医学
罪魁祸首
血栓
心脏病学
内科学
易损斑块
心肌梗塞
钙化
冠状动脉疾病
作者
Chao Fang,Yan-Wei Yin,Shuang Jiang,Shaotao Zhang,Jifei Wang,Yidan Wang,Lulu Li,Yini Wang,Junchen Guo,Huai Yu,Wei Guo,Fangmeng Lei,Tao Chen,Xia Ren,Jinfeng Tan,Lei Xing,Ruoxi Zhang,Jiannan Dai,Bo Yu
标识
DOI:10.1016/j.jcmg.2021.07.022
摘要
This study aimed to investigate the pancoronary plaque vulnerability (including culprit and nonculprit lesions) and layered phenotype in patients with ST-segment elevation myocardial infarction (STEMI) vs non-STEMI (NSTEMI).Pancoronary vulnerability should account for distinct clinical manifestations of acute myocardial infarction (AMI). Layered plaque is indicative of previous coronary destabilization and thrombosis.A total of 464 patients with AMI who underwent 3-vessel optical coherence tomography imaging were consecutively studied and divided into a STEMI group (318 patients; 318 culprit and 1,187 nonculprit plaques) and a NSTEMI group (146 patients; 146 culprit and 560 nonculprit plaques). Patients were followed up for a median period of 2 years.Compared with NSTEMI, culprit lesions in STEMI had more plaque rupture, thrombus, thin-cap fibroatheroma (TCFA), calcification, macrophage accumulation, and microvessels. The prevalence of plaque rupture (8.2% vs 4.8%; P = 0.018), microvessels (57.5% vs 45.2%; P < 0.001), and calcification (40.7% vs 30.2%; P = 0.003) at nonculprit lesions was higher in STEMI than NSTEMI. The layer area and thickness at the culprit and nonculprit lesions were significantly larger in STEMI than in NSTEMI. Multivariate analyses showed that culprit layer area (odds ratio: 1.443; 95% CI: 1.138-1.830; P = 0.002) was predictive of STEMI (vs NSTEMI), in addition to culprit TCFA, culprit thrombus, and non-left circumflex artery location of the culprit lesion. Although the type of AMI was not related to clinical outcomes, high-sensitivity C-reactive protein, culprit calcified nodule, and nonculprit TCFA predicted the 2-year major adverse cardiovascular events in patients with AMI.Patients with STEMI had increased plaque vulnerability (ie, more plaque rupture and microvessels) and distinct layered phenotype at the culprit and nonculprit lesions compared with patients with NSTEMI. Culprit lesion features of large layer area, TCFA, thrombus, and non-left circumflex artery location predicted the clinical presentation of STEMI.
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