Patients with SARS-CoV-2 infection, the virus that causes COVID-19, are at increased risk for heart attack, acute coronary syndrome, and stroke for up to a year, research finds.
RT’s Three Key Takeaways:
- COVID-19 Linked to Coronary Plaque Growth – SARS-CoV-2 infection is associated with accelerated plaque buildup in the arteries, raising the risk of cardiovascular events.
- Increased Heart Attack and Stroke Risk – Patients with COVID-19 had a higher likelihood of developing high-risk plaques and coronary inflammation, increasing their risk for heart attacks and strokes for up to a year.
- Effects Persist Beyond Infection – The cardiovascular risks remained even in patients without preexisting conditions, underscoring the need for ongoing monitoring and preventive care.
A new study found severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection was associated with the rapid growth of plaque in the coronary arteries and an increased risk of cardiovascular events.
The results were published in Radiology, a journal of the Radiological Society of North America.
“COVID-19, caused by SARS-CoV-2, is initially characterized by acute lung injury and respiratory failure,” says the study’s senior author, Junbo Ge, MD, professor and director of the cardiology department at Zhongshan Hospital, Fudan University in Shanghai, China, in a release. “However, emerging evidence indicates COVID-19 also involves an extreme inflammatory response that can affect the cardiovascular system.”
According to Ge, this systemic inflammation produces consequences for the heart beyond the first month of infection, leading to high mortality and unfavorable outcomes.
The researchers investigated the impact of SARS-CoV-2 infection using coronary CT angiography (CCTA) to assess coronary inflammation, determined by analyzing changes in tissue surrounding the coronary arteries, as well as plaque burden and type.
The retrospective study included patients who underwent CCTA between September 2018 and October 2023. The final study group of 803 patients (mean age, 63.9 years, 543 men) included 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.
The research team analyzed a total of 2,588 coronary artery lesions, including 2,108 lesions among SARS-CoV-2 patients and 480 lesions among uninfected patients.
Findings: Faster Plaque Growth and Increased Risk
For all patients, researchers compared baseline and follow-up measurements of plaque volume changes, the presence of high-risk plaque, and inflammation. They also analyzed the relationship between SARS-CoV-2 and cardiovascular events, such as a heart attack or revascularization procedure.
At baseline, the mean stenosis, or narrowing of the artery, per lesion was 31.3%. Only 8.1% of lesions had diameter stenosis of 50% or more. Compared to the uninfected patients, the plaque volumes grew faster in SARS-CoV-2 patients. Lesions in patients with SARS-CoV-2 infection had a higher incidence of developing into high-risk plaques (20.1% versus 15.8%) and coronary inflammation (27% versus 19.9%).
Patients with COVID-19 also had a higher risk of target lesion failure (10.4% versus 3.1%), an indicator of increased heart attack or stroke risk.
Long-Term Cardiovascular Implications
“Inflammation following COVID-19 can lead to ongoing plaque growth, particularly in high-risk, noncalcified plaques,” says Ge in a release. “Patients with SARS-CoV-2 infection are at increased risk for myocardial infarction, acute coronary syndrome, and stroke for up to a year.”
He adds that these effects persist during the aftermath of COVID-19, regardless of comorbidities such as age, hypertension, and diabetes. “Effective management strategies for these patients are imperative,” he says in a release.
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.
“It’s crucial to anticipate a heavier cardiovascular patient burden in the future as most infected individuals recover from acute SARS-CoV-2 infection,” Ge says.
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