100Culprit plaque morphology in patients with and without preinfarction angina: an optical coherence tomography imaging study

Abstract

Abstract Background The relation between culprit plaque morphology and the clinical presentation of an acute myocardial infarction (AMI) has not been examined in detail. Purpose To study the culprit plaque morphology in patients with AMI with or without preinfarction angina using optical coherence tomography (OCT) imaging. Methods A total of 102 patients with AMI (32 STEMI, 70 NSTEMI) who underwent OCT imaging before percutaneous coronary intervention were enrolled. Patients were classified as: i) having either intermittent chest pain in the six hours preceding the final episode of pain, or unstable angina (or both) in the week preceding AMI (preinfarction angina group); or ii) having a single episode of chest pain without unstable symptoms in the preceding week (no preinfarction angina group). Culprit plaque was classified as plaque rupture (PR) or intact fibrous cap (IFC), as previously described. Prati thrombus score was calculated, and the prevalence of calcification, neovascularization, and OCT-defined macrophage accumulation was assessed. Results Patients with preinfarction angina showed a significantly higher prevalence of IFC than PR, while those without preinfarction angina showed a significantly higher prevalence of PR than IFC (Figure). PR in patients with preinfarction angina were more frequently associated with macrophage accumulation, while those in patients without preinfarction angina were not (Figure). White thrombus tended to be more frequent in patients with preinfarction angina than in those without (85.7% vs. 63.6%, p=0.097), and Prati thrombus score tended to be lower [22.0 (15.8–30.3) vs. 38.5 (12.8–67.5), p=0.145]. Calcifications were significantly less frequent in patients with preinfarction angina than in those without (22.0% vs. 40.4%, p=0.045), while neovascularization tended to be more frequent (58.0% vs. 42.3%, p=0.113). Conclusions Patients with preinfarction angina have a distinct culprit plaque phenotype, frequently characterized by IFC and a relatively lower thrombotic burden, probably reflecting a prevalence of reparative mechanisms and spontaneous thrombolytic activity in these patients.