Increased Vulnerability and Distinct Layered Phenotype at Culprit and Nonculprit Lesions in STEMI Versus NSTEMI

被引:16
|
作者
Fang, Chao [1 ,2 ]
Yin, Yanwei [1 ,2 ]
Jiang, Senqing [1 ,2 ]
Zhang, Shaotao [1 ,2 ]
Wang, Jifei [1 ,2 ]
Wang, Yidan [1 ,2 ]
Li, Lulu [1 ,2 ]
Wang, Yini [1 ,2 ]
Guo, Junchen [1 ,2 ]
Yu, Huai [1 ,2 ]
Wei, Guo [1 ,2 ]
Lei, Fangmeng [1 ,2 ]
Chen, Tao [1 ,2 ]
Ren, Xuefeng [1 ,2 ]
Tan, Jinfeng [1 ,2 ]
Xing, Lei [1 ,2 ]
Hou, Jingbo [1 ,2 ]
Dai, Jiannan [1 ,2 ]
Yu, Bo [1 ,2 ]
机构
[1] Harbin Med Univ, Affiliated Hosp 2, Dept Cardiol, 246 Xuefu Rd, Harbin 150086, Peoples R China
[2] Chinese Minist Educ, Key Lab Myocardial Ischem, 246 Xuefu Rd, Harbin 150086, Peoples R China
基金
中国国家自然科学基金;
关键词
KEY WORDS layered plaque; NSTEMI; optical coherence tomography; pancoronary; plaque vulnerability; STEMI; OPTICAL COHERENCE TOMOGRAPHY; ACUTE CORONARY SYNDROME; ELEVATION MYOCARDIAL-INFARCTION; ST-SEGMENT ELEVATION; INTRAVASCULAR ULTRASOUND; PLAQUE CHARACTERISTICS; NATURAL-HISTORY; ARTERY-DISEASE; MORPHOLOGY; INTERVENTION;
D O I
10.1016/j.jcmg.2021.07.022
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
OBJECTIVES 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).BACKGROUND Pancoronary vulnerability should account for distinct clinical manifestations of acute myocardial infarction (AMI). Layered plaque is indicative of previous coronary destabilization and thrombosis.METHODS 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.RESULTS 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.CONCLUSIONS 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. (J Am Coll Cardiol Img 2022;15:672-681)(c) 2022 by the American College of Cardiology Foundation.
引用
收藏
页码:672 / 681
页数:10
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