Report: Severe COVID can catalyze arterial plaque growth, sparking deadly heart problems

COVID-19
Cardiac arrest

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Severe COVID-19 infection can trigger extensive inflammation, resulting in the rapid growth of plaque in the coronary arteries and a higher risk of heart attack, stroke, and other life-threatening cardiovascular events for as long as 1 year, reports a Fudan University–led research team in China.

The retrospective analysis of a prospective study, published yesterday in Radiology, included 803 patients who underwent serial coronary computed tomography angiography (CCTA) between September 2018 and October 2023. The researchers assessed 2,108 coronary artery lesions in 690 COVID-19 patients and 480 lesions in 113 matched uninfected patients.

The median time between the first and second CCTA was 3 years, while a median of 7 months elapsed between COVID-19 infection and the second CCTA, and median follow-up was 9 months after the second CCTA. The average patient age was 63.9 years, and 67.6% were men. Similar proportions of infected and uninfected participants were vaccinated against COVID-19 (about 89%) and received boosters (about 56%).

20% vs 16% developed high-risk plaques

At baseline, the average stenosis, or narrowing of an artery, per lesion was 31.3%, and only 8.1% of lesions had a stenosis diameter of 50% or greater. COVID-19 infection was tied to a larger increase in percentage of stenosis diameter (1.0% vs 0.4% per year in uninfected patients), leading to a higher average percentage of stenosis diameter (34.2% vs 32.5%) and proportion of lesions with a stenosis diameter of 50% or more (12.6% vs 8.5%) at follow-up.

COVID-infected patients showed accelerated progression rates of total coronary atherosclerotic volume (0.90% vs 0.62%), with diverse effects on different kinds of plaques, including a reduction in calcified plaque constituents (0.12% vs 0.20% per year) and greater advancement of noncalcified segments of atherosclerotic lesions (0.78% vs 0.42%).

Target lesion failures (composite of cardiac death, target-lesion heart attack, and target-lesion revascularizations) occurred in 150 lesions (6 cardiac deaths, 40 target-lesion heart attacks, and 104 target-lesion revascularizations) in infected patients and in 13 lesions (0 cardiac deaths, 2 target-lesion heart attacks, and 11 target-lesion revascularizations) in their uninfected counterparts. 

Relative to plaque volumes in uninfected patients, volumes grew faster in COVID-19 patients, whose lesions developed into high-risk plaques at a greater rate (20.1% vs 15.8%). Infected patients also were more likely to have coronary inflammation (27% vs 19.9%) and a higher risk of target lesion failure (10.4% vs 3.1%), an indicator of increased risk of heart attack or stroke. Previous infection was associated with worse cardiovascular outcomes (adjusted hazard ratio, 2.9).

Bracing for heavier cardiovascular burden

"COVID-19, caused by SARS-CoV-2, is initially characterized by acute lung injury and respiratory failure," senior author Junbo Ge, MD, of Fudan University, said in a press release from the Radiological Society of North American, which publishes the journal. "However, emerging evidence indicates COVID-19 also involves an extreme inflammatory response that can affect the cardiovascular system."

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

It's crucial to anticipate a heavier cardiovascular patient burden in the future, as most infected individuals recover from acute SARS-CoV-2 infection.

Junbo Ge, MD

The authors said that while mechanisms underlying the link between COVID-19 and greater susceptibility to heart attack and stroke post-infection aren't completely understood, some experts speculate that SARS-CoV-2 promotes atherosclerosis through direct infection of vascular cells, systemic inflammation, and outsized inflammatory responses. 

While pulmonary manifestations are the most common consequence, COVID-19 infection causes systemic inflammation with cardiac problems such as damage to the heart muscle, cardiac insufficiency, abnormal heart rhythms, and irregular blood-clotting, they said.

These effects persist post-infection, regardless of age and underlying conditions such as high blood pressure and diabetes, said Ge, who called for further research into the underlying mechanisms to enable development of preventive and therapeutic strategies. "It's crucial to anticipate a heavier cardiovascular patient burden in the future, as most infected individuals recover from acute SARS-CoV-2 infection," he said.

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