4.6 Article

Air Pollution and Coronary Plaque Vulnerability and Instability An Optical Coherence Tomography Study

Journal

JACC-CARDIOVASCULAR IMAGING
Volume 15, Issue 2, Pages 325-342

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jcmg.2021.09.008

Keywords

acute coronary syndrome; air pollution; inflammation; myocardial infarction; optical coherence tomography; plaque rupture; vulnerable plaque

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This study investigated the relationship between exposure to air pollutants and mechanisms of coronary instability in patients with acute coronary syndrome. The findings suggest that higher concentrations of air pollutants are associated with the presence of vulnerable plaque features and plaque rupture as a mechanism of coronary instability.
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 in-filtrates (M & Oslash;I) 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 M & Oslash;I 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 in-flammatory activation may explain these findings. (C) 2022 by the American College of Cardiology Foundation.

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