, Caracas, Edición del Congreso de la República, 1986. Same author, ed., La hora de Vargas, Caracas,
Academia Nacional de la Historia, 1986. Andrés Eloy Blanco, Vargas, El albacea de la angustia, Caracas, Ediciones
del Ministerio de Educación Nacional, 1947. Elías Pérez
Sosa, La casa de Vargas, Caracas, Editorial Latorre, 1938.
54.
Ibid.
55.
AGPR, Tribunal de Justicia Mayor, Ponce, 183049, ‘Caso civil contra la testamentaría de Joaquín Vargas’.
Boxes without number.
56.
AHN, Ultramar, Vol. III, leg. 2.014, No. 4.
57.
See note 48.
58.
Ibid.
59.
See note 50.
60.
Miguel Vargas was established as a merchant in
Caracas in 1786: Manuel Lucena Salmoral, op. cit.
61.
AGPR, Tribunal de Justicia Mayor, Ponce, 183049, op. cit. Vargas, Médicos cirujanos, op. cit., p. 148. The
wife of Lavarthé was Josefa María Vargas Ponce.
62.
AGPR, Tribunal de Justicia Mayor de Ponce, ibid.
63.
AGPR, FGE, ‘Lista de los vecinos blancos de Ponce’. The property had 351 cuerdas, 46 slaves, and a value of
over 50,000 Spanish pesos in 1825.
64.
Carmen Campos Esteve, ‘La política del comercio:
Los comerciantes de San Juan, 1837-1844’, unpub. MA thesis, University of Puerto Rico, Río Piedras, 1986.
65.
Del Toro, op. cit., Acta No. 107, 20 July 1812.
66.
Pedro Tomás de Córdova, Memorias geográficas,
históricas, económicas y estadísticas de la Isla de Puerto
Rico, 5 tomos, San Juan, Puerto Rico, Instituto de Cultura
Puertorriqueña, 1968, Vol. 4, pp. 260-261.
RESUMEN
A principios del sigloXIX Puerto Rico
se encotraba en una una situación crítica
con una ausencia crónica de médicos, medicinas y facilidades hospitalarias. Pero, la
llegada de emigrantes de diferentes partes
del mundo contribuyó al desarrollo socioeconómico, a la mejoría de las condiciones
de la salud y al cuidado médico. Las Guerras de Independencia que arroparon a las
colonias hispanoamericanas (1808-1826)
resultaron en movimientos de poblamiento en la Isla, particularmente de Tierra Firme (Venezuela), como también de España
(1808-1814). En 30 años la población se
dobló. Entonces, Puerto Rico contó con 44
médicos, 13 farmaceúticos y 48 “curanderos”; el Municipio de Ponce tuvo 6 médicos
y 2 farmaceúticos. El progreso alcanzado
por la sociedad sureña fue notable. Los de
Venezuela fueron de los emigrantes más
beneficiados durante ese tiempo. Se caracterizaron por su educación, conocimiento
de idiomas, comercio, agricultura, ciencias
y la medicina. Esto propició el progreso y
el bienestar social y económico de Puerto
Rico.
OO
ACKNOWLEDGMENTS
n behalf of the Puerto Rico Medical As
sociation and Editorial Board we wish to THANK
the following AUTHORS and REVIEWERS for
their contribution in creation and development of
Volume 101, 2009 of the ‘Boletin AMPR’:
Humberto Lugo-Vicente MD
Editor-in-Chief ‘Boletin’ AMPR
AUTHORS
Abdiel Cruz MS
Ada M. Laureano EdD
Ada Rivera MD
Alejandro López Mas MD
Alexis Canino Rodríguez MD
Alfonso Martínez Taboas PhD
Alfredo E. Mercado Quiñones MD
Algia Ojeda MD
Ana Michelle García MD
Annette Pagán MD
Arturo Medina Ruíz MD
Awilda Alvarado Pomales MS
Beatriz Ramírez MD
Carene Oliveras García MD
Carlos Camacho MD
Carlos Claudio MD
Carlos Ramos MD
Carmen Gurrea MD
Charles D. Johnson, MD
Christine Fabelo MD
Cid Quintana Rodríguez MD
Claudia P. Rosales Álvarez MD
Cristina Ramos Romey MD
Diana Díaz MD
Dilka I. González Ortiz MD
Dorcas L. Ruiz Rodríguez MD
Doris H. Toro MD
Elías Bou Prieto MD
Félix A. Flecha MPH
Fernando Cabanillas MD
Fernando Santiago MD
Fernando Soto Torres MD
Frank Madera MD
Gabriel García MD
Gabriel L. Martínez MD
