JACC: Cardiovascular Imaging ( IF 14.0 ) Pub Date : 2021-10-13 , DOI: 10.1016/j.jcmg.2021.09.008 Rocco A Montone 1 , Massimiliano Camilli 2 , Michele Russo 2 , Claudio Termite 2 , Giulia La Vecchia 2 , Giulia Iannaccone 2 , Riccardo Rinaldi 2 , Filippo Gurgoglione 2 , Marco Giuseppe Del Buono 2 , Tommaso Sanna 3 , Carlo Trani 3 , Giovanna Liuzzo 3 , Filippo Crea 3 , Giampaolo Niccoli 4
Objectives
We assessed the relationship between exposure to air pollutants and mechanisms of coronary instability evaluated by optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS).
Background
Air pollution is an emerging key player in determining the residual risk of coronary events. However, pathophysiological mechanisms linking air pollution and coronary events have been not adequately investigated.
Methods
Patients with ACS undergoing OCT imaging were retrospectively selected. Mechanism of culprit lesion instability was classified as plaque rupture (PR) or intact fibrous cap (IFC) by OCT, and the presence of macrophage infiltrates (MØI) and thin-cap fibroatheroma (TCFA) at the culprit site was also assessed. Based on each case’s home address, exposure to several pollutants was evaluated, including particulate matter 2.5 (PM2.5), PM10, and carbon monoxide (CO). Only patients with >2 years of available data on air pollution exposure prior to ACS were enrolled.
Results
We included 126 patients (median age: 67.0 years of age; IQR: 55.5-76.0; 97 male patients [77.0%]). Sixty-six patients (52.4%) had PR as the mechanism of plaque instability. Patients with PR were exposed to significantly higher PM2.5 levels than to IFC, and PM2.5 was independently associated with PR (odds ratio: 1.194; 95% CI: 1.036 to 1.377; P = 0.015). Moreover, exposure to higher levels of PM2.5 was independently associated with the presence of TCFA and of MØI at the culprit site. Interestingly, PM2.5, PM10, and Co levels were positively and significantly correlated with serum levels of C-reactive protein.
Conclusions
We provide novel insights into the missing link between air pollution and increased risk of coronary events. In particular, exposure to higher concentrations of air pollutants is associated with the presence of vulnerable plaque features and with plaque rupture as a mechanism of coronary instability. An enhanced systemic and plaque inflammatory activation may explain these findings.
中文翻译:
空气污染和冠状动脉斑块的脆弱性和不稳定
目标
我们通过光学相干断层扫描 (OCT) 在急性冠状动脉综合征 (ACS) 患者中评估了暴露于空气污染物与冠状动脉不稳定机制之间的关系。
背景
空气污染是确定冠状动脉事件残余风险的新兴关键因素。然而,尚未充分研究将空气污染与冠状动脉事件联系起来的病理生理机制。
方法
回顾性选择接受OCT成像的ACS患者。通过 OCT 将罪魁祸首病变不稳定性的机制分类为斑块破裂 (PR) 或完整的纤维帽 (IFC),并且还评估了罪魁祸首部位是否存在巨噬细胞浸润 (MØI) 和薄帽纤维粥样斑块 (TCFA)。根据每个病例的家庭住址,评估了对几种污染物的暴露情况,包括颗粒物 2.5 (PM2.5)、PM10 和一氧化碳 (CO)。只有在 ACS 之前具有 > 2 年空气污染暴露可用数据的患者被纳入研究。
结果
我们纳入了 126 名患者(中位年龄:67.0 岁;IQR:55.5-76.0;97 名男性患者 [77.0%])。66 名患者 (52.4%) 以 PR 作为斑块不稳定的机制。PR 患者的 PM2.5 水平显着高于 IFC,PM2.5 与 PR 独立相关(比值比:1.194;95% CI:1.036 至 1.377;P = 0.015)。此外,暴露于较高水平的 PM2.5 与罪魁祸首 TCFA 和 MØI 的存在独立相关。有趣的是,PM2.5、PM10 和 C o水平与血清 C 反应蛋白水平呈正相关且显着相关。
结论
我们对空气污染与冠状动脉事件风险增加之间缺失的联系提供了新的见解。特别是,暴露于较高浓度的空气污染物与易损斑块特征的存在以及作为冠状动脉不稳定机制的斑块破裂有关。增强的全身和斑块炎症激活可以解释这些发现。