Metabolic syndrome and coronary artery disease: is there a gender specific effect?

INTRODUCTION: Clustering of cardiovascular risk factors is observed in metabolic syndrome (MS), but the relative contribution of different factors to determine outcomes remains largely unknown. We investigated the influence of gender in the effect of MS in coronary vascular lesions in 385 patients who underwent first time coronary artery disease (CAD) assessment through coronary angiography. MATERIALS AND METHODS: Patients were stratified in two groups: metabolic syndrome (MS, N = 190) and non-metabolic syndrome (NMS, N = 195), according to standard criteria. Two vascular scores related to extension and severity of vascular lesions were determined by systematic analysis of 20 coronary segments. RESULTS AND CONCLUSIONS: MS was more prevalent in females (58.7 vs. 39.7%, p = 0.0005) and hypertension and low-HDL were the leading prevalent factors in the MS group. Scores for extension and severity of lesions were higher in the MS than in the NMS group (2.10 +/- 1.75 vs. 1.75 +/- 1.58; p = 0.01, and 1.49 +/- 1.29 vs. 1.25 +/- 1.15; p = 0.03, respectively). The impact of MS in CAD scores was more pronounced in females (OR 2.2, 95% CI 1.1-4.3, p = 0.02) than in males (OR 1.5, 95% CI 0.8-2.7, p = 0.17). Non-HDL cholesterol was the only risk factor influencing the scores in a gender specific manner, showing an increased impact in the female gender. Normal coronary angiograms were more frequent in females (p = 0.0001), especially in NMS. Collectively, these data suggest that MS is related to higher extension and severity of vascular lesions in this population regardless of gender but lipids and anthropometric parameters may differentially modulate the MS effect in a particular gender.

Angiotensinogen M235T polymorphism is associated with coronary artery disease severity.

INTRODUCTION: Previous reports relating coronary artery disease and functional variants of the renin-angiotensin system have been contradictory in establishing the role of these polymorphisms in coronary artery disease (CAD) development. The aim of the present study is to determine if there is an association between the M235T variant of the angiotensinogen gene and severity of coronary artery disease in patients with clinically suspected disease undergoing cineangiogram. METHODS: The angiotensinogen M235T variant was analyzed in 871 consecutive patients with clinically suspected coronary artery disease submitted to coronary angiography study. Three different angiographic scores were used to determine severity of the disease analyzing 20 coronary segments. All patients were evaluated considering classical risk factors for coronary artery disease throughout a medical oriented questionnaire, anthropometric measures, and blood glucose and lipid profile determination. RESULTS: Presence of the 235T allele was associated with higher angiographic extension scores in univariate analysis (p < 0.05). The 235T allele was also associated with an increased risk of presenting 3-vessel disease (p < 0.05). In addition, the T allele was significantly associated with higher Gensini's scores both in univariate (p = 0.05) and multivariate analyses (p < 0.05). Finally, a 1.86 fold increase in the risk of multivessel disease (95% CI: 1.174-2.947) was associated with the TT genotype independently of other cardiovascular risk factors associated with disease extension. CONCLUSION: The data hereby provide further support for the association between angiotensinogen M235T polymorphism and CAD severity independently of other cardiovascular risk factors.

Effect of glycoprotein IIIa PlA2 polymorphism on outcome of patients with stable coronary artery disease and effect of smoking.

A polymorphism of glycoprotein IIb/IIIa has been associated with myocardial infarction and restenosis after percutaneous coronary intervention. The influence on outcome and the interaction of the Pl(A1) genotype with classic risk factors for coronary artery disease (CAD) were characterized in patients with chronic CAD followed prospectively for 3 years. Pl(A1) genotypes were assessed in 592 patients enrolled in the Medical, Angioplasty, or Surgery Study II, a randomized trial comparing treatments for patients with CAD and preserved left ventricular function. The incidence of the composite end point of cardiac death, myocardial infarction, and refractory angina requiring revascularization were determined in each genotype group. Risk was assessed with the Cox proportional-hazards model. The clinical characteristics and treatment of each genotype were similar. Although the composite end point tended to be more common in patients with the Pl(A2) allele, only smokers with the Pl(A2) allele had a significantly increased incidence of the composite end point (p = 0.01). Moreover, a 2.2-fold increased risk was apparent in smokers with the Pl(A2) allele (p = 0.03). Thus, taken together, these data provide support for the interaction effect between smoking and the Pl(A1) gene variant. Smokers with the Pl(A2) polymorphism of platelet glycoprotein IIIa are at greater risk for subsequent cardiac events in stable coronary disease.