A new study has identified an association between prior SARS-CoV-2 infections and a more rapid progression of atherosclerotic plaque in coronary arteries as well as an elevated risk of adverse cardiovascular outcomes.
In the retrospective analysis of a prospective study, published in Radiology, investigators examined 803 patients (mean age = 63.9 years, 67.6% male) who underwent serial coronary computed tomography angiography (CCTA) between September 2018 and October 2023. A total of 2,588 coronary artery lesions were analyzed—2,108 from patients with SARS-CoV-2 infections and 480 from those without infections.
The investigators found that patients with SARS-CoV-2 infections demonstrated accelerated plaque growth and a heightened incidence of high-risk plaque characteristics compared with those without infections.
Lesions in patients with prior SARS-CoV-2 infections exhibited a faster annualized progression of total percent atheroma volume (PAV) compared with those in uninfected patients (0.90% per year ± 0.91 vs 0.62% per year ± 0.68, P < .001). Noncalcified PAV also progressed more rapidly (0.78% per year ± 0.79 vs 0.42% per year ± 0.45, P < .001).
"Emerging evidence indicates that [SARS-CoV-2 infections are] also characterized by an extreme inflammatory response, known as a cytokine storm, with resultant endothelial inflammation, microvascular thrombosis, and multiorgan failure," stressed lead study author Neng Dai, of the Department of Cardiology at Zhongshan Hospital at Fudan University at the Shanghai Institute of Cardiovascular Diseases, and colleagues.
The study also revealed that lesions in patients with SARS-CoV-2 infections were more likely to evolve into high-risk plaques (21.0% [n = 442/2,108] vs 15.8% [n = 76/480], P = .03) and demonstrate elevated pericoronary adipose tissue (PCAT) attenuation—an indicator of coronary inflammation (27.1% [n = 571/2,108] vs 19.8% [n = 95/480], P < .001).
Clinical outcomes reflected the imaging findings, with patients who had SARS-CoV-2 infections experiencing a significantly higher risk of target lesion failure, a composite endpoint that included cardiac death, target lesion myocardial infarction, and clinically driven target lesion revascularizations (10.4% vs 3.1%, adjusted hazard ratio = 2.90, 95% confidence interval = 1.68–5.02, P < .001).
The investigators highlighted the importance of understanding the long-term cardiovascular risks associated with SARS-CoV-2 infections. Despite the resolution of acute symptoms, ongoing coronary inflammation and plaque progression may predispose patients to future cardiovascular events.
The study underscored the need for clinicians to remain vigilant when evaluating cardiovascular health in patients recovering from SARS-CoV-2 infections. Further research may elucidate the mechanisms underlying plaque progression and inform strategies for mitigating cardiovascular risks in this patient population.
No conflicts of interest were disclosed in the study.
