Pneumonia as a cause of chronic cardiac disease

Pneumonia as a cause of chronic cardiac disease

Grant Waterer1,2, Adil Rajwani3

1Department of Medicine, University of Western Australia, Perth, Australia; 2Department of Medicine, Northwestern University, Chicago, USA; 3Department of Cardiology, Royal Perth Hospital, Perth, Australia

Correspondence to: Dr. Grant Waterer, MBBS, PhD. Level 4 MRF Building, Royal Perth Hospital, GPO Box X2213, Perth 6847, Australia. Email:

Provenance: This is a Guest Editorial commissioned by Section Editor Mi Zhou, MM (No. 152 Central Hospital of PLA, Pingdingshan, China).

Comment on: Eurich DT, Marrie TJ, Minhas-Sandhu JK, et al. Risk of heart failure after community acquired pneumonia: prospective controlled study with 10 years of follow-up. BMJ 2017;356:j413.

Received: 29 March 2017; Accepted: 30 March 2017; Published: 04 May 2017.

doi: 10.21037/arh.2017.04.21

Traditionally clinicians who treat patients with pneumonia generally consider their job well done when the patient is safely discharged from hospital.

In recent years, there has been an increasing awareness that survivors of pneumonia have significantly worse long term health outcomes than population controls (1-8). The explanation for the adverse health outcomes in pneumonia survivors remains to be fully elucidated, but a significant excess of cardiovascular disease is a major factor (3,9-11).

Adding to the weight of literature about adverse cardiac consequences of pneumonia is a recent study published in the British Medical Journal by Eurich and colleagues (12). In this Canadian study of a prospectively collected database of adults with community acquired pneumonia, 4,988 patients with no prior history of heart failure were matched to between one and five controls based on age (5-year bands) and gender. Controls were obtained from patients presenting to hospital for other reasons at the same time of year as the pneumonia case. The principal finding of the study was that survivors of pneumonia had, over a median of 9.9 years of follow up, an incident rate of heart failure of 11.9% compared to 7.4% in controls [hazard ratio 1.61, 95% confidence interval (CI): 1.44–1.81]. Unsurprisingly older patients developed more heart failure. In keeping with other published data overall mortality was also higher in pneumonia survivors than controls (38.4% vs. 23.9%, P<0.001). Of clinical importance the difference between cases and controls was established within 90-day of discharge and appears to be maximal by one year. Unfortunately due to the nature of the database additional data on severity and cause of pneumonia as well as the severity of the subsequent heart failure could not be assessed.

The findings of Eurich and colleagues are not surprising. Analysis of the Cardiovascular Health Study (CHS), a large prospective population cohort study initiated in the 1990’s, by Corrales-Medina and colleagues (13) also found that an episode of pneumonia predicted a subsequent significantly greater risk of a new diagnosis of cardiac failure. In this study the hazard ratio for new onset heart failure was maximal at 31–90 days (6.9, 95% CI: 4.46–10.63) and declined slowly to 2.6 (95% CI: 1.64–4.04) at 1-year but was still 2.0 (95% CI: 1.56–2.58) after 5 years.

What then explains the greater incidence of heart failure in pneumonia survivors? There is abundant evidence that acute myocardial infarction is a common complication in patients with pneumonia (14-18), increasing with severity of the pneumonia to as high as 15% in the most severe disease (15). This is not just observation of elevation of cardiac enzymes as is seen commonly in severe sepsis, but also abnormalities consistent with myocardial ischaemia on electrocardiographs. While the majority of myocardial ischaemia is not ST-elevation myocardial infarction, in one series these were as much as 16% of all events (16). A reasonable hypothesis is therefore that myocardial infarction precipitated by the acute pneumonia, both recognized and unrecognized, causes cardiac damage sufficient to lead to early cardiac failure.

Why are acute coronary events higher in pneumonia survivors? The persistence of radiological infiltrates for months in some patients suggests a continued low-level inflammatory response (19,20). Even small elevations of systemic inflammatory markers such as c-reactive protein have been associated with substantial increases in subsequent cardiac events (21,22), and patients with the highest level of inflammatory markers at discharge from hospital with CAP have the worst 1-year outcomes (23).