Gerald Isenberg MD
Gloria González Tejera MD
Gloria M. Suau MD
Héctor Brunet MD
Héctor E. Marcano MD
Helen Rovira MD
Hilton Franqui Rivera MD
Humberto Lugo Vicente MD
Ignacio Echenique MD
Iván González Cancel MD
Iván Pacheco MD
Ivette Pérez Vega PhD
Ivonne Z Jiménez Velázquez MD
Jadira Irizarry Padilla MD
Jaime Martínez Souss MD
Jaime Román MD
Janice Cáceres MD
Javier Jardón BS
Jenniffer González MD
Joanna J. Mercado Alvarado MD
Joel De Jesús Caraballo MD
Jorge J. Ferrer PhD
Jorge L. Falcón Chévere MD
Jorge Ortega Gil MD
Jorge Yarzebski MD
José Eugenio López MD
José G. Cabañas Rivera MD
José M. Busquets MD
José Martínez Toro MD
José Pereyó Díaz MD
José R. Rodríguez Gómez MD
José Ramírez Rivera MD
Juan A. González Sánchez MD
Juan C. Portela MD
Juan Carlos Zevallos MD
Juan J González Concepción MD
Juanita Centeno MPH
Judith Rodríguez PhD
Karen G. Martínez MD
Karen Rodríguez Maldonado MD
Karen Santiago MD
Kenneth Geil MD
Lelis Nazario MD
Linnette Rodríguez Figueroa PhD
Liza Paulo MD
Luis A. Serrano MD
Luis F Acevedo MD
Luis F. Rodríguez Ospina MD
Luis Marrero MD
Luis Muñoz MD
Luz N. Colon Martí MD
Maralexis Rivera MD
Marcia Cruz Correa MD
Mari González PhD
Maria Correa MD
María del Mar Estremera MD
María Isabel Dueño MD
María Ramos Fernández MD
Mariel Silva MD
Marielys Colón BS
Mario García Palmieri MD
65
Miguel González Manrique MD
Myrangelisse Ríos Pelati MD
Natalio J. Izquierdo Encarnación MD
Nelson E. Aguilar MD
Nereida González Berríos MD
Néstor J. Galarza MD
Priscila Hernández Vélez MD
Rafael Rodríguez MD
Ramón K. Sotomayor Ramírez, MD
Randy Quiñones Maldonado MS
Raquel Herrero MD
Raúl García Rinaldi MD
Ricardo G. Colacioppo Saavedra MD
Roberto Ayala MD
Rolance G. Chavier Roper MD
Rosa Janet Rodríguez PhD
Roxana Soltero MD
Salvador Villanueva MD
Samuel Olmeda ORT
Susan Corey PhD
Tamara Arroyo Cordero MD
Tania Díaz MD
Vangie Texidor MS
Vilma McCarthy, MD
Vylma Velazquez MD
Wayca R Céspedes Gómez MD
Weldon Mauney MD
William Cáceres MD
Yadiel A. Alameda MD
Yadira Ramos Arias MD
Eduardo Rodríguez MD
Eduardo Santiago Delpín MD
Enrique Vázquez Quintana MD
Félix Seda MD
Francisco J. Muñiz Vázquez MD
Francisco Joglar Pesquera MD
Frank Escobar Roger MD
Humberto Lugo Vicente MD
Ibrahim Pérez MD
Jorge Bertrán Pasarell MD
Jorge Martínez Díaz MD
José A. Franceschini Carlo MD José Escabí Mendoza MD
José Ginel Rodríguez MD
José Ramírez Rivera MD
José Rodríguez Gómez MD
José Serrano Muñoz MD
Juan Aranda Ramírez MD
Luis Izquierdo Mora MD
Luis Rodríguez Ospina MD
Mario García Palmieri MD
Melvin Bonilla Félix MD
Miguel Campos MD
Natalio J. Izquierdo Encarnación MD
Néstor J. Galarza MD
Pablo Marrero MD
Pedro Mayol MD
Rafael Ruiz Quijano MD
Raúl Armstrong Mayoral MD
Roberto Muñoz Marín MD
Walter Frontera MD
Yocasta Brugal MD
REVIEWERS
Albert de la Vega MD
Anette Pagan MD
Carlos G. Díaz MD
Carlos González Oppenheimer MD
Special thanks to Mr. Juan Laborde and his expert
intellectual computerized ability in forging every
page design of the print and web version of Volume 101, 2009 of the ‘Boletin’.
PRENSA MédicA
El periódico dirigido a
la comunidad médica y
el paciente puertorriqueño
ido
Conten
Núm. 2
Año 21
p.3
sidente,
je del Pre
Mensa
Noticias,
a la
Afiliado
Médica
Asociación
Americana
ca ció n
de la
ión
As oc iac
o
de Pu ert
M éd ica
Año 21
Ri co •
Medicina
de
y la salud
bióticos
Los pre
D,
los niños ner Lugo, LN
Mi
Dennice
r
al provee
la calidad eso y
antía de
el acc
mejor gar que garantice ientes. La
pac
ión
un sistema cción de los
investigac arrosele
enta la
la libre
des
