RESUMEN

OBJECTIVE: Drug-eluting stents (DES) have reduced restenosis rates compared with bare-metal stents. P27 and P53 play important roles in the signal transduction leading to neointimal growth inhibition and induction of apoptosis of smooth muscle cells due to rapamycin and paclitaxel. We hypothesized that genetic variants of P27 and P53 influence the development of restenosis and the clinical outcome of patients receiving DES. METHODS: Polymorphisms in the genes encoding for P27 and P53 were tested for their association with restenosis and major adverse cardiac events. P27 C-79T and P53 G72C polymorphism genotypes were determined in a series of 433 consecutive patients receiving DES. Follow-up angiography after 6 months was performed in 87% of the patients. Genotyping was performed with PCR-based methods. RESULTS: For patients with the respective P27 C-79T and P53 G72C genotypes, the angiographic restenosis rates were between 5.0 and 22.0%, and the clinical restenosis rates were between 0.0 and 16.3%, without significant differences for the studied genotypes (p > 0.19). There was no association of the studied genotypes with the 1-year incidences of death and myocardial infarction. CONCLUSION: This study could not demonstrate a clinically relevant role of P27 and P53 polymorphisms in the processes leading to in-stent restenosis.

Asunto(s)

Angioplastia Coronaria con Balón , Enfermedad de la Arteria Coronaria/terapia , Inhibidor p27 de las Quinasas Dependientes de la Ciclina/genética , Stents Liberadores de Fármacos/efectos adversos , Oclusión de Injerto Vascular/genética , Polimorfismo Genético , Proteína p53 Supresora de Tumor/genética , Anciano , Estudios de Cohortes , Femenino , Predisposición Genética a la Enfermedad , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Factores de Riesgo , Transducción de Señal

RESUMEN

Inflammation plays an important role in the pathogenesis of atherosclerosis and acute coronary syndromes. Cytokines IL-10 and TNF-alpha exert opposite functions in inflammatory reactions, IL-10 acting predominantly as an antiinflammatory and TNF-alpha as a proinflammatory factor. Functional single nucleotide polymorphisms in the genes of IL-10, TNF-alpha, and TNF-beta are associated with gene expression and plasma levels of IL-10 and TNF-alpha. The aim of the study was to assess whether these IL-10 and TNF gene polymorphisms are related to the risk of coronary artery disease (CAD) and myocardial infarction (MI). Consecutive, angiographically examined patients with significant coronary stenoses but without symptoms or signs of old or acute MI constituted the group with CAD (n=998) and patients with old or acute MI constituted the group with MI (n=793). Subjects with neither angiographic CAD nor symptoms or signs of MI (n=340) served as controls. They were matched with the patients for age and sex. Genotyping was performed with techniques based on the polymerase chain reaction. Allele frequencies, genotype distributions, and frequencies of allele combinations for three IL-10 promoter polymorphisms, -1082G/A, -819C/T and -592C/A, were similar between CAD patients, MI patients, and matched controls. Similarly, genetic analysis did not reveal group-specific differences for the TNF-alpha promoter polymorphisms -863C/A and -308G/A, as well as for the TNF-beta intron 1 polymorphism 252G/A. In addition, no relationship was found between specific combinations of IL-10 and TNF alleles, indicative of low IL-10 and high TNF-alpha production, respectively, and CAD or MI. The lack of association persisted also after adjusting for other cardiovascular risk factors. Our findings suggest that six different and functionally relevant polymorphisms of the genes coding for IL-10, TNF-alpha, and TNF-beta are neither separately nor in cooperation associated with the risk of CAD or MI in angiographically examined patients.

Asunto(s)

Enfermedad Coronaria/genética , Interleucina-10/genética , Linfotoxina-alfa/genética , Infarto del Miocardio/genética , Polimorfismo Genético , Factor de Necrosis Tumoral alfa/genética , Femenino , Frecuencia de los Genes , Genotipo , Humanos , Desequilibrio de Ligamiento , Masculino , Persona de Mediana Edad , Factores de Riesgo

