Institute of Cardiology, Catholic University of the Sacred Heart, Largo F. Vito 1, 00168 Rome, Italy.
Institute of Cardiology, Zagazig University, 44519, Ismailia - El-Zakazik Rd, Zagazig, Egypt.
Eur Heart J Cardiovasc Imaging. 2017 Nov 1;18(11):1271-1277. doi: 10.1093/ehjci/jew208.
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.
斑块破裂（PR）代表了至少 50%的冠状动脉血栓形成的最常见的基质。慢性低度炎症是动脉粥样硬化发展的常见背景；然而，斑块炎症的增加本身可能会导致 PR。在过去的十年中，通过光学相干断层扫描（OCT）进行的研究已经通过评估巨噬细胞浸润（MØI）来确定斑块炎症的严重程度。我们的回顾性研究旨在使用 OCT 评估急性冠状动脉综合征（ACS）患者中 PR 与斑块炎症之间的关系。
我们纳入了 56 例 ACS 患者，这些患者在 OCT 确定的罪犯狭窄部位发生了 PR。根据 OCT 分析中是否存在 MØI，将患者分为两组，MØI 定义为信号丰富、明显或连续的点状区域，超过背景斑点噪声的强度。入院时通过乳胶增强免疫比浊法测量血清高敏 C 反应蛋白（CRP）。在 56 例 PR 患者中，有 37 例（66%）患者有 MØI，19 例（34%）患者没有 MØI。与没有 MØI 的患者相比，有 MØI 的患者 CRP 值>3mg/dL 的比例更高（92% vs. 47%，P=0.004）。相比之下，没有 MØI 的患者中高血压的患病率高于有 MØI 的患者（89% vs. 59%，P=0.021）。此外，有 MØI 的患者的富含脂质斑块比例显著更高（86% vs. 50%，P=0.008），多灶性病变的比例更高（59% vs. 10%，P<0.001），罪犯病变和远处病变均有 MØI 的比例也更高（97% vs. 0%，P<0.001）。多变量分析显示，CRP 值>3mg/dL 是罪犯斑块中 MØI 的唯一独立预测因子（OR 8.72，95%CI 1.78-41.67，P=0.007）。
总之，PR 可能是由炎症为主或非炎症为主的机制引起的，而这些机制在病理学观察中已知的共同的慢性低度炎症背景上占主导地位。