A less recognized but also clearly established cause of cardiac damage is direct myocardial invasion by the pneumonic pathogen(s). In the case of Streptococcus pneumoniae, the most common cause of community-acquired pneumonia, it has recently been documented in mice that direct translocation into the heart can occur but is associated with minimal inflammatory response and results in significant fibrosis (24). Disease severity correlated with levels of serum troponin and the number and size of cardiac microlesions. Similar microlesions were also demonstrated in cardiac samples from human patients who had died from invasive pneumococcal disease. In a murine model of burn trauma, S. pneumoniae inoculation led to a significant further depression of cardiac function (25) (Sheeran et al., J Surg Research, 1998). Myocarditis has also been described in the setting of pneumonia with a variety of other common bacterial pathogens (26-29). In the case of viral disease myocarditis may be even more common, especially with influenza (30,31).

In the case of both coronary artery occlusion and direct myocardial invasion the extent that subclinical disease is present during pneumonia and contributes to subsequent adverse cardiac outcomes is unknown. Two lines of evidence suggest subclinical involvement may be substantial. The first is the high rate of arrhythmias in acute pneumonia (10,11,14,17,32), and especially atrial fibrillation, and that the onset of a new arrhythmia during admission predicts worse subsequent outcomes (10,32). While a variety of problems may contribute to a higher risk of arrhythmia including hypoxia and electrolyte disturbance, subclinical myocarditis may also contribute. The second suggestive evidence is that significant elevations of cardiac enzymes are common in patients with pneumonia and predict a worse prognosis in the short term (16,33-35), and after discharge (35). Similar results have been observe for b-type natriuretic peptide (4,36-38), but these studies are complicated by premorbid cardiac disease.

The evidence is therefore extremely strong that pneumonia causes cardiac disease and that when it does, outcomes are significantly worse. Furthermore the evidence is also strong that pneumonia survivors have significantly more cardiac disease over the subsequent months to years. Antibiotics may rapidly clear bacteria from cardiac tissue, but this does not appear to be sufficient to prevent the adverse development of cardiac fibrosis (24). Can we do anything else about the increased cardiovascular risk? There is some evidence to suggest anti-platelet agents may reduce coronary artery occlusion in acute pneumonia (39-43), but further studies are needed. Longer-term interventions now standard in patients who have had myocardial ischaemia like anti-platelet agents, statins, angiotensin-converting enzyme inhibitors and beta-blockers have not been studied in pneumonia survivors. It is likely that therapies in development to improve ‘healthy’ recovery from brain and cardiac injury may also be important in the setting of pneumonia, especially severe disease. We do not need any more studies like that of Eurich and colleagues (12) to tell us that the whole area of short and long term cardiac disease precipitated by pneumonia is now urgently in need of significant research investment.




Conflicts of Interest: The authors have no conflicts of interest to declare.


