Impacto de los polimorfismos de las glucoproteínas plaquetarias sobre la enfermedad coronaria
Salud(i)ciencia (Impresa); 12 (4), 2004
Publication year: 2004
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 Iba, 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 Iba 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.
Glicoproteínas, Polimorfismo Genético, Cardiopatías, Activación Plaquetaria, Angioplastia, Aspirina, Efectos Colaterales y Reacciones Adversas Relacionados con Medicamentos, Enfermedad de la Arteria Coronaria, Enfermedades Cardiovasculares, Factor de von Willebrand, Glicoproteínas de Membrana Plaquetaria, Infarto del Miocardio, Inhibidores de Hidroximetilglutaril-CoA Reductasas, Vasos Coronarios, Trombosis