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Risk for MI increases after influenza, pneumonia
Physicians should be mindful of the increased risk for MI in patients during and after acute infections such as influenza and pneumonia, according to a review published in The New England Journal of Medicine.
Daniel M. Musher, MD, distinguished service professor and professor of microbiology and molecular virology at Baylor College of Medicine in Houston, and colleagues analyzed available evidence on acute viral and bacterial infections and an increased risk for MI.
CVD and acute infections
An increased risk for CVD during influenza epidemics has been recognized since the early 20th century, but the associations between the two were not established until decades later, according to the study. The risk for MI has been shown to increase with pneumonia, influenza, acute bronchitis and other chest infections, in addition to respiratory syncytial virus, influenza virus and other respiratory viruses.
The risk for MI typically peaks at the onset of the pneumonia infection and is relative to the severity of the illness. In a case series with U.S. veterans, the risk for MI increased during the first 15 days after a patient was hospitalized for acute bacterial pneumonia. The risk for MI was 48 times higher than it was the year before and the year after the onset of infection, the researchers wrote.
This increased risk for MI related to acute infections can persist beyond the short-term period after infection, although it returned to baseline within a few months after resolution of a mild respiratory infection or urinary tract infection. The risk related to pneumonia also decreases over time, but it is higher than it was at baseline for up to 10 years after the infection, according to the study.
The association between an increased risk for MI and infections may be a causal relationship, with the infection and host response to it determining the strength of the relationship. Infection in the body can generate circulating inflammatory cytokines that activates inflammatory cells in atherosclerotic plaques. In addition, the risk for coronary thrombosis in areas of plaque disruption can also result from the procoagulant, prothrombotic state linked to acute infection, the researchers wrote.
Platelet activation and an increased risk for MI is associated with the influenza virus and other respiratory viruses. Fever and inflammation related to infections increase the metabolic needs of peripheral organs and tissues, which can shorten the filling time during diastole and compromise coronary perfusion, according to the study.
Decreased risk with vaccines
A meta-analysis found that patients who received the influenza vaccine had a 36% decreased risk for a composite of CV events compared with those who were not vaccinated. This benefit was greater when analyzing patients with known CAD. Limited data are available for patients who received a pneumococcal vaccination, the researchers wrote.
Future research should focus on the use of statins and other drugs in patients with acute infection, specifically those without clinical indications for these treatments. In addition, more data are needed to characterize the associations between acute infections and other CV events such as arrhythmias, HF and strokes, according to the study.
“Practitioners may be able to influence the risk of postinfection myocardial infarction if they remain mindful of the increased risk of myocardial infarction during and after acute infections and if they do not dismiss elevated troponin levels as ‘troponin leak,’” Musher and colleagues wrote. – by Darlene Dobkowski
Disclosures: The authors report no relevant financial disclosures.