Laboratory-confirmed influenza significantly increases the risk of acute myocardial infarction

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Jeffrey Kwong

Jeffrey C Kwong (Institute for Clinical Evaluative Sciences, Toronto, Canada) and others report in The New England Journal of Medicine that patients with laboratory-confirmed influenza have a six-fold increased risk of having an acute myocardial infarction within the first seven days of a diagnosis. Although previous studies have found a link between respiratory disease and myocardial infarction, most have used non-specific measures of identifying influenza. 

According to Kwong et al, the hypothesis that influenza may “trigger acute cardiovascular events and death” has been around since the 1930s. However, they note that the studies that looked at this association were “neither sensitive nor specific” for influenza and observe that the few studies that did use laboratory-confirmed influenza as a measure were underpowered and had inconsistent findings. “We sought to evaluate the association between laboratory confirmed influenza infection and acute myocardial infarction using the self-controlled case series study design,” the authors write.

In the study, Kwong et al grouped hospitalisations for patients who had an acute myocardial infarction and a laboratory-confirmed diagnosis of influenza (364) into two cohorts: hospitalisations for acute myocardial infarction that occurred within the first seven days of an influenza diagnosis (20; the risk interval); and those that occurred a year before or a year after the diagnosis of influenza (344; the control interval). They comment: “The incidence ratios for days one through three and for days four through seven were 6.3 and 5.78, respectively. We observed no significant increase in the incidence on days eight through 14 or on days 15 through 28”. According to the authors, the incidence ratio patios were highest for older adults, for patients with influenza B infection, and for patients who had their first acute myocardial infarction.

The risk of acute myocardial infarction after influenza was increased regardless of whether the patient had received a vaccine. However, Kwong et al comment that this finding should not be seen as evidence of lack of vaccine effectiveness but rather—since vaccination of adults is only approximately 40% to 60% effective—as evidence that vaccinated patients who go on to have laboratory-confirmed influenza have a similar increased risk of acute myocardial infarction as those who were not vaccinated.

The authors suggest that an infectious illness may cause an acute coronary syndrome “through acute inflammation, biomechanical stress, and vasoconstriction”, noting: “Infections create a thrombogenic environment through platelet activation and endothelial dysfunction.”

They say that their findings, and those of previous studies, support current guidelines that advocate influenza immunisation to persons older than 65 years of age to protect against ischaemic coronary events. They add that other strategies to mitigate the risk of cardiovascular events include maximising the uptake of existing vaccines for other respiratory pathogens, developing more effective influenza vaccines, and “promoting established infection prevention practices”.

Kwong told Cardiovascular News that patients with an acute respiratory infection “whether due to influenza or another respiratory virus” should “probably stay home, avoid physical exertion that would further strain their heart, and drink enough fluids to avoid dehydration”. However, he adds that patients who are at high risk of myocardial infarction and who experience typical myocardial infarction symptoms (eg. chest pain) when they have an acute respiratory infection “should seek medical attention promptly”.

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