COVID-19 Accelerates Progression of Atherosclerotic Plaque, Increases Risk for Cardiovascular Events

Patients with COVID-19 were more likely to have plaque (lesions) growth in the arteries compared to patients who did not have SARS-CoV-2, according to a new study published in the journal Radiology.¹

“Compared with lesions in patients without SARS-CoV-2 infection, lesions in patients with SARS-CoV-2 infection demonstrated more rapid progression of overall [percutaneous aortic valve] PAV (0.90% per year ± 0.91 vs 0.62% per year ± 0.68, respectively; P < .001) and noncalcified PAV (0.78% per year ± 0.79 vs 0.42% per year ± 0.45, respectively; P < .001),” the authors wrote.¹

“COVID-19, caused by SARS-CoV-2, is initially characterized by acute lung injury and respiratory failure,” the study’s senior author, Junbo Ge, MD, professor and director of the Cardiology Department at Zhongshan Hospital, Fudan University in Shanghai, China, said in a statement. “However, emerging evidence indicates COVID-19 also involves an extreme inflammatory response that can affect the cardiovascular system.”²

Study Parameters

This was a retrospective study that included patients who underwent coronary CT angiography (CCTA) between September 2018 and October 2023. The study included 803 total patients with 543 men and a mean age of 63.9 years. There were 329 patients (41%) imaged before the COVID-19 pandemic and 474 patients imaged during the pandemic. Of those, 25 patients were infected with SARS-CoV-2 before imaging.²

The researchers investigated the impact of SARS-CoV-2 infection using CCTA to assess coronary inflammation, determined by analyzing changes in tissue surrounding the coronary arteries, as well as plaque burden and type.²

The investigators analyzed a total of 2,588 coronary artery lesions, including 2,108 lesions among SARS-CoV-2 patients and 480 lesions among uninfected patients.²

For all patients, researchers compared baseline and follow-up measurements of plaque volume changes, the presence of high-risk plaque and inflammation.²

Cardiovascular Events

In addition to studying plaque formation for the primary clinical outcome, the secondary clinical outcome was major adverse cardiovascular events, which included all-cause mortality, myocardial infarction, and hospital admission for unstable angina. According to the investigators, in patients with multivessel disease or multiple lesions, the classification according to target lesions was based on the lesions exhibiting the highest number of high-risk characteristics. Any mortality was considered to have a cardiac origin unless an unequivocal noncardiac cause could be established. ¹

“Target lesion failures…occurred in 150 lesions (6 cardiac deaths, 40 target lesion myocardial infarctions, and 104 target lesion revascularizations) in patients with SARS-CoV-2 infection and in 13 lesions (no cardiac deaths, two target lesion myocardial infarctions, and 11 target lesion revascularizations) in patients without SARS-CoV-2 infection,” the investigators wrote.¹

Ge said these effects persist during the aftermath of COVID-19, regardless of comorbidities such as age, hypertension, and diabetes. The findings suggest that SARS-CoV-2 infection may exacerbate cardiovascular risk by accelerating the progression of susceptible plaques and coronary inflammation. However, a more comprehensive understanding of the biological mechanisms is required to formulate preventative and therapeutic approaches.²

“Inflammation following COVID-19 can lead to ongoing plaque growth, particularly in high-risk, noncalcified plaques.” Ge said. “Patients with SARS-CoV-2 infection are at increased risk for myocardial infarction, acute coronary syndrome and stroke for up to a year.”²

References
1. Dai N, Tang X, Hu Y, et al. SARS-CoV-2 Infection Association with Atherosclerotic Plaque Progression at Coronary CT Angiography and Adverse Cardiovascular Events. Radiology. 2025;314(2):e240876. doi:10.1148/radiol.240876
2. Virus That Causes COVID-19 Increases Risk of Cardiac Events. Radiological Society of North America press release. February 4, 2025. Accessed February 5, 2025.
https://press.rsna.org/timssnet/media/pressreleases/14_pr_target.cfm?ID=2564