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URL: https://www.clinicaltrials.gov. Unique identifier: NCT02041650.

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Presence of LRP in the nonculprit regions of the target vessel by OCT predicts increased risk for future NC-MACE, which is primarily driven by revascularization for recurrent ischemia. Lipid-rich plaque with longer lipid length, wider lipid arc, and higher degree of stenosis identified patients at higher risk of future cardiac events. (The Massachusetts General Hospital Optical Coherence Tomography Registry; NCT01110538).

Compared with those with culprit plaque rupture, patients with acute coronary syndrome caused by culprit plaque erosion had a smaller number of nonculprit plaques and the lower levels of panvascular instability, affirming that distinct pathophysiologic mechanisms operate in plaque erosion and plaque rupture.

BackgroundDiabetes mellitus (DM) is a major risk factor for cardiovascular events. We aimed to investigate the coronary plaque phenotype of diabetic patients who presented with acute coronary syndromes by optical coherence tomography.Methods and ResultsA total of 322 patients with acute coronary syndromes who underwent preintervention optical coherence tomography imaging of the culprit lesion were included. Culprit plaque characteristics were compared between patients with DM (n=95) and those without DM (n=227). In the subgroup of 250 patients in whom sufficient length of nonculprit region in the culprit vessel was imaged by optical coherence tomography, the characteristics of nonculprit plaques were also evaluated. Patients with DM had a higher prevalence of lipid‐rich plaque (58.9% versus 44.9%, P=0.030) and macrophage accumulation (60.0% versus 44.9%, P=0.019) in the culprit lesion compared with patients without DM. The prevalence of plaque rupture (33.7% versus 30.4%, P=0.896) and plaque erosion (21.1% versus 22.0%, P=0.458) was similar. In the nonculprit lesions, the DM group had greater maximal lipid arc (248.9°±83.9° versus 179.9°±58.3°, P=0.006), thinner fibrous cap thickness (103.3±56.2 μm versus 140.7±70.0 μm, P=0.013), and a higher prevalence of thin‐cap fibroatheroma (17.2% versus 6.3%, P=0.031), compared with the non‐DM group.ConclusionsCompared with patients without DM, those with DM had more vulnerable features in both culprit and nonculprit lesions, thus indicating a higher level of panvascular instability.Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT01110538.

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