Abstract
Abstract Background It is currently well-known that inflammation plays an essential role in all phases of atherosclerosis. Recent CT studies showed that atherosclerotic plaques found in the right coronary arteries (RCA) display a greater number of features that increase their susceptibility to destabilization compared to plaques found in left coronary arteries (LCA). COVID-19’s impact on regional coronary inflammation is not well understood, despite extensive research on its effects on cardiovascular diseases. Objectives This study aimed to evaluate the regional differences between local inflammation at the level of left versus right coronary circulation in patients who had CCTA examinations for chest pain in the early stages after COVID-19 infection. Methods In total, 172 patients with chest pain and CCTA data available were included in the study, divided into two groups: Group 1 (n = 80) with recent COVID-19 infection, and Group 2 (n = 92) with no known COVID infection. Attenuation of epicardial fat density was calculated in all patients using the FAI technology available from Caristo (Oxford, UK), and the associated FAI score and CaRi Heart® score of related cardiovascular risk were calculated. Results CaRi Heart® Risk (p < 0.0001) and Duke Score (p < 0.0001) were significantly higher for the COVID-negative patients, who presented a significantly higher FAI score (p = 0.001). This difference was also present in all the three coronary arteries: LAD (p = 0.05), LCX (p = 0.05), RCA. In the COVID-19 positive group the FAI score was significantly higher at the RCA level (p = 0.0002), but the non-COVID-19 presented no significant differences of inflammation levels between the left and right coronary circulation. Conclusions COVID-19 infection is associated with a higher risk of inflammation in the pericoronary epicardial fat. In post- COVID-19 patients, this inflammation seems to be more pronounced at the level of the RCA, which indicates a potential role of local hemorheological factors in the complex process of inflammation-mediated plaque vulnerabilization after COVID.
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