Differences in intravascular ultrasound and histological findings in culprit coronary plaques between ST-segment elevation myocardial infarction and stable angina
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- Lee, C.W., Hwang, I., Park, CS. et al. J Thromb Thrombolysis (2014) 37: 443. doi:10.1007/s11239-013-0975-z
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A comprehensive evaluation of culprit coronary lesions may help to understand vulnerable plaques responsible for ST-segment elevation myocardial infarction (STEMI). We compared intravascular ultrasound (IVUS) and histological findings in culprit coronary plaques from 94 patients with STEMI (n = 54) or stable angina (n = 40). Tissue specimens were obtained by directional coronary atherectomy and IVUS was performed before percutaneous coronary intervention. IVUS and histological data were analyzed. Clinical characteristics were largely similar between the two groups. Plaque rupture and thrombi were more frequently found in the STEMI group than in the stable angina group. There were no significant differences between plaque types or proximal and distal reference measurements in the two groups. However, the site of minimal lumen area had a greater vessel area, remodeling index, and plaque burden with lesser lumen area in the STEMI group than in the stable angina group. Plaque areas immunopositive for CD68 and CD31 were significantly larger in the STEMI group, while the area immunopositive for α-smooth muscle actin was larger in the stable angina group. In conclusion, culprit lesions in STEMI patients showed a greater plaque burden, remodeling index, and more frequent thrombi with increased inflammation and neovascularization compared to the stable angina group, supporting the current concept of vulnerable plaques being responsible for STEMI.