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Management of Acute Myocardial Infarction During the COVID-19 Pandemic 2018 ESC/EACTS Guidelines on myocardial revascularization - The Task Force on myocardial revascularization of the European Society of Cardiology (ESC) and European Association for Cardio- Thoracic Surgery (EACTS) Prognostic significance of QRS fragmentation and correlation with infarct size in patients with anterior ST-segment elevation myocardial infarction treated with percutaneous coronary intervention: Insights from the INFUSE-AMI trial Comparison of Physician Visual Assessment With Quantitative Coronary Angiography in Assessment of Stenosis Severity in China Comparison of Delay Times Between Symptom Onset of an Acute ST-elevation Myocardial Infarction and Hospital Arrival in Men and Women <65 Years Versus ≥65 Years of Age.: Findings From the Multicenter Munich Examination of Delay in Patients Experiencing Acute Myocardial Infarction (MEDEA) Study Silent Myocardial Infarction and Long-Term Risk of Heart Failure: The ARIC Study 2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI) PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock What's new in the Fourth Universal Definition of Myocardial infarction? Fourth Universal Definition of Myocardial Infarction (2018)

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.