CBS 2019
CBSMD教育中心
English

科学研究

科研文章

荐读文献

Guiding Principles for Chronic Total Occlusion Percutaneous Coronary Intervention 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society Rotational Atherectomy Followed by Drug-Coated Balloon Dilation for Left Main In-Stent Restenosis in the Setting of Acute Coronary Syndrome Complicated with Right Coronary Chronic Total Occlusion Individualizing Revascularization Strategy for Diabetic Patients With Multivessel Coronary Disease Derivation and Validation of a Chronic Total Coronary Occlusion Intervention Procedural Success Score From the 20,000-Patient EuroCTO Registry:The EuroCTO (CASTLE) Score Thin Composite-Wire-Strut Zotarolimus-Eluting Stents Versus Ultrathin-Strut Sirolimus-Eluting Stents in BIONYX at 2 Years Treatment of higher-risk patients with an indication for revascularization: evolution within the field of contemporary percutaneous coronary intervention Heart Disease and Stroke Statistics-2019 Update: A Report From the American Heart Association Acute Myocardial Injury in Patients Hospitalized With COVID-19 Infection: A Review Universal Definition of Myocardial Infarction

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.