713 Culprit plaque morphology and healing capacity in patients with and without preinfarction angina: an optical coherence tomography imaging study

Abstract

Abstract Aims The relationship between culprit plaque morphology, healed culprit plaques prevalence and clinical presentation of acute myocardial infarction (AMI) remains largely unexplored. We hypothesized that angina preceding the occurrence of AMI (pre-infarction angina, PIA) may reflect a distinct morphologic phenotype of culprit plaques and potentially different healing capacity. Methods and results We conducted a retrospective observational study in patients with AMI who underwent intracoronary optical coherence tomography (OCT) imaging of the culprit lesion before PCI at the Fondazione Policlinico A. Gemelli–Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome. Based on the clinical history, patients were classified into two groups: (i) PIA group, defined as either intermittent chest pain within 6 h preceding the final episode of chest pain, or unstable angina (or both) in the week preceding AMI or (ii) no-PIA group, defined as a single episode of chest pain without prodromal symptoms in the preceding week. Culprit plaques were classified as plaque rupture (PR) or intact fibrous cap (IFC), and presence of layered appearance (healed plaque, HP) was assessed. Thrombus burden (TB) was estimated, and prevalence of diffuse calcification, neovascularization, and OCT-defined macrophage accumulation were evaluated. A total of 102 patients with AMI were included (50 PIA, 52 no-PIA). Patients with PIA showed a higher prevalence of IFC than PR (58% vs. 42%, P = 0.030). PR in patients with PIA were more frequently associated with macrophage accumulation (71.4% vs. 28.6% P = 0.001), and TB tended to be lower [22.0 (15.8–30.3) vs. 38.5 (12.8–67.5), P = 0.145]. Diffuse calcifications were significantly less frequent in patients with PIA (22.0% vs. 40.4%, P = 0.045), while neovascularization tended to be more frequent (58.0% vs. 42.3%, P = 0.113). HPs prevalence was significantly higher in the PIA than in the no-PIA group (66.0% vs. 25.0%, P < 0.001). Conclusions Patients with PIA have a distinct culprit plaque phenotype, more frequently characterized by IFC and a relatively lower TB, with a significantly higher prevalence of plaque healing.