SARS-CoV-2 Infection Associated With Increased Plaque in Coronary Arteries, Higher Risk of Cardiac Events

Infection with SARS-CoV-2, the virus that causes COVID-19, is associated with a rapid buildup of plaque in coronary arteries and a corresponding increased risk of cardiovascular events, according to new results published by investigators in Radiology, a journal of the Radiological Society of North America (RSNA).^1,2

COVID-19 can cause an increase in inflammation in multiple areas of the body. | Image Credit: © Yingyaipumi - stock.adobe.com

In the early stages of the COVID-19 pandemic, research centered around COVID-19 being characterized by acute lung injury and respiratory failure. Now, nearly 5 years since the pandemic began, emerging data indicate that COVID-19 is also characterized by inflammation present in the heart and other organs, which could lead to thrombosis or multiorgan failure. Chronic inflammation in patients following COVID-19 infection can increase cardiovascular mortality and is a risk factor for atherosclerotic development and progression, the investigators of the study wrote.^1,3,4

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

Methods to evaluate coronary inflammation, such as coronary CT angiography (CCTA), are available, but it remains unknown whether infection with SARS-CoV-2 would have an impact on coronary inflammation, plaque buildup, and clinical outcomes. Using CCTA, the investigators sought to assess the impact of SARS-CoV-2 on cardiac outcomes by analyzing changes in peri-coronary adipose tissue (PCAT) while elucidating the burden and type of plaque that impacts survivors of COVID-19.^1,2

A total of 803 patients who underwent CCTA between September 2018 and October 2023 were included in the retrospective study, with 329 patients enrolled prior to the COVID-19 pandemic and 474 patients imaged during the pandemic. Investigators analyzed 2588 coronary artery lesions among the trial participants, including 2108 lesions among patients with SARS-CoV-2 and 480 among uninfected patients.^1,2

To garner their data, the researchers compared baseline and follow-up measurements of plaque volume changes, inflammation, and indications of high-risk plaque. Furthermore, the relationship between SARS-CoV-2 and cardiovascular events like heart attacks or revascularization procedures was examined to see if there was an association. First, the investigators examined the impact of SARS-CoV-2 infection on coronary atherosclerosis progression.^1,2

At baseline, 8.1% of lesions had a diameter stenosis of 50% or larger. Results indicate that SARS-CoV-2 infection was associated with an increase in the percentage of diameter stenosis, leading to a higher proportion of lesions with stenosis of 50% or more at follow-up among patients with SARS-CoV-2 infection than those without. Regarding plaque concentration, percent atheroma volume (PAV) at the first CCTA examination was similar among patients with and without SARS-CoV-2 infection. Upon the second examination, though, it was revealed that annual progression of coronary lesion PAV was faster in patients with prior SARS-CoV-2 infection than those without (0.90% per year ± 0.91 vs 0.62% per year ± 0.68, respectively; P < .001). An interesting observation was that COVID-19 vaccination had no effect on the progression of atherosclerosis among those with SARS-CoV-2, but it did have a protective value among uninfected patients.^1,2

The impact of infection on cardiovascular outcomes was described. Two major factors of cardiovascular burden—target lesion failures and target lesion revascularizations—were observed in 150 lesions in patients with SARS-CoV-2 infection and in 13 lesions in patients who were not infected. Compared with those without SARS-CoV-2 infection, the lesions of infected patients showed an increased percentage of target lesion failure. Lastly, in a major indicator of increased cardiovascular risk, patients with SARS-CoV-2 had a greater percentage of major adverse cardiovascular events compared with those who were not infected (20.1% vs 3.8%; HR, 4.82; 95% CI: 1.77-13.11; P = .002).¹

“Effective management strategies for these patients are imperative,” Ge continued. “It’s crucial to anticipate a heavier cardiovascular patient burden in the future as most infected individuals recover from acute SARS-CoV-2 infection.”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). doi:10.1148/radiol.240876

2. RSNA. Virus that causes COVID-19 increases risk of cardiac events. EurekAlert! News Release. Released February 4, 2025. Accessed February 11, 2025. https://www.eurekalert.org/news-releases/1071914

3. Gallagher A. COVID-19 infection could be detected in lungs, heart, causing inflammatory damage. Pharmacy Times. Published June 2, 2023. Accessed February 11, 2025. https://www.pharmacytimes.com/view/covid-19-infection-could-be-detected-in-lungs-heart-causing-inflammatory-damage

4. Ridker PM, Lüscher TF. Anti-inflammatory therapies for cardiovascular disease. Euro Heart Journ. 2014;35(27):1782-1791. doi:10.1093/eurheartj/ehu203