encia fom ovación en el
pet
de
com
ología,
a y la inn
científic icamentos y tecn problemas
los
llo de med respondan a
que
6
manera
página
a en la
Continú
idos
Distingu
s
scritore
se
ones
as profesi
es; amb de observar a
escritor
ica
un
profesión, La tarea méd
es como
va.
za de su
nóstico
naturale de una narrati
Un diag intuición y la
, por la
n
ración.
, la
iente
icos son la construcció
e una nar
eriencia
Los méd
de
l produc a al unir la exp
con su pac
vínculo
historia
lucrado
tienen el e y recopilar su lve más complej temente invo
cien
un pacient la trama se vue e estar lo sufi
de
deb
don
ico
méd
texto,
tación. El
interpre
nado, MD
a
Médic
Prensa 9387
9387
po Box n pr 00908san JUa
Uested
vICe req
e ser
CHanG
rd
t standa
presor
taGe
U.s. pos
paId
n, p.r.
san JUa 3007
no.
perMIt
Anunciarse en Prensa Médica:
Publishing Resources, Inc.
Ron Chevako 787-647-9343
tor, p.4
del Edi
nidad
r con dig
Envejece rdo Mora, MD
uie
Luis Izq
, p12
n I. Maldo
Norma
p3
ritorio
Del Esc
pez león
zada del va
La pun
p.14
evako Ba
Terry Ch de Emergencia,
Sería
nte
tentes.
Preside
s pre exis que exista la
er, MD,
dicione
vier Rop
l, aun
, se
por con
e G. Cha
en el cua
pública
Rolanc
presiun sistema de una opción uradoras
gestión
aseg
o de la
ciación
posibilidad“exchange” de
puedan
comienz
, la Aso
do los
personas
Desde el Barack Obama
ría un
las
yan
alda
crea
de
resp
de
que se dilua
s, en don
Rico ha
cepto
dencial
privada de tal manera
prim
de Puerto de salud y el con como
una
dica
rse
ga
Mé
agr upa
socied, tal y
manten
reforma
gos y se os. En nuestra es la
planes de universal a la salu actual.
los ries
ia
tod
ión
petenc
le para
de acceso e la administrac
accesib
a la com
átic
pon
ocr
pro
los
r un
dad dem
en crea
se basa
ine
puesta
discrim
Esta pro el cual no se
en
sistema
Médico
2
Geriatría
Pu bli
e
cepto d les
o al con
ra
Respald n fondos fede ara
p
de
parida aid y Medicare os
n
ic
de Med anos america
d
o
a
ic
d
R
u
o
ci
los
uert
tes en P
residen
, AMPR
Médicos
• Núm.
MBA
, p.15
Nutrición
o
o métod
omía com
a
La vasect ción masculin
liza
de esteri uer-Merino, MD
Pedro Piq
ía, p.15
Urolog
es
La diabet tiago, MD
San
Luis A. , p. 16
Medicina
y te
barazada
¡Estás em un sonograma!
n,
ordenaron rdo-Encarnació
e, a la
ión. Deb
uie
compas te para ser
Luis Izq
a tenerle
cien
como par la distancia sufi el escritor,
6
MD
y
r
logía, p.1
vez, tene bos, el médico la vida de
Gineco
Am
ad por
exosid
crítico.
sus
ades y
ten la curi
de
un
compar por sus necesid
incluye
ser vicio
que
ás,
ectura al
los dem una curiosidad
o. Tanto
ias;
resultad
La arquit : de París
cesu
pro
perienc
car
ina
comuni
an de un
la medic
deseo de el otro particip
ificado
n
o
del sign
sentido,
das
uno com
a San Jua uierdo, MD
entendi
ción de
Izq
y
o
es
so de crea ncias que no son l del caso,
tali
art
Na
ina y las
de experie nte. El historia rtes de
La medic 19
repo
ame
ico, los casos en
p.
complet
nte méd
Letras,
de
el expedie presentación
, todas
o, la
s médicas
de
progres
ferencia orias.
prolapso
ios y con
seminar de éstas son hist
ia
iento del
Tratam vés de la histor
y cada una
litetra
stras de
e, MD, a
recto a
obras mae
les de
sic
Echeniqu
l que las diferentes nive
Al igua
Ignacio inosa, MD, Jes
tienen
dades pre- es
que
rme
ra,
Esp
ratu
enfe
idad
Ángel
sión, las
complej
MD
22
va.
compren plicaciones y
Marrero, medicina, p.
ión narrati
de
de
sentan com ejan a una ficc
después
Historia
un
cy, quien
que se asem
lter Per
virtió en
El Dr. Wa erculosis se con decía que
o,
r tub
complet compartían
contrae
a tiempo
tas
itor
elis
nov
escr
to el
