CBS 2019
CBSMD教育中心
English

科学研究

科研文章

荐读文献

Change in Kidney Function and 2-Year Mortality After Transcatheter Aortic Valve Replacement Conceptual Framework for Addressing Residual Atherosclerotic Cardiovascular Disease Risk in the Era of Precision Medicine Prognostic Value of Intravascular Ultrasound in Patients With Coronary Artery Disease Serial intravascular ultrasound analysis of the main and side branches in bifurcation lesions treated with the T-stenting technique A risk score to predict postdischarge bleeding among acute coronary syndrome patients undergoing percutaneous coronary intervention: BRIC-ACS study Percutaneous Coronary Intervention of Left Main Disease: Pre- and Post-EXCEL (Evaluation of XIENCE Everolimus Eluting Stent Versus Coronary Artery Bypass Surgery for Effectiveness of Left Main Revascularization) and NOBLE (Nordic-Baltic-British Left Main Revascularization Study) Era Coronary calcium as a predictor of coronary events in four racial or ethnic groups Infective endocarditis after transcatheter aortic valve implantation: a nationwide study Extracellular Myocardial Volume in Patients With Aortic Stenosis Computed tomography angiography-derived extracellular volume fraction predicts early recovery of left ventricular systolic function after transcatheter aortic valve replacement

Original Research2019 May 14;73(18):2253-2263.

JOURNAL:J Am Coll Cardiol. Article Link

Healed Culprit Plaques in Patients With Acute Coronary Syndromes

Fracassi F, Crea F, Jang IK et al. Keywords: coronary vulnerability; healed plaques; inflammation; layered plaquesoptical coherence tomography; subclinical thrombosis

ABSTRACT


BACKGROUND - Healed plaques, morphologically characterized by a layered phenotype, are frequently found in subjects with sudden cardiac death. However, in vivo data are lacking.

 

OBJECTIVES- The purpose of this study was to determine the prevalence, morphological characteristics, and clinical significance of healed culprit plaques in patients with acute coronary syndromes (ACS) using optical coherence tomography (OCT).

 

METHODS - A total of 376 ACS patients (252 ST-segment elevation myocardial infarction [MI] and 124 nonST-segment elevation acute coronary syndrome) who had undergone pre-intervention OCT imaging of the culprit lesion were enrolled. Patients were stratified according to the presence of layered phenotype, defined as layers of different optical density at OCT. Clinical and laboratory data, OCT characteristics, and 1-year outcome were compared between the 2 groups.

 

RESULTS- Among 376 patients, 108 (28.7%) healed plaques were identified. Hyperlipidemia, diabetes, and history of MI were more frequent in patients with healed plaques (44.4% vs. 33.2%; p = 0.041; 35.2% vs. 23.5%; p = 0.021; and 15.7% vs. 6.3%; p = 0.009, respectively). High-sensitivity C-reactive protein was significantly higher in patients with healed plaques (median 4.98 mg/l [interquartile range: 1.00 to 11.32 mg/l] vs. 3.00 mg/l [interquartile range: 0.30 to 10.15 mg/l]; p = 0.029). Plaque rupture (64.8% vs. 53.0%; p = 0.039), thin cap fibroatheroma (56.5% vs. 42.5%; p = 0.016), and macrophage accumulation (81.1% vs. 63.4%; p = 0.001) were common in the layered group. OCT also revealed greater area stenosis in plaques with layered phenotype (79.2 ± 9.5% vs. 74.3 ± 14.3%; p = 0.001). The incidence of major adverse cardiovascular events was similar between the 2 groups, except that the all-cause rehospitalization rate was higher among healed plaques (32.7% vs. 16.5%; p = 0.013).

 

CONCLUSIONS- Healed plaques, a signature of prior plaque destabilization, were found at the culprit site in more than one-quarter of ACS patients. Such patients more frequently were diabetic, were hyperlipidemic, or had a history of MI. Healed plaques frequently showed OCT features of vulnerability with evidence of local and systemic inflammation. The combination of plaque vulnerability, local inflammation, and greater plaque burden in addition to systemic inflammation may outweigh the protective mechanism of plaque healing and predispose those plaques to develop occlusive thrombus.