Why Your Heart Is Still at Risk After the Flu or COVID?
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As a cardiologist, I often remind patients that the heart and immune system are inextricably linked. Every infection—whether a simple cold, the flu, or COVID-19—sets off a cascade of inflammation throughout the body. For most people, that inflammation resolves quickly. But for some, it leaves behind dangerous echoes that can increase the risk of a heart attack or stroke for weeks, months, or even longer.
A new evidence review published in the Journal of the American Heart Association confirms what many of us in cardiovascular medicine have suspected: both influenza and COVID-19 substantially raise the short- and long-term risk of serious cardiovascular events.
The Evidence: Skyrocketing Risk After Infection
According to the review, people are four times more likely to have a heart attack and five times more likely to have a stroke within the first 30 days after infection with influenza. The danger window is narrow but critical—most events occur in the first two weeks, but the risk remains elevated for at least a month.
COVID-19, meanwhile, produces a longer-lasting effect. The data show that individuals are three times more likely to experience a heart attack or stroke within 14 weeks of infection, and that risk remains elevated for up to a year. This means that even after recovering from COVID, many people’s cardiovascular systems are still under siege.
These findings are consistent with prior studies from Canada, the Netherlands, and the United Kingdom, which have shown a marked increase in myocardial infarction (MI) and ischemic stroke rates following viral infections. The mechanism is not purely respiratory—it’s systemic.
Why Viral Infections Stress the Heart?
When a virus like influenza or SARS-CoV-2 enters the body, the immune system responds with inflammation, fever, and the release of signaling proteins called cytokines. While these responses are crucial to fighting infection, they can also destabilize vulnerable atherosclerotic plaques in the arteries.
In simple terms, infection can trigger plaque rupture—the event that precedes most heart attacks. Fever, dehydration, and elevated heart rate add further strain by increasing the heart’s oxygen demand just as oxygen supply may be compromised. In addition, inflammation can make blood more prone to clotting, which raises the risk of stroke.
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Is the Flu Shot A Cardioprotective Vaccine?
One of the most encouraging insights from this body of research is that the influenza vaccine reduces the risk of heart attack and stroke by about 34% in adults. This isn’t just about avoiding the flu—it’s about avoiding the cardiovascular storm that follows it.
A 2021 study in JAMA Network Open found that people who received the flu vaccine had significantly lower rates of major adverse cardiovascular events, particularly among those with preexisting heart disease. Another large analysis presented at the European Society of Cardiology Congress found similar results: the vaccine reduced cardiovascular mortality by up to one-third within a year.
It’s worth noting that while the flu vaccine doesn’t prevent every case of influenza, it dramatically reduces the severity of illness and the systemic inflammation that accompanies it. The same principle may apply to COVID vaccination, which has been shown to mitigate both acute and post-infection cardiovascular complications.
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What is the Longer Tail of COVID?
COVID-19 continues to challenge our understanding of cardiovascular risk. Several large-scale studies—including those from the U.S. Department of Veterans Affairs and Nature Medicine—have shown that even after “mild” COVID, patients face a persistent elevation in cardiovascular risk for at least 12 months.
This includes not just heart attacks and strokes but also myocarditis (inflammation of the heart muscle), arrhythmias, and new-onset heart failure. We are still learning exactly why, but ongoing inflammation, microvascular damage, and immune dysregulation likely all play roles.
In my practice, I’ve seen many patients—some previously healthy—develop unexplained fatigue, shortness of breath, or palpitations after COVID. Cardiac imaging often reveals subtle changes consistent with inflammatory injury. While most recover, some do not return fully to baseline for months.
Who Is Most at Risk?
The elevated risk after infection affects everyone, but it’s most pronounced among those with underlying cardiovascular disease, diabetes, hypertension, or smoking history. Age amplifies the risk, but even younger adults are not immune. In fact, a 2022 study in Circulation showed that adults under 45 had a measurable increase in heart attack incidence after COVID, especially those who were unvaccinated.
For people with established heart disease, catching the flu or COVID can act as a “final straw.” The infection adds stress to an already burdened cardiovascular system—raising heart rate, thickening the blood, and tipping the balance toward plaque rupture or clot formation.
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The Mechanisms—In Brief
While we’re still learning the finer details, three mechanisms are thought to underlie the post-viral spike in cardiovascular risk:
Inflammation: Viral infections trigger an inflammatory surge that destabilizes arterial plaques and increases clotting tendency.
Endothelial Dysfunction: Viruses damage the inner lining of blood vessels, impairing vasodilation and promoting thrombosis.
Autonomic Imbalance: Fever and systemic stress increase heart rate and blood pressure, adding oxygen demand and strain on the heart.
These processes can linger for weeks or months, explaining why the elevated risk persists long after the initial illness.
What Patients Can Do?
The good news is that there are clear, actionable steps to reduce risk:
Get vaccinated: The flu vaccine, and COVID boosters, significantly cut both infection severity and cardiovascular complications.
Prioritize rest after illness: Even when symptoms resolve, the heart may still be recovering. Avoid intense physical exertion for several weeks post-infection.
Monitor your numbers: Check blood pressure, heart rate, and cholesterol regularly—especially after recent infection.
Don’t ignore symptoms: New or unexplained chest pain, shortness of breath, dizziness, or weakness in the limbs after viral illness should prompt immediate medical evaluation.
We often think of viral infections as short-term inconveniences—something you “get over.” But for the heart, they can be silent saboteurs. The weeks following the flu or COVID represent a critical window when vigilance pays off.
Vaccination isn’t just about preventing illness—it’s a cardiovascular intervention. By reducing infection-related inflammation, we protect our arteries, our brain, and our future.
This winter, as flu season overlaps with COVID circulation, I’ll be reminding every patient: protecting your heart might be as simple as rolling up your sleeve.
Sources
Journal of the American Heart Association. “Risk of Acute Myocardial Infarction and Stroke After Influenza and COVID-19 Infection.” (2025) Link
JAMA Network Open. “Influenza Vaccination and Major Adverse Cardiovascular Events: A Meta-Analysis.” 2021. Link
Kwong JC et al. “Acute Myocardial Infarction after Laboratory-Confirmed Influenza Infection.” New England Journal of Medicine. 2018. Link
Xie Y et al. “Long-Term Cardiovascular Outcomes of COVID-19.” Nature Medicine. 2022. Link
European Heart Journal. “Influenza Vaccination and Cardiovascular Mortality: Insights from Randomized Trials.” 2020. Link
CDC. “Flu and Heart Disease.” Updated 2024. Link