icos y los idénticas. Tan
1
los méd
as
Médica
analític
Prensa
4
destrezas
página
a en la
Continú
Usted puede descargar este formulario y encontrar instrucciones y costo de cuotas en
ww.asociacionmedicapr.org
(In vitro data; clinical significance unknown.
Full course of therapy is complete in 7 days.)1,2
n
ZYMAR® ophthalmic solution rapidly eradicates
key pathogens in vitro, including:
S aureus: eradicated in 15 minutes1,*
S epidermidis: eradicated in 30 minutes1,*
S pneumoniae: eradicated in 10 minutes2,*
H influenzae: eradicated in 5 minutes2,*
* Time to reach kill threshold. 10 CFU/mL is the lower limit of detection and is
indistinguishable from complete kill.
ZYMAR® ophthalmic solution is indicated for the treatment of bacterial conjunctivitis caused by susceptible strains
of the following organisms: Corynebacterium propinquum,† Staphylococcus aureus, Staphylococcus epidermidis,
Streptococcus mitis,† Streptococcus pneumoniae, and Haemophilus influenzae. (†Efficacy for this organism was studied
in fewer than 10 infections.)
Important Safety Information: NOT FOR INJECTION. ZYMAR® ophthalmic solution should not be injected
subconjunctivally, nor should it be introduced directly into the anterior chamber of the eye. As with other antiinfectives, prolonged use may result in overgrowth of nonsusceptible organisms, including fungi. If superinfection
occurs, discontinue use and institute alternative therapy. Patients should
be advised not to wear contact lenses if they have signs and symptoms of
bacterial conjunctivitis.
®
The most frequently reported adverse events occurring in approximately 5%
to 10% of the overall study population were conjunctival irritation, increased
lacrimation, keratitis, and papillary conjunctivitis.
Please see brief prescribing information on adjacent page.
1. O’Brien TP. Antimicrobial efficacy of ZYMAR® and Vigamox® against Staphylococcus species. Refract Eyecare Ophthalmol. 2003;7(12):15-18. 2. Novosad BD, Callegan MC.
Killing of Streptococcus pneumoniae, methicillin-resistant Staphylococcus aureus (MRSA), and Haemophilus influenzae ocular isolates by fourth-generation fluoroquinolones.
Poster presented at: 78th Annual Meeting of the Association for Research in Vision and Ophthalmology; April 30-May 4, 2006; Fort Lauderdale, FL.
©2009 Allergan, Inc., Irvine, CA 92612 www.allergan.com ® marks owned by Allergan, Inc.
ZYMAR® is licensed from Kyorin Pharmaceutical Co., Ltd., Tokyo, Japan. APC50TC09 803807

S aureus: eradicated in - Asociacion Medica de Puerto Rico

Transcription

Similar documents

Nivel 2 - Aspectos Culturales

Presentación de PowerPoint

Nivel 3

Estudio de la electromecánica cardíaca mediante postprocesado de

Cardiología Nuclear - Human Health Campus

dossier microdacyn

Circulatorio

PROGRAMA DE RESIDENCIA SERVICIO DE CARDIOLOGIA Período 2009-2010

Mexico - Smithsonian Latino Center

St. Peter Chanel Catholic Church

Rivercenter Mall restores history

Alta Costura, costura de altura en los años 50

Descargar PDF - Newton College

Biodeterioro algal en monumentos históricos mayas de la zona

Agosto 2014 - Recinto de Arecibo - Universidad Interamericana de

p11 p11 - Manhattan Times News

Validación antibiótica de plantas medicinales del noroeste de

Bitter sweet mural blessing for San Anto

Protocolo diaganóstico y terapéutico en perros sospechosos de

memoria de investigación hospital clínico san carlos

Estudio del sistema nervioso autónomo en la enfermedad de

Caracterización de proteínas con actividad antifúngica producidas