RESUMEN

Inflammatory mechanisms play an important role in the process of restenosis after percutaneous coronary interventions, with cell adhesion molecules, including Mac-1 (CD11b/CD18), as key mediators. A single nucleotide polymorphism, 1323C/T, located in exon 11 of the CD18 gene has been previously described, but its functional and clinical significances have not yet been studied. We assessed whether an association exists between this polymorphism and restenosis after coronary stenting. Clinical and angiographic measures of restenosis were evaluated over 1 year after coronary stent placement in 1,207 consecutive patients. Angiographic restenosis was defined as a > or =50% diameter stenosis at follow-up angiography. Determination of the CD18 1323C/T genotype was based on the polymerase chain reaction technique. The frequency of the T allele was 0.34 and its presence reduced the 1-year risk of a major adverse cardiac event (death, myocardial infarction, target vessel revascularization) by 29% (p = 0.011). Carriers of the T allele had a significantly lower risk of angiographic restenosis compared with noncarriers (odds ratio 0.71, 95% confidence interval 0.55 to 0.92). The incidence of restenosis decreased as a function of the number of T alleles: 38.1% in patients with genotype CC, 31.7% in patients with genotype CT, and 26.0% in patients with genotype TT (p = 0.004). Thus, the 1323T allele of the CD18 gene is associated, in a gene dose-dependent manner, with a lower incidence of angiographic restenosis after coronary stenting. This finding suggests that Mac-1 is involved in the development of restenosis after coronary stent placement.

Asunto(s)

Angioplastia Coronaria con Balón , Antígenos CD18/genética , Enfermedad Coronaria/terapia , Reestenosis Coronaria/genética , Exones , Femenino , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Polimorfismo Genético

RESUMEN

Platelets are thought to contribute to development of restenosis following percutaneous coronary interventions. The glycoprotein Ia/IIa complex is a major platelet collagen receptor, its surface expression being influenced by two, linked single nucleotide polymorphisms (C807T and G873A) in the glycoprotein Ia gene. T807 is associated with increased expression of this integrin receptor. We assessed whether T807 is associated with an increased risk of restenosis in 1769 consecutive patients treated with coronary stenting. 6-month follow-up angiograms were available in 82.4% of the patients. C807T genotype distribution was CC in 35.8%, CT in 47.6% and TT in 16.6% of the patients. Restenosis (diameter stenosis > or =50% at follow-up angiography) occurred in 32.9% of CC, 31.5% of CT and 32.1% of TT patients (P=0.87). The rate of major adverse cardiac events (death, myocardial infarction or need of reintervention) within 1 yr was 21.6% for CC, 21.7% for CT and 21.2% for TT patients (P=0.98). Thus, carriage of the GP Ia T807 allele is not associated with an increased risk of restenosis or unfavorable late outcome following coronary artery stenting.

Asunto(s)

Enfermedad Coronaria/genética , Enfermedad Coronaria/terapia , Integrinas/genética , Adhesividad Plaquetaria/genética , Polimorfismo Genético , Stents/efectos adversos , Anciano , Secuencia de Bases , Intervalos de Confianza , Angiografía Coronaria , Enfermedad Coronaria/diagnóstico , Femenino , Marcadores Genéticos , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Datos de Secuencia Molecular , Oportunidad Relativa , Reacción en Cadena de la Polimerasa , Valor Predictivo de las Pruebas , Probabilidad , Pronóstico , Estudios Prospectivos , Receptores de Colágeno , Recurrencia , Medición de Riesgo , Factores de Riesgo , Sensibilidad y Especificidad , Índice de Severidad de la Enfermedad

RESUMEN

OBJECTIVES: To test the hypothesis that interleukin-1 receptor antagonist (IL-1ra) gene polymorphism contributes to the risk of restenosis after coronary stenting. BACKGROUND: Cytokines of the interleukin-1 (IL-1) family play a central role in regulating inflammatory responses. There is strong evidence to support IL-1 involvement in smooth muscle cell mitogenesis and extracellular matrix metabolism. The IL-1ra counters the proinflammatory effects of IL-1. The interleukin-1 receptor antagonist gene (IL-1RN) contains several well-characterized polymorphic sites that correlate with altered IL-lra levels. METHODS: In 1,850 consecutive patients, clinical and angiographic measures ofrestenosis were evaluated over one year after coronary stent placement. Repeat angiography at six months was achieved in 84% of the patients; angiographic restenosis was defined < or =50% diameter stenosis at follow-up. Genotyping for an exon 2 polymorphism (+2,018) of IL-1RN (alleles 1 and 2) was based on a polymerase chain reaction technique. RESULTS: Allele 2 frequency was 0.28. Carriers of allele 2 had a significantly lower risk for angiographic restenosis, odds ratio (OR) of 0.78 (95% confidence interval, 0.63 to 0.97) and target vessel revascularization, OR of 0.73 (0.58 to 0.92) compared with noncarriers. Risk reduction was especially significant in patients <60 years (n = 696), with OR of 0.63 (0.43 to 0.91) for angiographic restenosis and 0.55 (0.39 to 0.78) for target vessel revascularization. CONCLUSIONS: Allele 2 of the IL-1ra gene was associated with a lower incidence of restenosis after coronary stenting, particularly in younger patients. This finding supports a role of inflammation in the development of restenosis after stent placement.

