Not all plaque ruptures are born equal: an optical coherence tomography study

医学 光学相干层析成像 罪魁祸首 炎症 急性冠脉综合征 内科学 胃肠病学 心脏病学 狭窄 纤维帽 回顾性队列研究 冠状动脉疾病 C反应蛋白 放射科 心肌梗塞
作者
Giancarla Scalone,Giampaolo Niccoli,Hesham Refaat,Rocco Vergallo,Italo Porto,Antonio Maria Leone,Francesco Burzotta,Domenico D’Amario,Giovanna Liuzzo,Francesco Fracassi,Carlo Trani,Filippo Crea
出处
期刊:European Journal of Echocardiography [Oxford University Press]
卷期号:18 (11): 1271-1277 被引量:52
标识
DOI:10.1093/ehjci/jew208
摘要

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 (MØI). Our retrospective study aimed at assessing the role of plaque inflammation in PR among patients with acute coronary syndrome (ACS) using OCT.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 MØI 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 MØI at the site of PR, whereas 19 (34%) patients had no evidence of MØI. Patients with MØI showed a higher rate of CRP values >3 mg/dL as compared with those without MØI (92% vs. 47%, P = 0.004). In contrast, patients without MØI had a higher prevalence of hypertension compared with those with MØI (89% vs. 59%, P = 0.021). Furthermore, the group with MØI 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 MØI in both culprit and remote lesions (97% vs. 0%, P < 0.001) compared with those without MØI. At multivariate analysis, CRP value >3 mg/dL was the only independent predictor of MØI in the culprit plaque (OR 8.72, 95% CI 1.78-41.67, P= 0.007).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.

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