医学
罪魁祸首
急性冠脉综合征
内科学
心脏病学
狼牙棒
心肌梗塞
不稳定型心绞痛
冠状动脉疾病
易损斑块
血运重建
狭窄
经皮冠状动脉介入治疗
作者
Gereon Nelles,Youssef S. Abdelwahed,Claudio Seppelt,Denitsa Meteva,B E Staehli,N Kraenkel,Julia Steiner,Carsten Skurk,Matthias Riedel,Lara Sieronski,Aiden Haghikia,David Sinning,Ulf Landmesser,Michael Joner,David M. Leistner
标识
DOI:10.1093/eurheartj/ehab724.1300
摘要
Abstract Aims Cholesterol chrystals (CC) represent a feature of advanced plaque remodeling. Optical coherence tomography (OCT) allows for detailed morphological assessment of the culprit lesion, including the presence of CCs, in vivo. Since CCs have been identified as prognostically relevant plaque feature in coronary artery disease (CAD), the present analysis aims to further characterize their impact on adverse cardiovascular outcome in a large cohort of patients, presenting with acute coronary syndrome (ACS). Methods Within the translational OPTICO-ACS study program, 371 consecutive ACS-patients were included into the final analysis. OCT-characteristics, including the presence of CCs, were assessed by a standardized CoreLab analysis following universal consensus standards for OCT-derived plaque features. All patients were followed up for 12 months after the index event and major adverse cardiac events (MACE) consisting of death, myocardial infarction, target vessel revascularization plus re-hospitalization due to unstable or progressive angina pectoris were documented. Results 215 patients (58.1%) presented with cholesterol chrystals (CCs) at the culprit lesion. Plaque rupture (RFC-ACS) represented the primary ACS-causing pathophysiology (75.3%) in those patients. Further, the presence of CCs was associated with other high-risk features within the culprit lesion, i.e. the presence of thin cap fibroatheroma (77.7% vs. 63.2%; p<0.05), plaque calcification (80.5% vs. 67.1; p<0.01) and microchannels (80.1% vs. 70.1; p<0.05) as well as an increased area stenosis (0.77 vs. 0.73 mm2; p<0.01) and a greater maximum lipid arc (282.8 vs. 242.6°; p<0.01) as compared to culprit lesions free of CCs. Of note, there was a strong association among the occurrence of macrophages within the plaque and cholesterol crystals. Finally, and most importantly MACE during 12 months follow-up, consisting of cardiac death, myocardial infarction, target vessel revascularization and re-hospitalization due to progressive or unstable angina pectoris, occurred with nearly twice the frequency in CC-patients (20.3% vs. 10.6%; p<0.01) as compared to patients without CCs at the culprit site. Conclusion The present analysis introduces cholesterol chrystals as a novel prognostically relevant high-risk plaque feature allowing individual risk stratification for patients after ACS. Funding Acknowledgement Type of funding sources: None.
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