Acute infection and myocardial infarction
The risk of myocardial infarction after infection is well known, and for inpatients with pneumococcal pneumonia, it is 7 to 8%. This risk is higher at the onset of infection, is proportional to severity of pneumonia, and persists for at least 5 weeks. The risk declines slowly after this period but persists for several years. The explanation for this fact is complex. Some individuals may suffer from type 2 infarction, when there are atherosclerosis and plaques in coronary arteries, but no acute obstruction. In such cases, the metabolic demand of myocardial cells exceed the blood capacity to supply oxygen. Others may have type 1 infarction, i.e., acute myocardial ischemia caused by coronary occlusion related to plaque disruption and thrombosis. Infection leads to a procoagulant and inflammatory activity in atheromatous plaques. Myocardial lesions can occur in pneumonia and sepsis with vacuolization or necrosis of myocytes. The same facts occur in septic shock and related cytokine storm. The association of infection and myocardial infection is also observed in individuals with influenza and other respiratory virus infections.
Influenza vaccine reduces the risk of cardiovascular events by 36%, when comparing individuals at the same age who were vaccinated or not. Pneumococcal vaccine has demonstrated protection against myocardial infarction risk.
Musher DM, Abers MS, Corrales-Medina VF. Acute infection and myocardial infarction. N Engl J Med. 2019;380(2):171-6. doi: 10.1056/NEJMra1808137.