María Guadalupe Valades-Mejía1, María Lilia Domínguez-López1, José Luis Aceves-Chimal2, Alfredo Leaños Miranda3, Abraham Majluf-Cruz4, Irma Isordia-Salas5. 1. Escuela de Ciencias Biológicas. IPN, Mexico. 2. Servicio de Cirugía Cardiovascular, Centro Médico Nacional 20 de Noviembre, ISSSTE, Mexico. 3. Unidad de Investigación Médica en medicina Reproductiva, Unidad Médica de Alta Especialidad, Hospital de Ginecología y Obstetricia núm. 4, IMSS, Mexico. 4. Unidad de Investigación Médica en Trombosis, Hemostasia y Aterogénesis, Hospital General Regional Dr Carlos Mac Gregor Sánchez Navarro, IMSS, Mexico. 5. Unidad de Investigación Médica en Trombosis, Hemostasia y Aterogénesis, Hospital General Regional Dr Carlos Mac Gregor Sánchez Navarro, IMSS, Mexico. irmaisordia@yahoo.com.mx.
Abstract
BACKGROUND: Acute myocardial infarction is the first cause of morbidity and mortality in the world, resulting in the combination of genetic and environmental factors. It has been postulated that the R353Q polymorphism of the coagulation FVII gene represents a protective factor for acute myocardial infarction, whereas the N700S polymorphism in the thrombospondin-1 gene is associated with an increased risk for acute myocardial infarction; however, the results are still contradicted. The objective of the study was to examine the possible association of the FVII R353Q and N700S polymorphism and acute myocardial infarction in Mexican patients with acute myocardial infarction younger than 45 years old. METHODS: Case-control study that included 252 patients who were diagnosed with acute myocardial infarction and 252 apparently healthy, age- and gender-matched individuals without a history of coronary artery disease. R353Q and N700S polymorphisms were determined in all participants by PCR-RFLP. RESULTS: There was no statistical significant difference in genotype distribution (p = 0.06) between the acute myocardial infarction and control groups. Also, there was a similar genotype distribution of N700S polymorphism between stroke and control groups (p = 0.50). Hypertension, diabetes mellitus, family history of coronary disease and dyslipidemia represented independent risk factors for acute myocardial infarction. CONCLUSIONS: Polymorphisms R353Q and N700S do not represent a protective or risk factor for acute myocardial infarction in young Mexican individuals.
BACKGROUND:Acute myocardial infarction is the first cause of morbidity and mortality in the world, resulting in the combination of genetic and environmental factors. It has been postulated that the R353Q polymorphism of the coagulation FVII gene represents a protective factor for acute myocardial infarction, whereas the N700S polymorphism in the thrombospondin-1 gene is associated with an increased risk for acute myocardial infarction; however, the results are still contradicted. The objective of the study was to examine the possible association of the FVII R353Q and N700S polymorphism and acute myocardial infarction in Mexican patients with acute myocardial infarction younger than 45 years old. METHODS: Case-control study that included 252 patients who were diagnosed with acute myocardial infarction and 252 apparently healthy, age- and gender-matched individuals without a history of coronary artery disease. R353Q and N700S polymorphisms were determined in all participants by PCR-RFLP. RESULTS: There was no statistical significant difference in genotype distribution (p = 0.06) between the acute myocardial infarction and control groups. Also, there was a similar genotype distribution of N700S polymorphism between stroke and control groups (p = 0.50). Hypertension, diabetes mellitus, family history of coronary disease and dyslipidemia represented independent risk factors for acute myocardial infarction. CONCLUSIONS: Polymorphisms R353Q and N700S do not represent a protective or risk factor for acute myocardial infarction in young Mexican individuals.
Entities:
Keywords:
Coagulation FVII; acute myocardial infarction; factor VII de la coagulación; infarto agudo de miocardio; polimorfismo; polymorphism; thrombospondin-1; trombospondina-1