Metabolic syndrome is associated with extension of coronary artery disease in patients with non-ST segment elevation acute coronary syndromes.

Yuksek Ihtisas Education and Research Hospital, Cardiology Clinic, Sihhiye, Turkey.
Coronary Artery Disease (Impact Factor: 1.11). 09/2005; 16(5):287-92. DOI: 10.1097/00019501-200508000-00005
Source: PubMed

ABSTRACT Metabolic syndrome (MS) comprises a group of factors that are associated with increased risk for cardiovascular events. Acute coronary syndromes account for the most important part of cardiovascular events with considerable morbidity and mortality. We aimed to investigate the association of MS with extension of coronary artery disease in patients presenting with non-ST segment elevation (NSTE) acute coronary syndromes (ACS).
Three hundred and six consecutive patients (220 men, 86 women patients) with the diagnosis of NSTE ACS, who were hospitalized within the first 24 h of their chest pain in the coronary care unit, were prospectively enrolled into our study. Patients with elevation of troponins (T or I) were classified as NSTE myocardial infarction (MI) and otherwise as unstable angina pectoris (USAP). Components of MS were noted as previously identified. Coronary angiograms were evaluated by two authors, who were blinded to the study plan and each other, via Sullivan's method.
MS was noted in 49% of all patients, and was significantly more common in women than in men (62.8 versus 43.6%, P=0.003). The mean total stenosis score of patients with MS was significantly higher than for those without MS (16+/-6 versus 12+/-5, P<0.001), and the mean extension score of patients with MS was significantly higher than for those without MS (63+/-29 versus 44+/-26, P<0.001). The presence of MS together with some clinical factors and poor total cholesterol/high-density lipoprotein cholesterol ratio, hypertension and diabetes mellitus, was found to be independently predictive of extension of coronary artery disease (CAD) in a group of patients presenting with NSTE ACS.
MS is independently associated with CAD extension, and hence, might account for poor cardiovascular outcomes through CAD extension in patients with NSTE ACS.

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