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IMPACTO DE LOS POLIMORFISMOS DE LAS GLUCOPROTEINAS PLAQUETARIAS SOBRE LA ENFERMEDAD CORONARIA
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INICIO DEL TRATAMIENTO CON ESTATINAS Y PROGRESIÓN DE LA DIABETES
JAMA Internal Medicine
Difundido en siicsalud: 28 oct 2021

IMPACTO DE LOS POLIMORFISMOS DE LAS GLUCOPROTEINAS PLAQUETARIAS SOBRE LA ENFERMEDAD CORONARIA

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A pesar de la abundante literatura disponible, la significación clínica y el impacto de los polimorfismos en las glucoproteínas receptoras en las plaquetas como factores de riesgo potenciales para enfermedades multifactoriales, como la cardiopatía isquémica o la enfermedad coronaria, todavía son inciertos.
chriluc9.gif Autor:
Luc Christiaens
Columnista Experto de SIIC
Artículos publicados por Luc Christiaens
Coautor
Laurent Macchi.* 
Medicine doctor. Service d'Hématologie Centre Hospitalo-Universitaire de Poitiers France*
Recepción del artículo
19 de Diciembre, 2003
Primera edición
19 de Mayo, 2004
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
Generalmente, el infarto de miocardio es la consecuencia de la formación de trombos intravasculares sobreimpuestos a la rotura de una placa en una arteria coronaria. Las plaquetas desempeñan un papel fundamental en la iniciación y en la formación del trombo. Diferentes estudios, a menudo con resultados contradictorios, evaluaron las relaciones entre diversos polimorfismos de las glucoproteínas plaquetarias implicadas en la agregación y en la presencia de alteraciones oclusivas de las arterias coronarias. En esta revisión, destacamos el impacto terapéutico y clínico de diversos polimorfismos de las glucoproteínas plaquetarias (GP IIIa, GP Ia, GP Ibα, GP VI).El polimorfismo de la GP IIIa PIA1/A2 ejerce influencia sobre el receptor plaquetario para el fibrinógeno, el proceso de activación plaquetario y así podría modificar la trombogenicidad de las plaquetas, la respuesta al efecto antiplaquetario de la aspirina, la eficacia del tratamiento con estatinas y el riesgo de eventos adversos luego de la angioplastia. El impacto del polimorfismo GP IIIa PIA1/A2 en presencia de enfermedad cardiovascular isquémica en la población general es probablemente débil pero es más obvio en la minoría de hombres homocigotas PlA2/A2. El polimorfismo de GP Ia C807T influye sobre el receptor plaquetario para el colágeno y no está asociado con un aumento en el riesgo de infarto de miocardio o de eventos adversos luego del implante de stents coronarios. Diversos polimorfismos de GP Ibα pueden ejercer influencia sobre el receptor funcional para el factor de Von Willebrand y contribuir al desarrollo de trombosis intracoronaria. A pesar de los numerosos estudios, el impacto verdadero de los polimorfismos de las glucoproteínas plaquetarias no está todavía claro en aquellas enfermedades multifactoriales y multigénicas como el infarto de miocardio o la coronariopatía.

Palabras clave
Plaquetas, polimorfismo, arteria coronaria, stent, glucoproteína


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Abstract
Myocardial infarction is usually the consequence of intravascular thrombus formation superimposed upon ruptured plaque in a coronary artery. Platelets plays a pivotal role in the initiation and thrombus formation. A lot of conflicting studies have evaluated the relations between various platelet glycoprotein polymorphisms implicated in the platelet aggregability and the occurrence of coronary arterial occlusive disorders. In this review, we highlight the clinical and therapeutic impact of several platelet glycoprotein polymorphisms (GP IIIa, GP Ia, GP Ibα, GP VI).The GP IIIa PlA1/A2 polymorphism influence the platelet receptor for fibrinogen, the platelet activation process and then could modify the thrombogenicity of platelets, the response to the antiplatelet effect of aspirin, the efficacy of statin therapy and the risk of adverse event after angioplasty. The impact of the GP IIIa PlA1/A2 polymorphism on the occurrence of ischemic cardiovascular disease is probably weak in the general population but more obvious in the minority of men homozygous PlA2/A2. The GP Ia C807T polymorphism influence the platelet receptor for collagen and is not associated with an increased risk of myocardial infarction or adverse event after coronary stenting. Several platelet GP Ibα polymorphisms may influence the functional receptor for Von Willebrand factor and contribute to the development of intracoronary thrombosis. Despite numerous studies, the real impact of platelet glycoprotein polymorphisms is still unclear for such multifactorial and multigenic diseases as myocardial infarction or coronary artery disease.Abstract francésLes cardiopathies ischémiques sont en majorité secondaires au développement de thrombus au contact de plaques d'athérosclérose intra coronaires. Les plaquettes jouent un rôle central dans l'initiation et la formation des thromboses intra artérielles. De nombreuses mutations des gènes codant les glycoprotéines membranaires responsables de l'adhésion et de l'agrégation plaquettaire sont connues. L'évaluation de la responsabilité de ces polymorphismes dans la survenue de cardiopathies ischémiques a fait l'objet de nombreux travaux souvent controversés. Dans cette revue de la littérature nous analyserons l'impact clinique et thérapeutique des principaux polymorphismes des glycoprotéines plaquettaires (GPIIIa, Ia, Ibα et VI).Le polymorphisme PlA1/A2 de la GP IIb/IIIa, principal site de fixation plaquettaire du fibrinogène, intervient dans la formation de thrombus, dans l'efficacité de l'aspirine et des statines, et dans le risque d'événement après angioplastie coronaire. Le polymorphisme PlA1/A2 est un facteur de risque d'infarctus probablement faible dans la population générale mais semble un peu plus important en cas d'hommes jeunes homozygotes PlA2/A2. Le polymorphisme C807T de la GP Ia-IIa concerne les récepteurs plaquettaires au collagène et n'augmente pas le risque d'infarctus du myocarde. Plusieurs types de polymorphismes de la GP Ibα paraissent favoriser la survenue de thromboses intra coronaires par l'intermédiaire de la fixation du facteur Von Willebrand. En dépit de nombreuses études sur de larges cohortes de patients l'importance clinique de ces polymorphismes plaquettaires reste incertain, du fait de difficultés méthodologiques et du caractère multifactoriel des cardiopathies ischémiques.

Key words
Platelet, polymorphism, coronary artery, stent, glycoprotein


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Especialidades
Principal: Cardiología
Relacionadas: Cirugía, Hematología, Medicina Interna



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Bibliografía del artículo
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