Abstract 12048: Prevalence, Characteristics, and Clinical Significance of Healed Culprit Plaques in Acute Coronary Syndromes.

Introduction: Healed plaques, morphologically characterized by a layered phenotype, are frequently found in subjects with sudden cardiac death. However, in vivo data are lacking. Aim: To determine the prevalence, morphologic characteristics, and clinical significance of healed culprit plaques of patients with acute coronary syndrome (ACS) by using optical coherence tomography (OCT). Methods: A total of 376 ACS patients (252 ST-elevation MI and 124 non ST elevation ACS) 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, laboratory, OCT characteristics, and 1-year outcome were compared between the two groups. Results: Among 376 patients, 108 (28.7%) healed plaques were identified. Hyperlipidemia, diabetes, and history of myocardial infarction (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; 15.7% vs 6.3%, p=0.009). High sensitive C-reactive protein was significantly higher in patients with healed plaques (4.98 [1.00-11.32] mg/L vs 3.00 [0.30-10.15] mg/L, p=0.029). Plaque rupture (64.8% vs 53.0%, p=0.039), TCFA (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 two groups, except that all cause rehospitalization rate was higher in the healed plaque group (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 were more frequently diabetic, 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. [ABSTRACT FROM AUTHOR]