Asunto(s)

Enfermedad Coronaria/terapia , Receptores de Interleucina-1/antagonistas & inhibidores , Sialoglicoproteínas/farmacología , Stents , Anciano , Enfermedad Coronaria/fisiopatología , Femenino , Humanos , Proteína Antagonista del Receptor de Interleucina 1 , Masculino , Persona de Mediana Edad , Polimorfismo Genético , Receptores de Interleucina-1/genética , Recurrencia , Sialoglicoproteínas/genética

RESUMEN

OBJECTIVE: We designed this prospective study to test the hypothesis that platelet antigen (PlA) polymorphism of glycoprotein (GP) IIIa is associated with an increased risk for adverse events after coronary stent placement. BACKGROUND: Platelets play a central role in arterial thrombosis. The PlA polymorphism of GP IIIa, a constituent of the fibrinogen receptor, may influence the platelet function and, thereby, the early outcome of patients after coronary stent placement. METHODS: The study included 1,759 consecutive patients with stable or unstable angina and successful coronary stent placement. Platelet antigen genotypes were determined by allele-specific restriction enzyme analysis. The end point of the study was a composite of death, myocardial infarction and urgent revascularization during the first 30 days after stent placement. RESULTS: The PlA1 genotype of the patients included was: 70.2% were homozygous for platelet antigen 1 (PlA1), 2.6% homozygous for platelet antigen 2 (PlA1), and 27.2% were heterozygous (PlA1/A2). The incidence of the composite end point was 5.5% among PlA2 carriers and 5.4% in homozygous PlA1 subjects (p = 0.94). It was 5.4% in PlA1/A1 patients, 4.8% in PlA1/A2 patients and 13.0% in PlA2A2 patients (p = 0.06). The combined incidence of death or myocardial infarction was 4.3% in PlA1/A1 patients, 4.2% in PlA1/A2 patients and 13.0% in PlA2/A2 patients (p = 0.02). CONCLUSIONS: The isolated presence of the PlA2 allele in heterozygous patients is not associated with any detectable increase in the risk for an adverse 30-day outcome after coronary stenting. This study suggests also that an increased risk is likely to be present in homozygous carriers of the PlA2 allele, but this should be confirmed in a much larger series of patients.

Asunto(s)

Antígenos CD/genética , Antígenos de Plaqueta Humana/genética , Trombosis Coronaria/genética , Glicoproteínas de Membrana Plaquetaria/genética , Polimorfismo Genético , Stents/efectos adversos , Anciano , Alelos , Angina de Pecho/cirugía , Antígenos CD/metabolismo , Antígenos de Plaqueta Humana/sangre , Angiografía Coronaria , Trombosis Coronaria/sangre , Trombosis Coronaria/complicaciones , Trombosis Coronaria/diagnóstico por imagen , ADN/análisis , Cartilla de ADN/química , Epítopos/sangre , Epítopos/genética , Femenino , Marcadores Genéticos , Genotipo , Humanos , Integrina beta3 , Integrinas/sangre , Integrinas/genética , Masculino , Persona de Mediana Edad , Infarto del Miocardio/sangre , Infarto del Miocardio/diagnóstico por imagen , Infarto del Miocardio/etiología , Oportunidad Relativa , Glicoproteínas de Membrana Plaquetaria/metabolismo , Reacción en Cadena de la Polimerasa , Pronóstico , Estudios Prospectivos , Factores de Riesgo

