Association between cholesterol crystals and culprit lesion vulnerability in patients with acute coronary syndrome: An optical coherence tomography study

被引:41
作者
Dai, Jiannan [1 ]
Tian, Jinwei [1 ]
Hou, Jingbo [1 ]
Xing, Lei [1 ]
Liu, Shengliang [1 ]
Ma, Lijia [1 ]
Yu, Huai [1 ]
Ren, Xuefeng [1 ]
Dong, Nana [1 ]
Yu, Bo [1 ]
机构
[1] Harbin Med Univ, Dept Cardiol, Affiliated Hosp 2, Key Lab Myocardial Ischemia,Chinese Minist Educ, 246 Xuefu Rd, Harbin 150086, Peoples R China
基金
中国国家自然科学基金; 中国博士后科学基金;
关键词
Atherosclerosis; Cholesterol crystals; Acute coronary syndrome; Optical coherence tomography; THIN-CAP FIBROATHEROMA; INTRAVASCULAR ULTRASOUND; BIOLOGICAL-MEMBRANES; PLAQUE RUPTURE; ATHEROSCLEROSIS; FEATURES; EROSION; EVENTS;
D O I
10.1016/j.atherosclerosis.2016.02.010
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Cholesterol Crystals (ChCs) are recognized as a hallmark of advanced atherosclerotic lesions. Previous animal and histopathology studies have revealed that Cholesterol crystallization trigger a local inflammatory response and plaque rupture. We sought to investigate the in vivo relationship between ChCs and culprit lesion vulnerability in patients with acute coronary syndrome (ACS). Methods: 206 culprit lesions from 206 patients with ACS who underwent optical coherence tomography (OCT) imaging were divided into 2 groups based on the presence or absence of ChCs. Culprit lesions characteristics were compared between ChCs and Non-ChCs groups. Results: For overall ACS patients, culprit lesions with ChCs had higher incidence of macrophages accumulation (77.8% vs. 40.0%, p < 0.001), microchannel (67.9% vs. 24.8%, p < 0.001), plaque rupture (58.0% vs. 36.0%, p = 0.001), thrombosis (66.7% vs. 49.6%, p = 0.016) and spotty calcification (35.8% vs. 10.4%, p < 0.001). In addition, the mean lipid arc (274.2 +/- 57.6 degrees vs. 228.1 +/- 66.3 degrees, p < 0.001) was larger and the lipid index (3826.1 +/- 2111.4 vs. 2855.0 +/- 1753.0, p = 0.001) was greater. The frequency of ChCs was significantly higher in patients with STEMI, as compared with NSTEACS (50.8% vs. 34.7%, p = 0.032). Larger lipid arc, higher incidence of macrophages accumulation and that of microchannel were observed in culprit lesions with ChCs in both STEMI (p = 0.028, p < 0.001, and p = 0.002 respectively) and NSTEACS (p < 0.001, p < 0.001, and p < 0.001 respectively) subgroups. Conclusion: ChCs were frequently associated with characteristics of vulnerable plaques in ACS culprit lesions as well as in STEMI and NSTEACS subgroups. ChCs and vulnerable plaque features were more often observed in culprit lesions of STEMI patients compared to NSTEACS patients. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:111 / 117
页数:7
相关论文
共 30 条
[1]   Cholesterol crystals piercing the arterial plaque and intima trigger local and systemic inflammation [J].
Abela, George S. .
JOURNAL OF CLINICAL LIPIDOLOGY, 2010, 4 (03) :156-164
[2]   Effect of Cholesterol Crystals on Plaques and Intima in Arteries of Patients With Acute Coronary and Cerebrovascular Syndromes [J].
Abela, George S. ;
Aziz, Kusai ;
Vedre, Ameeth ;
Pathak, Dorothy R. ;
Talbott, John D. ;
DeJong, Joyce .
AMERICAN JOURNAL OF CARDIOLOGY, 2009, 103 (07) :959-968
[3]   Cholesterol crystals rupture biological membranes and human plaques during acute cardiovascular events - A novel insight into plaque rupture by scanning electron microscopy [J].
Abela, GS ;
Aziz, K .
SCANNING, 2006, 28 (01) :1-10
[4]   Cholesterol crystals cause mechanical damage to biological membranes: A proposed mechanism of plaque rupture and erosion leading to arterial thrombosis [J].
Abela, GS ;
Aziz, K .
CLINICAL CARDIOLOGY, 2005, 28 (09) :413-420
[5]   Comparison of Tissue Characteristics Between Acute Coronary Syndrome and Stable Angina Pectoris An Integrated Backscatter Intravascular Ultrasound Analysis of Culprit and Non-Culprit Lesions [J].
Ando, Hirohiko ;
Amano, Tetsuya ;
Matsubara, Tatsuaki ;
Uetani, Tadayuki ;
Nanki, Michio ;
Marui, Nobuyuki ;
Kato, Masataka ;
Yoshida, Tomohiro ;
Yokoi, Kiminobu ;
Kumagai, Soichiro ;
Isobe, Satoshi ;
Ishii, Hideki ;
Izawa, Hideo ;
Murohara, Toyoaki .
CIRCULATION JOURNAL, 2011, 75 (02) :383-390
[6]  
Brown Adam J, 2015, EuroIntervention, V11, pe1, DOI 10.4244/EIJV11I2A38
[7]   Pathogenesis of Acute Coronary Syndromes [J].
Crea, Filippo ;
Liuzzo, Giovanna .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2013, 61 (01) :1-11
[8]   NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals [J].
Duewell, Peter ;
Kono, Hajime ;
Rayner, Katey J. ;
Sirois, Cherilyn M. ;
Vladimer, Gregory ;
Bauernfeind, Franz G. ;
Abela, George S. ;
Franchi, Luigi ;
Nunez, Gabriel ;
Schnurr, Max ;
Espevik, Terje ;
Lien, Egil ;
Fitzgerald, Katherine A. ;
Rock, Kenneth L. ;
Moore, Kathryn J. ;
Wright, Samuel D. ;
Hornung, Veit ;
Latz, Eicke .
NATURE, 2010, 464 (7293) :1357-U7
[9]   Update on acute coronary syndromes: the pathologists view [J].
Falk, Erling ;
Nakano, Masataka ;
Bentzon, Jacob Fog ;
Finn, Aloke V. ;
Virmani, Renu .
EUROPEAN HEART JOURNAL, 2013, 34 (10) :719-+
[10]   Relation of plaque lipid composition and morphology to the stability of human aortic plaques [J].
Felton, CV ;
Crook, D ;
Davies, MJ ;
Oliver, MF .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1997, 17 (07) :1337-1345