期刊
EUROPEAN HEART JOURNAL-CARDIOVASCULAR IMAGING
卷 18, 期 11, 页码 1271-1277出版社
OXFORD UNIV PRESS
DOI: 10.1093/ehjci/jew208
关键词
acute coronary syndrome; plaque rupture; optical coherence tomography; systemic inflammation; local inflammation
Aims Plaque rupture (PR) represents the most common substrate of coronary thrombosis, in at least 50% of cases. Chronic low grade inflammation is a common background for atherosclerosis development; however, increased plaque inflammation may predispose by itself to PR. In the last decade, studies performed by optical coherence tomography (OCT) have allowed to establish the severity of plaque inflammation by assessing macrophage infiltration (MOI). Our retrospective study aimed at assessing the role of plaque inflammation in PR among patients with acute coronary syndrome (ACS) using OCT. Methods and results We enrolled 56 patients with ACS exhibiting PR at the site of the culprit stenosis identified by OCT. Patients were divided into two cohorts according to the presence of MOI at OCT analysis, defined as signal-rich, distinct, or confluent punctate regions that exceed the intensity of background speckle noise. Serum high-sensitivity C-reactive protein (CRP) was measured on admission by latex-enhanced immunophelometric assay. Thirty-seven (66%) patients had MOI at the site of PR, whereas 19 (34%) patients had no evidence of MOI. Patients with MOI showed a higher rate of CRP values > 3 mg/dL as compared with those without MOI (92% vs. 47%, P = 0.004). In contrast, patients without MOI had a higher prevalence of hypertension compared with those with MOI (89% vs. 59%, P = 0.021). Furthermore, the group with MOI exhibited a significantly higher rate of lipid-rich plaques (86% vs. 50%, P = 0.008), a higher rate of multifocal disease (59% vs. 10%, P < 0.001), and an MOI in both culprit and remote lesions (97% vs. 0%, P < 0.001) compared with those without MOI. At multivariate analysis, CRP value> 3 mg/dL was the only independent predictor of MOI in the culprit plaque (OR 8.72, 95% CI 1.78-41.67, P = 0.007). Conclusions In conclusion, PR can be caused by predominant inflammatory or non-inflammatory mechanisms, over a common low-grade chronic inflammatory background well known from pathology observations.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据