Patients who are hospitalized for either viral infection should be screened for myocardial involvement, experts say.
Patients hospitalized for influenza are just as likely as those admitted for COVID-19 to have signs of myocardial involvement, according to a study out Ontario, Canada.
Though patients with COVID-19 were more likely than those with the flu to have their levels of troponin and natriuretic peptides tested, the proportion of patients with high concentrations of the biomarkers was similar in the two groups, researchers led by Finlay McAlister, MD (University of Alberta, Edmonton, Canada), report in a study published in the July 2025 issue of the Canadian Journal of Cardiology.
New clinical diagnoses of various cardiovascular conditions—including heart failure (HF), atrial fibrillation (AF), acute myocardial infarction, and myocarditis—were infrequent and not much different between groups, although 40% to 50% of patients overall met Canadian Cardiovascular Society-defined criteria for probable HF.
It’s not surprising to see cardiac biomarkers elevated to a similar degree in both COVID-19 and influenza, McAlister told TCTMD, noting that many patients referred to the heart function clinic at his center didn’t have ischemic heart failure but did have a preexisting viral upper respiratory tract infection.
In that context, this study should “raise that index of suspicion for clinicians to think of those potential [cardiac] complications and at least rule them out in patients” with any viral upper respiratory tract infection, McAlister said. “If people have elevated biomarkers, then probably we should be following those patients more closely postdischarge than we currently do.”
It’s also important to consider whether a patient hospitalized for influenza who is getting more dyspneic may, in fact, have HF and not just a viral infection affecting the lungs. “Because if people have early heart failure, if we’re intervening earlier with therapies like RAAS [renin-angiotensin-aldosterone-system] inhibitors and SGLT2 [sodium-glucose cotransporter 2] inhibitors, things like that, we can actually change the course of disease and have people improve their prognosis,” said McAlister.
Mortality Risk Greater With COVID-19
Myocardial involvement has long been recognized as a potential complication of viral upper respiratory tract infections, and early in the COVID-19 pandemic, it became clear that myocardial injury was common among patients with a severe SARS-CoV-2 infection. However, there isn’t the same heightened index of suspicion for cardiac complications when it comes to influenza, McAlister said.
For the current study, conducted within the GEMINI research collaborative, the investigators examined myocardial involvement in adults hospitalized across 29 centers in Ontario for either COVID-19 (n = 25,200) or influenza (n = 8,569) between April 2015 and March 2023. Those with COVID-19 tended to be younger (mean age 67 vs 72 years), were more likely to be men (56% vs 47%), and were less likely to have had prior cardiovascular disease (7% vs 13%; P < 0.001 for all comparisons).
Patients with COVID-19 versus influenza had higher rates of testing for troponin (84.2% vs 78.7%) and natriuretic peptides (21.6% vs 12.7%; P < 0.001 for both comparisons). The proportion of patients with elevated levels of biomarkers, however, was not significantly different between the COVID-19 and influenza groups for either troponin (42.7% vs 39.8%; adjusted risk ratio [RR] 1.07; 95% CI 0.99-1.15) or natriuretic peptides (72.3% vs 81.7%; adjusted RR 0.93; 95% CI 0.87-0.99).
Rates of new clinical diagnoses of HF and AF did not differ significantly between groups, with only slight significant differences in rates of acute MI and myocarditis.
Outcomes Through Discharge
|
COVID-19 (n = 25,200) |
Influenza (n = 8,567) |
Adjusted RR (95% CI) |
New HF |
2.4% |
2.6% |
1.18 (0.79-1.77) |
New AF |
3.4% |
5.2% |
0.89 (0.76-1.04) |
Acute MI |
0.4% |
0.3% |
1.73 (1.13-2.66) |
Myocarditis |
0.1% |
0.2% |
0.47 (0.22-0.98) |
COVID-19 was associated with a greater risk of dying compared with influenza (16.5% vs 5.7%; adjusted RR 2.43; 95% CI 2.27-2.60), as well as higher use of mechanical ventilation (14.0% vs 6.0%; adjusted RR 1.30; 95% CI 1.24-1.37), longer stays in the hospital (mean 12.0 vs 8.5 days) and in special or intensive care units (mean 2.7 vs 1.3 days), and an increased risk of 30-day readmission (9.8% vs 8.8%; adjusted RR 1.27; 95% CI 1.14-1.43).
The results were similar in a propensity score-matched analysis.
Don’t ‘Be Relaxed’ Because It’s Flu
Commenting on the findings for TCTMD, Martin Goldman, MD (Icahn School of Medicine at Mount Sinai, New York, NY), noted that prior research has indicated that at least some cardiac complications are similar when looking at COVID-19 and influenza. He cited, for example, a study he was involved in showing that atrial fibrillation/flutter was similarly frequent with either infection, with mortality higher in COVID-19.
Although the current study has some potential limitations related to how the data were collected at each hospital and how patients were selected for testing of cardiac biomarkers, Goldman said the major take-home message is that “a bad viral infection of any etiology, whether it be COVID or whether it be influenza, can have cardiac effects. . . . We shouldn’t be relaxed just because it’s influenza and not COVID as far as cardiac involvement.”
A bad viral infection of any etiology, whether it be COVID or whether it be influenza, can have cardiac effects. Martin Goldman
When patients come in with a severe viral infection, he said, potential cardiac involvement needs to be evaluated because when it’s found, it’s indicative of a much worse prognosis, he said. He pointed to another of his studies showing that the risk of in-hospital mortality in patients admitted for COVID-19 ranged from 5.2% in the absence of myocardial injury to 31.7% in the presence of both elevated troponin and echocardiographic abnormalities.
“An echocardiogram should be done in patients who are either manifesting some evidence of cardiac involvement or who have elevated troponin and BNP to detect if there is direct cardiac involvement, and those patients are at greater risk for cardiac arrhythmias,” Goldman said.
There is also research ongoing to look at the long-term cardiac consequences of viral infections, including arrhythmias and cardiomyopathies, as well as what might be done to mitigate them. COVID-19 provides a good opportunity to do this because the timing of the initial infection can be established relatively accurately, Goldman indicated.
For now, what can be learned from this study “is that viral infections involve the heart and people should be aware of that and not just say, ‘Oh, it’s the flu. I don’t have to worry about that as much as the COVID infection,’” he said.