COVID-19-causing virus linked to coronary plaque progression, risk for MI, death

ByScott Buzby

Fact checked byRichard Smith

Key takeaways:

The virus that causes COVID-19 may expedite progression of coronary lesions to high-risk plaque.
SARS-CoV-2 was linked to significantly elevated risk for cardiac death, MI and revascularization.

SARS-CoV-2 infection was associated with more rapid coronary plaque progression and significantly increased risk for adverse outcomes related to target lesion failure, such as heart attack and death, researchers reported.

A retrospective analysis of the CHART-VISION trial was conducted to assess the impact of SARS-CoV-2 on coronary plaque and adverse CV outcomes and was published in Radiology.

blood cell flow with plaque — The virus that causes COVID-19 may expedite progression of coronary lesions to high-risk plaque. *Image: Adobe Stock*

“COVID-19, caused by SARS-CoV-2, is initially characterized by acute lung injury, respiratory failure and death. However, emerging evidence indicates that COVID-19 is also characterized by an extreme inflammatory response, known as a cytokine storm, with resultant endothelial inflammation, microvascular thrombosis and multiorgan failure,” Neng Dai, MD, fellow in training in interventional cardiology at Zhongshan Hospital of Fudan University in Shanghai, and colleagues wrote. “Coronary CT angiography (CCTA) enables the detection and characterization of coronary plaques and provides an assessment of obstructive coronary artery disease. ... The aim of this study was to assess the impact of SARS-CoV-2 infection on coronary inflammation, plaques and clinical outcomes by using CCTA.”

SARS-CoV-2, coronary plaque and target lesion failure

For this retrospective analysis of CHART-VISION, Dai and colleagues included consecutive patients who underwent CCTA between September 2018 and October 2023. The researchers compared quantitative total and compositional percent atheroma volume, high-risk plaques and attenuation of lesion-specific pericoronary adipose tissue at baseline and follow-up among 803 patients with and without SARS-CoV-2 infection (mean age, 64 years; 68% men). Only patients with SARS-CoV-2 infection not requiring hospitalization were included in the analysis.

The primary composite outcome of interest was target lesion failure, which included cardiac death, target lesion MI and clinically driven target lesion revascularization.

The researchers reported that overall percent atheroma volume (0.9% per year vs. 0.62% per year; P < .001) and noncalcified percent atheroma volume (0.78% per year vs. 0.42% per year; P < .001) progressed more rapidly in patients with SARS-CoV-2 infection compared with no infection.

The rate of lesions becoming high-risk plaque was higher among patients with SARS-CoV-2 infection (21% vs. 15.8%; P = .03) as well as attenuation of lesion-specific pericoronary adipose tissue of 70.1 Hounsfield units or higher (27.1% vs. 19.8%; P < .001) in patients with SARS-CoV-2 infection compared with patients without infection, according to the study.

Moreover, researchers reported that patients with SARS-CoV-2 infection had a higher risk for the composite target lesion failure outcome compared with patients not infected (adjusted HR = 2.9; 95% CI, 1.68-5.02; P < .001).

“These results are consistent with previous studies showing an intensified inflammatory reaction in SARS-CoV-2-infected atherosclerotic lesions compared with nonatherosclerotic tissues,” the researchers wrote. “Thus, COVID-19 may affect pericoronary CT attenuation through systemic inflammatory processes and plaque structure, leading to an increased vulnerability level and altered patient outcomes.”

Link between COVID-19, CV events ‘concerning’

In a related editorial, Jonathan R. Weir-McCall, PhD, senior lecturer at King’s College London and cardiothoracic radiologist at the Royal Brompton Hospital in London, and Jack S. Bell, BMBCh, cardiology registrar and a National Institute for Health Research academic clinical fellow at the Liverpool Centre for Cardiovascular Science in Liverpool, U.K., wrote: “From a public health perspective, the association between mild COVID-19 infection, plaque progression and cardiovascular events is concerning as we approach 800 million confirmed COVID-19 cases worldwide. If these findings are replicated in other populations, and across the spectrum of COVID-19 severity, the question then becomes one of how best to integrate COVID-19 into the cardiovascular preventative care pathway. ... Action is required to bring together the clinical trials necessary to assess potential treatment strategies, such as anti-inflammatory medications and statins, to reduce inflammation and prevent plaque progression in patients at high risk for future cardiovascular events.”