Cardiovascular sequelae of pneumonia.

PURPOSE OF REVIEW: In this brief review, we discuss the current epidemiological data and latest results from basic research on the cardiovascular sequelae after lower respiratory tract infection. RECENT
FINDINGS: Novel epidemiological evidence substantiates the association between pneumonia and subsequent cardiovascular events (CVEs) in the short- and long-term after viral or bacterial acute infection. Biomarkers such as cardiac troponin or coronary artery calcium may represent useful predictive tools for the detection of cardiac involvement during and after pneumonia. Particularly, Streptococcus pneumoniae directly cause cardiac damage by invasion into the myocardium and formation of microscopic lesions finally leading to the development of cardiac scarring in rodents and nonhuman primates. In addition, a causal relationship between pulmonary inflammation and atherosclerotic plaque formation in systemic arteries has emerged that appears to involve a mechanistic role for neutrophil granulocytes. However, many key pathomechanisms by which pneumonia may trigger or promote subsequent CVEs still remain unclear.
SUMMARY: Pneumonia may deleteriously impact cardiovascular function. Direct cardiomyocyte destruction by pathogens as well as host inflammatory response associated effects including atherosclerotic plaque development and/or rupture have been observed. Details of underlying mechanisms need to be further investigated to deliver future perspectives for the prevention of CVEs subsequent to pneumonia.