Carotid plaque composition in stable and unstable coronary artery disease

Several pieces of evidence suggest that formation of complex atheromatous plaques may be influenced not only by local but also by systemic factors. Twenty-five patients (16 men/9 women, age 63 ± 10 years) with stable coronary artery disease (sCAD) and 61 (41 men/20 women, age 66 ± 16 years) with acute coronary syndromes (ACSs) underwent carotid ultrasonography within 2 days of cardiac catheterization. Complex coronary plaques were associated with intraluminal filling defect consistent with thrombus, ulceration, or irregularity. Complex carotid plaques had one or more of the following features: ( a) ulceration, ( b) irregular surface, ( c) mobile thrombi on plaque surface, ( d) predominant echolucency, and ( e) heterogeneity with intraplaque echolucent areas. Carotid intimamedia thickness and luminal diameter were not significantly different between patients with sCAD and those with ACS (0.95 ± 0.22 vs 1.0 ± 0.15 mm [ P = .23] and 6.1 ± 0.89 vs 6.20 ± 0.77 mm [ P = .60], respectively), whereas the interadventitial diameter was slightly greater in the latter (7.93 ± 1.05 vs 8.40 ± 0.97 mm, P = .0496). Both complex coronary plaques and complex carotid plaques were more common in patients with ACS than in those with sCAD (n = 52 [85.2%] vs n = 6 [24%] [ P < .0001] and n = 38 [62.3%] vs n = 5 [20%] [ P = .0009], respectively). The odds of having complex carotid plaques were increased >6-fold in patients with ACS compared with those with sCAD (OR 6.61, 95% CI 2.24-19.32). Complex coronary plaques are associated with complex carotid plaques and the high prevalence of both plaque types in patients with ACS is indicative of a systemic process contributing to complex plaque formation and instability.