Pathogenesis and prevention of risk of cardiovascular events in patients with pneumococcal community‐acquired pneumonia. (29th January 2019)

• Record Type: Journal Article
• Authors: Feldman, C.; Normark, S.; Henriques‐Normark, B.; Anderson, R.
• Is Part Of: Journal of internal medicine. Volume 285:Number 6(2019)
• Page Start: 635
• Page End: 652
• Publication Date: 2019-01-29
• Subjects: cardiovascular events -- community‐acquired pneumonia -- persistent antigenaemia -- pneumococcus -- pneumolysin -- vaccination; Internal medicine -- Periodicals; Medicine -- Periodicals; 616
• DOI: 10.1111/joim.12875
• Languages: English
• ISSNs: 0954-6820

Abstract

Abstract: It is now well recognized that cardiovascular events (CVE) occur quite commonly, both in the acute phase and in the long‐term, in patients with community‐acquired pneumonia (CAP). CVE have been noted in up to 30% of patients hospitalized with all‐cause CAP. One systematic review and meta‐analysis of hospitalized patients with all‐cause CAP noted that the incidence rates for overall cardiac events were 17.7%, for incident heart failure were 14.1%, for acute coronary syndromes were 5.3% and for incident cardiac arrhythmias were 4.7%. In the case of pneumococcal CAP, almost 20% of patients studied had one or more of these cardiac events. Recent research has provided insights into the pathogenesis of the acute cardiac events occurring in pneumococcal infections. With respect to the former, key involvements of the major pneumococcal protein virulence factor, pneumolysin, are now well documented, whilst systemic platelet‐driven neutrophil activation may also contribute. However, events involved in the pathogenesis of the long‐term cardiovascular sequelae remain largely unexplored. Emerging evidence suggests that persistent antigenaemia may predispose to the development of a systemic pro‐inflammatory/prothrombotic phenotype underpinning the risk of future cardiovascular events. The current manuscript briefly reviews the occurrence of cardiovascular events in patients with all‐cause CAP, as well as in pneumococcal and influenza infections. It highlights the close interaction between influenza and pneumococcal pneumonia. It also includes a brief discussion of mechanisms of the acute cardiac events in CAP. However, the primary focus is on the prevalence, pathogenesis and prevention of the longer‐term cardiac sequelae of severe pneumococcal disease, particularly in the context of persistent antigenaemia and associated inflammation.