RESUMEN

BACKGROUND: The renin-angiotensin system is thought to play a role in coronary thrombosis and restenosis. Plasma angiotensin I-converting enzyme (ACE) activity is associated with an insertion/deletion polymorphism in the gene coding for ACE. The objective of this study was to test the hypothesis that the D allele of the ACE gene is associated with a higher risk for restenosis after coronary stent placement. METHODS AND RESULTS: This prospective study included 1850 consecutive patients with coronary artery disease who underwent intracoronary stent implantation. The adverse clinical events recorded were death, myocardial infarction, and target vessel revascularization. The primary end point of the study was restenosis (>/=50% diameter stenosis at follow-up angiography performed in 84% of the patients). The secondary end point was clinical outcome 1 year after the procedure. The restenosis rate at the 6-month angiographic follow-up was 32.8% in patients with the II genotype, 34.0% for patients with the ID genotype, and 31.2% for patients with the DD genotype (P=0.62). One-year event-free survival was 77.7% in patients with genotype II, 75.2% in patients with genotype ID, and 75.5% in patients with genotype DD (P=0.54). The lack of association was also present in the subgroup of patients with a low risk for restenosis: the restenosis rate was 21.7% in II carriers, 23.4% in ID carriers, and 19.7% in DD carriers (P=0.83). CONCLUSIONS: The ACE DD genotype or D allele does not influence the 1-year clinical and angiographic outcome of patients undergoing coronary stent placement. These data suggest that routine determination of the ACE genotype may not help identify patients who are at a higher risk of thrombotic and restenotic events after coronary stent placement.

Asunto(s)

Trombosis Coronaria/genética , Eliminación de Gen , Peptidil-Dipeptidasa A/genética , Polimorfismo Genético , Stents , Anciano , Constricción Patológica , Angiografía Coronaria , Enfermedad Coronaria/epidemiología , Enfermedad Coronaria/genética , Enfermedad Coronaria/cirugía , Trombosis Coronaria/epidemiología , Trombosis Coronaria/cirugía , Femenino , Estudios de Seguimiento , Predisposición Genética a la Enfermedad , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Revascularización Miocárdica , Recurrencia , Factores de Riesgo , Resultado del Tratamiento

RESUMEN

The glycoprotein complex Ia/IIa (GP Ia/IIa) is a major collagen receptor on platelets and other cell types. Recently, linked polymorphisms within the coding region of the GP Ia gene (C807T and G873A) were identified that are related to GP Ia/IIa surface expression. The T807/A873 allele is associated with high expression, whereas the C807/G873 allele is associated with low surface expression of GP Ia/IIa. Subsequently, the T807 allele was found to be associated with coronary and cerebral infarction in younger patients. Platelet adhesion to the vessel wall plays a pivotal role in thrombosis after coronary artery stent placement. The goal of this study was to test whether C807T polymorphism is associated with a higher incidence of thrombotic events following coronary stenting. Consecutive patients treated with coronary stent placement (n = 1797) were genotyped for C807T polymorphism with polymerase chain reaction and allele-specific fluorogenic probes. The composite end point was defined as death, myocardial infarction, or urgent target vessel revascularization within 30 days of stent implantation. The genotype distribution of the study population was CC in 36.5%, CT in 46.7%, and TT in 16.8% of the patients. The incidence of the composite end point was 6.5% in T allele carriers and 5.3% in noncarriers (odds ratio for T allele carriage 1.23 [95% confidence interval, 0.81-1.86], P =.33). After adjusting for other baseline characteristics, the odds ratio for the composite end point was 1.15 (0.76-1.75). Therefore, C807T genotype has no significant influence on the major adverse events occurring after coronary artery stenting.

Asunto(s)

Enfermedad Coronaria/terapia , Integrinas/genética , Polimorfismo Genético , Stents/efectos adversos , Anciano , Sustitución de Aminoácidos , Angina de Pecho/diagnóstico por imagen , Angina de Pecho/terapia , Angina Inestable/diagnóstico por imagen , Angina Inestable/terapia , Angiografía Coronaria , Enfermedad Coronaria/diagnóstico por imagen , Enfermedad Coronaria/mortalidad , ADN/sangre , Femenino , Genotipo , Humanos , Integrina beta1/fisiología , Masculino , Persona de Mediana Edad , Reacción en Cadena de la Polimerasa , Receptores de Colágeno , Recurrencia , Factores de Riesgo

