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December 4, 2020

Influenza Vaccine for Patients With High-risk Cardiovascular Disease

Author Affiliations
  • 1Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia
JAMA. 2021;325(1):33-35. doi:10.1001/jama.2020.23948

Influenza and cardiovascular disease (CVD) are 2 of the most common causes of hospitalizations and deaths worldwide. These diseases share a reciprocal relationship because influenza may increase the risk of acute cardiovascular complications and underlying cardiovascular disease may increase the risk of influenza complications. Establishing a causal relationship can strengthen the rationale for wider use of influenza vaccines in patients with CVD worldwide.

Ecologic studies have examined the relationship between influenza and excess winter mortality, often related to cardiovascular complications, and estimated that the percentage of winter deaths attributable to influenza could range from 4% to 68%.1,2 However, biases were likely in these studies because the fraction of all-cause outcomes attributed to influenza exceeded measured influenza incidence. Carefully conducted observational studies have suggested that approximately 3% to 6% of hospitalizations and deaths from myocardial infarction may be related to influenza.1,3 More recently, epidemiologic studies that used self-controlled case series methodology documented 5- to 10-fold temporal increases in the risk of acute myocardial infarction within 1 week of laboratory-confirmed influenza.4,5 In a 2020 study of 80 261 laboratory-confirmed influenza hospitalizations from 13 states in the US, 12% had acute cardiovascular events, which were most commonly decompensated heart failure and acute ischemic heart disease.6 These findings are supported by pathogenesis studies in animal models that have linked infection from influenza viruses and other pathogens to atherogenesis with suggested pathways to disease, including hypoxia, increased metabolic demand, atherosclerosis and plaque rupture from inflammation, induction of a prothrombotic state, and direct viral infection.7,8