  1. Mortensen EM, Kapoor WN, Chang CC, et al. Assessment of mortality after long-term follow-up of patients with community-acquired pneumonia. Clin Infect Dis 2003;37:1617-24. [Crossref] [PubMed]
  2. Waterer GW, Kessler LA, Wunderink RG. Medium-term survival after hospitalization with community-acquired pneumonia. Am J Respir Crit Care Med 2004;169:910-4. [Crossref] [PubMed]
  3. Corrales-Medina VF, Alvarez KN, Weissfeld LA, et al. Association between hospitalization for pneumonia and subsequent risk of cardiovascular disease. JAMA 2015;313:264-74. [Crossref] [PubMed]
  4. Alan M, Grolimund E, Kutz A, et al. Clinical risk scores and blood biomarkers as predictors of long-term outcome in patients with community-acquired pneumonia: a 6-year prospective follow-up study. J Intern Med 2015;278:174-84. [Crossref] [PubMed]
  5. Sandvall B, Rueda AM, Musher DM. Long-term survival following pneumococcal pneumonia. Clin Infect Dis 2013;56:1145-6. [Crossref] [PubMed]
  6. Bruns AH, Oosterheert JJ, Cucciolillo MC, et al. Cause-specific long-term mortality rates in patients recovered from community-acquired pneumonia as compared with the general Dutch population. Clin Microbiol Infect 2011;17:763-8. [Crossref] [PubMed]
  7. Johnstone J, Eurich DT, Majumdar SR, et al. Long-term morbidity and mortality after hospitalization with community-acquired pneumonia: a population-based cohort study. Medicine 2008;87:329-34. [Crossref] [PubMed]
  8. Eurich DT, Marrie TJ, Minhas-Sandhu JK, et al. Ten-Year Mortality after Community-acquired Pneumonia. A Prospective Cohort. Am J Respir Crit Care Med 2015;192:597-604. [Crossref] [PubMed]
  9. Koivula I, Stén M, Mäkelä PH. Prognosis after community-acquired pneumonia in the elderly: a population-based 12-year follow-up study. Arch Intern Med 1999;159:1550-5. [Crossref] [PubMed]
  10. Cangemi R, Calvieri C, Falcone M, et al. Relation of cardiac complications in the early phase of Community-Acquired pneumonia to Long-Term mortality and cardiovascular events. Am J Cardiol 2015;116:647-51. [Crossref] [PubMed]
  11. Perry TW, Pugh MJ, Waterer GW, et al. Incidence of cardiovascular events after hospital admission for pneumonia. Am J Med 2011;124:244-51. [Crossref] [PubMed]
  12. Eurich DT, Marrie TJ, Minhas-Sandhu JK, et al. Risk of heart failure after community acquired pneumonia: prospective controlled study with 10 years of follow-up. BMJ 2017;356:j413. [Crossref] [PubMed]
  13. Corrales-Medina VF, Taljaard M, Yende S, et al. Intermediate and long-term risk of new-onset heart failure after hospitalization for pneumonia in elderly adults. Am Heart J 2015;170:306-12. [Crossref] [PubMed]
  14. Musher DM, Rueda AM, Kaka AS, et al. The association between pneumococcal pneumonia and acute cardiac events. Clin Infect Dis 2007;45:158-65. [Crossref] [PubMed]
  15. Ramirez J, Aliberti S, Mirsaeidi M, et al. Acute myocardial infarction in hospitalized patients with community-acquired pneumonia. Clin Infect Dis 2008;47:182-7. [Crossref] [PubMed]
  16. Cangemi R, Casciaro M, Rossi E, et al. Platelet activation is associated with myocardial infarction in patients with pneumonia. J Am Coll Cardiol 2014;64:1917-25. [Crossref] [PubMed]
  17. Viasus D, Garcia-Vidal C, Manresa F, et al. Risk stratification and prognosis of acute cardiac events in hospitalized adults with community-acquired pneumonia. J Infect 2013;66:27-33. [Crossref] [PubMed]
  18. Mandal P, Chalmers JD, Choudhury G, et al. Vascular complications are associated with poor outcome in community-acquired pneumonia. QJM 2011;104:489-95. [Crossref] [PubMed]
  19. El Solh AA, Aquilina AT, Gunen H, et al. Radiographic resolution of community-acquired bacterial pneumonia in the elderly. J Am Geriatr Soc 2004;52:224-9. [Crossref] [PubMed]
  20. Bruns AH, Oosterheert JJ, El Moussaoui R, et al. Pneumonia recovery: discrepancies in perspectives of the radiologist, physician and patient. J Gen Intern Med 2010;25:203-6. [Crossref] [PubMed]
  21. Pischon T, Möhlig M, Hoffmann K, et al. Comparison of relative and attributable risk of myocardial infarction and stroke according to C-reactive protein and low-density lipoprotein cholesterol levels. Eur J Epidemiol 2007;22:429-38. [Crossref] [PubMed]
  22. Ahmadi-Abhari S, Luben RN, Wareham NJ, et al. Seventeen year risk of all-cause and cause-specific mortality associated with C-reactive protein, fibrinogen and leukocyte count in men and women: the EPIC-Norfolk study. Eur J Epidemiol 2013;28:541-50. [Crossref] [PubMed]
