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Pneumonia possible risk factor for CVD
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New data published in JAMA suggest that hospitalization for pneumonia increased the risk for cardiovascular disease.
Although the risk was highest (fourfold) within the first 30 days after pneumonia, the risk was still increased in subsequent years: approximately 1.5-fold higher.
“Most people think that pneumonia is an acute illness, and once they recover from this acute illness, there are no long-term consequences,” Sachin Yende, MD, MS, vice president of critical care at VA Pittsburgh, and associate professor in the department of critical care at the University of Pittsburgh, told Infectious Disease News. “Our study suggests that pneumonia hospitalization increases the risk of heart disease or stroke several months or years later. The risk is similar to the risk observed for smoking, hypertension and diabetes.”
The researchers conducted a matched-cohort study nested in two cohorts: the Cardiovascular Health Study (CHS) and the Atherosclerosis Risk in Communities (ARIC) study. Each participant hospitalized with pneumonia was matched to two controls. The researchers evaluated the risk for CVD at different times within the first 10 years after the pneumonia occurred. Each cohort was analyzed separately due to differences in baseline clinical characteristics between them.
The CHS cohort included 1,773 participants: 591 pneumonia cases and 1,182 controls. Among patients with pneumonia, 206 had CVD events over 10 years after hospitalization; 104 were myocardial infarctions, 35 were stroke and 36 were fatal coronary heart disease events. The risk for 10-year CVD risk was higher among patients with pneumonia compared with controls, and the risk was highest during the first year: 0-30 days, 10.6% vs. 0.5% (HR=4.07; 95% CI, 2.86-5.27); 31-90 days, 2.9% vs. 0.8% (HR=2.94; 95% CI, 2.18-3.7); and 91 days to 1 year, 6.4% vs. 5.2% (HR=2.1; 95% CI, 1.59-2.6).
The ARIC cohort included 2,040 participants: 680 patients with pneumonia and 1,360 controls. Among the pneumonia cases, 112 had CVD events over 10 years after hospitalization: 33 MI, 36 strokes and 43 with fatal coronary heart disease. Similar to the CHS cohort, the patients with pneumonia had a higher risk of CVD over the 10 years, and the risk was highest during the first year.
“Pneumonia or influenza vaccine may not only prevent these infections, but may also reduce the risk of heart disease,” Yende said. “Physicians caring for patients with pneumonia or sepsis should be aware that these individuals are at higher risk for heart disease and stroke over the subsequent months.”
Yende said that they are currently leading a large, NIH-funded study to understand why pneumonia and sepsis are linked to an increased risk for cardiovascular disease. – by Emily Shafer
Disclosure: Yende reports no relevant disclosures.
Perspective
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Thomas File, MD
The findings add to the already robust level of evidence for an association of pneumonia hospitalization and subsequent risk of cardiovascular events (CVEs). Numerous studies and review papers support this association, which include a variety of cardiovascular events: Arrhythmias; new or worsening heart failure; myocardial infarction; stroke; and acute coronary syndrome (Peyrani P et al). There is biologic plausibility for this association related to a variety of potential factors: Atherosclerotic plaque instability related to the host systemic inflammatory response from the pneumonia; cardiovascular stress produced by hypoxemia associated with pneumonia; and the tachycardia associated with systemic infection. The hypercoagulability state associated with sepsis may play a role in the subsequent development of CVEs.
As the Corrales-Medina et al indicated in their discussion, the focus now should be on strategies to reduce the burden of this association. Assuming host inflammatory response is a key, it would seem intuitive that an anti-inflammatory approach might be beneficial. It is of interest that several studies suggest combination therapy with a macrolide results in better outcomes for serious pneumonia, in part because of its effect on the host immune response, and its anti-inflammatory effect. However, there are some studies — refuted by others — suggesting the use of macrolides, specifically azithromycin, can be associated with an increased risk of sudden death based on arrhythmia potential. One study (Mortensen EM et al) showed a decrease death in a VA population but a small increase risk of myocardial infarction. Corrales-Medina et al did not assess the effect based on specific therapy (eg, macrolide vs. non-macrolide therapy). Adjunctive therapies directed at the host response rather than the pathogens are attractive targets for intervention. Corticosteroids, statins, ACE inhibitors, and anticoagulants have been used with some encouraging results, although data are still scarce.
Another obvious potential strategy is prevention of pneumonia in the first place by immunization. The authors did not assess for this effect in the present study, but evidence does suggest a reduction of CVEs after vaccination for influenza (Udell JA et al). However, there are conflicting findings related to pneumococcal vaccine and reduction of CVEs. It will be interesting to observe if there is a more substantial beneficial effect with the increasing use of the conjugate vaccine among adults, which has been shown to reduce non-invasive pneumonia.
Certainly, more evidence will be published regarding the association between CVEs in hospitalized patients with pneumonia, both short- and long-term. Future research will be necessary to identify patients at risk for CVEs during or after an episode of pneumonia. Other interventions beyond antibiotics may be indicated in these patients during and after hospitalization. The question as to best strategies for reduction of the burden of CVEs after pneumonia remains unanswered and should be a focus of future investigations.
For more information:
Mortensen EM. JAMA. 2014; 311:2199-2208.
Peyrani P. Infect Dis Clin N Am. 2013;27:205–210.
Sibila O. Infect Dis Clin N Am. 2013;27:133–147.
Udell JA. JAMA. 2013;310:1711-20.
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