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Clinical Course of Optical Coherence Tomography-Detected Lipid-Rich Coronary Plaque After Optimal Medical Therapy.

ABSTRACT: Background: The aim of this study was to evaluate optical coherence tomography (OCT)-detected lipid-rich coronary plaques (LRCPs) with coronary computed tomography angiography (CCTA) 10 months after optimal medical therapy (OMT). Methods and Results: Baseline OCT detected 28 LRCPs in non-culprit lesions. High-risk plaque features (HRPFs), such as positive remodeling, very low attenuation plaques, napkin-ring sign, and spotty calcification, were observed in 67.9%, 67.9%, 21.4%, and 64.3% of LRCPs, respectively, at the 10-month follow-up CCTA. Lesions with ≥3 HRPFs were defined as high-risk LRCPs (n=12); the remaining were defined as low-risk LRCPs (n=16). The maximum lipid arc on baseline OCT was larger in high- than low-risk LRCPs (221±62° vs. 179±44°, respectively; P=0.04). Receiver operating characteristic curve analysis indicated that a maximum lipid arc >154° on baseline OCT was the optimal cut-off value to predict high-risk LRCPs 10 months after OMT. Patients with high-risk LRCPs had worse clinical outcomes, defined as a composite of cardiac death, target lesion-related myocardial infarction, and target lesion-related revascularization, during follow-up than those with low-risk LRCPs (33.3% vs. 0%; P=0.01). Conclusions: A high-risk LRCP at follow-up CCTA was correlated with a larger maximum lipid arc on baseline OCT. Further aggressive treatment for patients with large LRCPs may reduce vulnerable plaque features and prevent future cardiac events.

SUBMITTER: Sugiura J

PROVIDER: S-EPMC8710641 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ImportancePatients with culprit plaque rupture are known to have pancoronary plaque vulnerability. However, the characteristics of nonculprit plaques in patients with acute coronary syndromes caused by plaque erosion are unknown.ObjectiveTo investigate the nonculprit plaque phenotype in patients with acute coronary syndrome according to culprit plaque pathology (erosion vs rupture) by 3-vessel optical coherence tomography imaging.Design, setting, and participantsIn this observational cohort study, between August 2010 and May 2014, 82 patients with acute coronary syndrome who underwent preintervention optical coherence tomography imaging of all 3 major epicardial coronary arteries were enrolled at the Massachusetts General Hospital Optical Coherence Tomography Registry database. Analysis of the data was conducted between November 2016 and July 2017. Patients were classified into 2 groups based on the culprit lesion pathology: 17 patients with culprit plaque erosion and 34 patients with culprit plaque rupture. Thirty-one patients with the absence of culprit rupture or erosion were excluded from further analysis.ExposuresPreintervention 3-vessel optical coherence tomography imaging.Main outcomes and measuresPlaque characteristics at the culprit and nonculprit lesions evaluated by optical coherence tomography.ResultsIn 51 patients (37 men; mean age, 58.7 years), the characteristics of 51 culprit plaques and 216 nonculprit plaques were analyzed. In patients with culprit erosion, the mean (SD) number of nonculprit plaques per patient was smaller (3.4 [1.9] in erosion vs 4.7 [2.1] in rupture, P = .05). Patient-based analysis showed that none of 17 patients with culprit plaque erosion had nonculprit plaque rupture, whereas 26% of the patients (9 of 34) with culprit plaque rupture had nonculprit plaque rupture (P = .02). Plaque-based analysis showed that, compared with the culprit rupture group (n = 158), the culprit erosion group (n = 58) had lower prevalence of plaque rupture (0% vs 8%; P < .001), macrophage accumulation (29% vs 53%; P = .01), microvessels (21% vs 42%; P = .003), and spotty calcium (5% vs 22%; P = .006) in the nonculprit lesions. The prevalence of lipid-rich plaque, thin-cap fibroatheroma, and thrombus did not differ between the groups.Conclusions and relevanceCompared 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.

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Clinical Course of Optical Coherence Tomography-Detected Lipid-Rich Coronary Plaque After Optimal Medical Therapy.

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