RESUMEN

Platelet fibrinogen receptor (glycoprotein [GP] IIb/IIIa) plays a fundamental role in atherothrombosis. The human platelet antigen (HPA) -1 and the HPA-3 are the most extensively studied polymorphisms of GPIIIa and GPIIb, respectively. This study was designed to test, in a large population, the hypothesis that these polymorphisms represent a risk factor for the occurrence of coronary artery disease (CAD) and myocardial infarction (MI). Consecutive, angiographically examined patients with significant coronary stenoses but without symptoms or signs of old or acute MI constituted the group with CAD (CAD, n = 998) and those with old or acute MI constituted the group with MI (MI, n = 793). As controls served subjects, matched with patients for age and sex, with neither angiographic CAD nor symptoms or signs of MI (matched controls [MC], n = 340) as well as a group of blood donors without cardiac symptoms or signs of CAD (BD, n = 104). Genotype distribution was similar across the groups; HPA-1a/a: HPA-1a/b: HPA-1b/b was 75.0%: 22.1%: 2.9% in BD, 72.6%: 24.7%: 2.6% in MC, 70.5%: 26.8%: 2.7% in CAD, and 70.7%: 26.4%: 2.9% in MI; HPA-3a/a: HPA-3a/b: HPA-3b/b was 39.4%: 40.4%: 20.2% in BD, 33.5%: 50.0%: 16.5% in MC, 35.0%: 46.4%: 17.0% in CAD, and 37.1%: 48.0%: 16.5% in MI. There was no interaction between these polymorphisms, nor between each of these polymorphisms and other risk factors. Thus, the HPA-1 and HPA-3 polymorphisms are neither separately nor in concert associated with any measurable increase of the risk for CAD or MI in angiographically evaluated subjects.

Asunto(s)

Antígenos de Plaqueta Humana/genética , Enfermedad Coronaria/genética , Infarto del Miocardio/genética , Complejo GPIIb-IIIa de Glicoproteína Plaquetaria/genética , Polimorfismo Genético , Anciano , Donantes de Sangre , Angiografía Coronaria , Enfermedad Coronaria/diagnóstico por imagen , Femenino , Frecuencia de los Genes , Predisposición Genética a la Enfermedad , Genotipo , Humanos , Integrina beta3 , Masculino , Persona de Mediana Edad , Infarto del Miocardio/diagnóstico por imagen , Factores de Riesgo

RESUMEN

C825T polymorphism in the G protein beta3 subunit gene (GNB3) has been associated with arterial hypertension, coronary artery disease and myocardial infarction. On the cellular level, C825T polymorphism is associated with altered transmembrane signaling via adenylyl cyclase inhibiting (G(i)) G proteins. This study was designed to test whether C825T polymorphism has an impact on the processes leading to restenosis and thrombosis following coronary stenting. The primary endpoint of the study was angiographic restenosis (> or =50% diameter stenosis) at 6-month follow-up. Secondary endpoint was angiographically proven stent thrombosis within 30 days of implantation. In the 562 consecutive patients C825T genotype was CC, 46.1%, CT, 45.2% and TT, 8.7%. The incidence of angiographic restenosis was 32.7% in homozygous carriers of the C allele, 28.2% in CT patients and 33.3% in homozygous carriers of the T allele (P = 0.563). C825T genotype distribution in 34 consecutive patients with subacute stent thrombosis (44.0% CC, 50.0% CT, and 6.0% TT) was not different from that of 451 patients with angiographically patent stented vessel (45.4% CC, 44.6% CT, 10.0% TT; P = 0.644). In conclusion, C825T polymorphism has no appreciable impact on the mechanisms leading to thrombosis and restenosis following coronary stent placement.

Asunto(s)

Puente de Arteria Coronaria/efectos adversos , Enfermedad Coronaria/genética , Enfermedad Coronaria/cirugía , Trombosis Coronaria/genética , Proteínas de Unión al GTP/genética , Oclusión de Injerto Vascular/genética , Anciano , Secuencia de Bases , Angiografía Coronaria , Puente de Arteria Coronaria/métodos , Enfermedad Coronaria/diagnóstico por imagen , Trombosis Coronaria/epidemiología , Femenino , Estudios de Seguimiento , Proteínas de Unión al GTP/análisis , Genotipo , Oclusión de Injerto Vascular/epidemiología , Humanos , Incidencia , Modelos Logísticos , Masculino , Persona de Mediana Edad , Datos de Secuencia Molecular , Análisis Multivariante , Reacción en Cadena de la Polimerasa , Polimorfismo Genético , Factores de Riesgo , Stents/efectos adversos

