Abstract 18045: Can Metabolic Syndrome Predict the Vulnerable Plaque in Patients with Stable Angina Pectoris?: Virtual Histology-Intravascular Ultrasound Analysis
Background- Vulnerable plaque (VP) in coronary artery can progress to plaque rupture and thrombosis, and have a strong potential to induce acute coronary syndrome. Many studies have demonstrated that metabolic syndrome (MS) is associated with increased risk for cardiovascular diseases and related mortalities. This study aimed to determine the predictive value of MS on VP in the patients with stable angina pectoris (SAP).
Methods and Results- From September 2007 to June 2010, a total of 239 patients with SAP who underwent coronary angiogram and intravascular ultrasound were categorized into two groups: MS group (n = 100, 56 men, 64.7 ± 9.5 years) and non-MS group (n = 139, 98 men, 60.2 ± 8.4 years). National Cholesterol Education Program-Adult Treatment Panel III guideline was used to determine the presence of MS and diverse variables containing IVUS findings were compared between two groups. MS group were older age and more likely to be women than non-MS group (p <0.001, p = 0.021, respectively). MS group showed more frequent multivessel involvement (p = 0.026) and had more distal target vessel in coronary artery (p = 0.005) than non-MS group, but IVUS finding containing the plaque burden showed no significant difference between two groups. In addition, low high density lipoprotein (HDL) cholesterol level as the criteria of MS (male <40 mg/dl, female <50 mg/dl) was observed in VP group more than stable plaque group (p = 0.020), but the prevalence of MS and other components of MS were not different between two groups. Multivariate analysis using logistic regression for the presence of VP showed that the independent predictor is the low HDL cholesterol level (odds ratio = 3.563, 95% confidence interval = 1.370-9.269, p = 0.009).
Conclusions- Low HDL cholesterol level, but not MS, is the independent predictor of VP as a culprit lesion in SAP patients.
- © 2011 by American Heart Association, Inc.