Abstract 1988: Non-culprit Coronary Plaque Morphology in Patients WIth Acute Myocardial Infarction : An Optical Coherence Tomography Study in Vivo
Background: In vivo imaging studies in patients with acute myocardial infarction (AMI) have demonstrated important lesions at sites other than the culprit. However, it is not well assessed whether non-culprit plaques in the non-infarct-related artery have similar markers of plaque instability compared to non-culprit plaques in the infarct-related artery. The aim of this study is to investigate the morphologic features of the non-culprit plaque in infarct-related artery in comparison with that in non-infarct-related artery for AMI patients using optical coherence tomography (OCT) in vivo.
Methods: OCT examinations were attempted prospectively using motorized pullback in all 3 major coronary arteries (at least 2/3 segment of each artery) for 34 AMI patients. In 34 patients, 118 focal plaques were identified (3.5 plaques per patient). Qualitative OCT analyses for each focal atherosclerotic plaque were performed using the previously validated criteria. TCFA was defined as a plaque with lipid content in a quadrant and the thinnest part of a fibrous cap measuring <65 μm. A plaque rupture contained a cavity that communicated with the lumen with an overlying residual fibrous cap fragment. A thrombus was defined as an irregular mass protruding into the lumen. Non-culprit plaques were divided into two groups according to their location:
plaques in infarct-related artery (n=35) and
plaques in non-infarct-related artery (n=83).
Results: Non-culprit TCFA, plaque rupture, and thrombus were observed in 50 lesions of 26 patients (76%), 14 lesions of 11 patients (34%), and 27 lesions of 15 patients (44%), respectively. OCT analyses are shown in the Table⇓.
Conclusions: The morphology of non-culprit plaques in AMI patients is similar whether these plaques occur in the infarct-related artery or the non-infarct-related artery. This suggests that plaque destabilization is a systemic phenomenon rather than a local, artery-specific process.