Abstract 3269: Does The Metabolic Syndrome Promote Progression of Coronary Atherosclerosis Beyond The Impact of its Component Risk Factors? Observations From Intravascular Ultrasound
he mechanism that confers an adverse cardiovascular prognosis in the metabolic syndrome (MetS) remains unclear. We sought to investigate the extent and progression of atherosclerosis in patients with or without the MetS. A systematic review was performed of 3459 patients with angiographic coronary artery disease in clinical trials that measured changes in coronary atheroma burden by intravascular ultrasound. Subjects have been stratified according to the presence or absence of the MetS at baseline. Patients with or without the MetS were compared with regard to clinical characteristics, coronary atheroma burden at baseline and change on serial evaluation. According to the baseline status 1997 (55%) patients had MetS. In addition to a predictably higher prevalence of obesity, hypertension, hypertriglyceridemia, hyperglycemia and low HDL cholesterol, patients with the MetS were younger and more likely to be female and had higher levels of CRP (3.2 vs 1.9 mg/L, p<0.001). At baseline patients with MetS did not have a greater percent atheroma volume (PAV, 38.7+/−9.1 vs 38.5+/−9.0 %, p=0.56) or total atheroma volume (TAV, 194+/−85.6 vs 189+/−79.0 mm3, p=0.19). Despite a high rate of use of medical therapies in both groups, the presence of the MetS was associated with greater progression of PAV (+0.51+/−0.2 vs +0.22+/−0.2 %, p=0.003) and TAV values (−2.3+/−1.7 vs −3.4+/−1.7 mm3, p=0.09). Patients with the MetS were more likely to demonstrate substantial progression (>5% increase PAV, 27.2 vs 22.6%, p=0.001) and less likely to demonstrate regression (>5% decrease PAV, 18 vs 21%, p=0.03). On multivariate analysis, after controlling for differences in clinical characteristics, the presence of the MetS did not independently predict plaque progression (p= 0.95). The greater progression of coronary atherosclerosis in the presence of the MetS is not evident after controlling for the presence of its individual defining factors. This suggests that the proatherogenic effect of the MetS simply results from the overall risk factor burden, rather than due to the presence of the syndrome itself.