RESUMEN

Both glycoprotein (GP) IIb and IIIa of platelet fibrinogen receptor are polymorphic proteins. Unlike GPIIIa, there is little information about the clinical significance of the GPIIb polymorphism. We designed this prospective study to assess whether patients with the human platelet antigen (HPA)-3 polymorphism of GPIIb are more susceptible to developing thrombosis and restenosis after coronary stent placement. We included 2,178 consecutive patients with coronary artery disease who underwent intracoronary stent implantation, 789 (36.2%) with HPA-3a/a, 1,023 (47.0%) with HPA-3a/b, and 366 (16.8%) with HPA-3b/b genotype. The incidence of stent thrombosis was 1.7% in HPA-3a/a, 1.7% in HPA-3a/b, and 1.6% in HPA-3b/b patients (p = 0.999). The incidence of stent restenosis was 37.3% in HPA-3a/a, 36.2% in HPA-3a/b, and 34.6% in HPA-3b/b patients (p = 0.724). Event-free survival 1 year after stent placement was 76.1% for HPA-3a/a, 76.5% for HPA-3a/b, and 76.4% for HPA-3b/b patients (p = 0.968). We conclude that the HPA-3 polymorphism of platelet GPIIb is not associated with an increase in the risk of thrombosis and restenosis over 1 year after coronary stent placement. These data indicate that unlike the HPA-1 polymorphism of GPIIIa, the HPA-3 polymorphism of GPIIb may not serve as a useful genetic marker for the risk assessment of patients treated with intracoronary stenting.

Asunto(s)

Angioplastia Coronaria con Balón/instrumentación , Enfermedad Coronaria/genética , Trombosis Coronaria/genética , Complejo GPIIb-IIIa de Glicoproteína Plaquetaria/genética , Polimorfismo Genético/genética , Stents , Adulto , Anciano , Angiografía Coronaria , Enfermedad Coronaria/terapia , Trombosis Coronaria/terapia , Femenino , Estudios de Seguimiento , Frecuencia de los Genes , Predisposición Genética a la Enfermedad/genética , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Recurrencia , Resultado del Tratamiento

RESUMEN

BACKGROUND: Platelets play a central role in the process of restenosis after percutaneous coronary interventions. A polymorphism of platelet glycoprotein IIIa (PlA) has been associated with a higher risk of coronary thrombosis. We designed this prospective study to test the hypothesis that PlA polymorphism of glycoprotein IIIa is associated with an increased risk for restenosis after coronary stent placement. METHODS AND RESULTS: The study included 1150 consecutive patients with successful coronary stent placement and 6-month follow-up with coronary angiography. The end point of the study was the incidence of angiographic restenosis (>/=50% diameter stenosis) at follow-up. Of the 1150 patients, 72.5% were homozygous for PlA1, 24.7% were heterozygous (PlA1/A2), and 2.8% were homozygous for PlA2. Patients with the PlA2 allele demonstrated a significantly higher restenosis rate than did those without (47% versus 38%; OR, 1.42; 95% CI, 1.09 to 1.84). The risk was highest in homozygous carriers of PlA2 (53.1% restenosis rate). After adjustment for several clinical and angiographic characteristics, the presence of the PlA2 allele remained a significantly independent risk factor for restenosis (adjusted OR, 1.35; 95% CI, 1.07 to 1.70). The influence of the PlA2 allele on restenosis was stronger in women. Women with PlA2 had a restenosis rate of 52% compared with the 33% incidence among women homozygous for PlA1 (OR, 2.21; 95% CI, 1.27 to 3.85). CONCLUSIONS: This study showed a significant association between the PlA polymorphism of glycoprotein IIIa and the risk of restenosis after coronary stent placement. The risk was more pronounced in patients homozygous for PlA2 allele and in female patients.

Asunto(s)

Enfermedad Coronaria/terapia , Complejo GPIIb-IIIa de Glicoproteína Plaquetaria/genética , Polimorfismo Genético , Stents , Adulto , Anciano , Alelos , Enfermedad Coronaria/etiología , Femenino , Genotipo , Humanos , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Recurrencia , Riesgo