  23. Yende S, D'Angelo G, Kellum JA, et al. Inflammatory markers at hospital discharge predict subsequent mortality after pneumonia and sepsis. Am J Respir Crit Care Med 2008;177:1242-7. [Crossref] [PubMed]
  24. Brown AO, Mann B, Gao G, et al. Streptococcus pneumoniae translocates into the myocardium and forms unique microlesions that disrupt cardiac function. PLoS Pathog 2014;10:e1004383. [Crossref] [PubMed]
  25. Sheeran PW, Maass DL, White DJ, et al. Aspiration pneumonia-induced sepsis increases cardiac dysfunction after burn trauma. J Surg Res 1998;76:192-9. [Crossref] [PubMed]
  26. Chuang TY, Lin CJ, Lee SW, et al. Rapidly fatal community-acquired pneumonia due to Klebsiella pneumoniae complicated with acute myocarditis and accelerated idioventricular rhythm. J Microbiol Immunol Infect 2012;45:321-3. [Crossref] [PubMed]
  27. Ishimaru N, Suzuki H, Tokuda Y, et al. Severe legionnaires' disease with pneumonia and biopsy-confirmed myocarditis most likely caused by legionella pneumophila serogroup 6. Intern Med 2012;51:3207-12. [Crossref] [PubMed]
  28. Durel CA, Saison J, Chidiac C, et al. A case of interstitial pneumonia, myocarditis and severe sepsis caused by Chlamydia pneumoniae. BMJ Case Rep 2015;2015. pii: bcr2015211788.
  29. Bodur H, Savran Y, Koca U, et al. Legionella pneumonia with acute respiratory distress syndrome, myocarditis and septic shock successfully treated with Drotrecogin Alpha (activated) Eur J Anaesthesiol 2006;23:808-10. [Crossref] [PubMed]
  30. Kumar K, Guirgis M, Zieroth S, et al. Influenza myocarditis and myositis: case presentation and review of the literature. Can J Cardiol 2011;27:514-22. [Crossref] [PubMed]
  31. Ukimura A, Ooi Y, Kanzaki Y, et al. A National survey on myocarditis associated with influenza H1N1pdm2009 in the pandemic and postpandemic season in Japan. J Infect Chemother 2013;19:426-31. [Crossref] [PubMed]
  32. Soto-Gomez N, Anzueto A, Waterer GW, et al. Pneumonia: an arrhythmogenic disease? Am J Med 2013;126:43-8. [Crossref] [PubMed]
  33. Moammar MQ, Ali MI, Mahmood NA, et al. Cardiac troponin I levels and alveolar-arterial Oxygen gradient in patients with community-acquired pneumonia. Heart Lung Circ 2010;19:90-2. [Crossref] [PubMed]
  34. Lee YJ, Lee H, Park JS, et al. Cardiac troponin I as a prognostic factor in critically ill pneumonia patients in the absence of acute coronary syndrome. J Crit Care 2015;30:390-4. [Crossref] [PubMed]
  35. Vestjens SM, Spoorenberg SM, Rijkers GT, et al. High-sensitivity cardiac troponin T predicts mortality after hospitalization for community-acquired pneumonia. Respirology 2017. [Epub ahead of print]. [Crossref] [PubMed]
  36. Christ-Crain M, Breidthardt T, Stolz D, et al. Use of B-type natriuretic peptide in the risk stratification of community-acquired pneumonia. J Intern Med 2008;264:166-76. [Crossref] [PubMed]
  37. Usuda D, Sangen R, Hashimoto Y, et al. Validation of a B-type natriuretic peptide as a prognostic marker in pneumonia patients: a prospective cohort study. BMJ Open 2016;6:e010440. [Crossref] [PubMed]
  38. Li J, Ye H, Zhao L. B-type natriuretic peptide in predicting the severity of community-acquired pneumonia. World J Emerg Med 2015;6:131-6. [Crossref] [PubMed]
  39. Oz F, Gul S, Kaya MG, et al. Does aspirin use prevent acute coronary syndrome in patients with pneumonia: multicenter prospective randomized trial. Coron Artery Dis 2013;24:231-7. [Crossref] [PubMed]
  40. Falcone M, Russo A, Cangemi R, et al. Lower mortality rate in elderly patients with community-onset pneumonia on treatment with aspirin. J Am Heart Assoc 2015;4:e001595. [Crossref] [PubMed]
  41. Gross AK, Dunn SP, Feola DJ, et al. Clopidogrel treatment and the incidence and severity of community acquired pneumonia in a cohort study and meta-analysis of antiplatelet therapy in pneumonia and critical illness. J Thromb Thrombolysis 2013;35:147-54. [Crossref] [PubMed]
  42. Falcone M, Russo A, Farcomeni A, et al. Septic shock from community-onset pneumonia: is there a role for aspirin plus macrolides combination? Intensive Care Med 2016;42:301-2. [Crossref] [PubMed]
  43. Storey RF, James SK, Siegbahn A, et al. Lower mortality following pulmonary adverse events and sepsis with ticagrelor compared to clopidogrel in the Plato study. Platelets 2014;25:517-25. [Crossref] [PubMed]
doi: 10.21037/arh.2017.04.21
Cite this article as: Waterer G, Rajwani A. Pneumonia as a cause of chronic cardiac disease. Ann Res Hosp 2017;1:19.