An Inflammatory Response: Cardiovascular Complications of Pneumonia

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The strongest risk factor for cardiovascular complications in patients with pneumonia is pre-existing CVD.
The strongest risk factor for cardiovascular complications in patients with pneumonia is pre-existing CVD.

Each year, community-acquired pneumonia (CAP) affects an estimated 5 to 6 million Americans and leads to 60,000 deaths.1 In addition to its respiratory effects, CAP and other acute infections can cause or exacerbate cardiovascular (CV) complications through various mechanisms. A systematic review and meta-analysis published in 2011 reported that 18% of patients with CAP developed CV complications within 30 days of CAP diagnosis, with higher rates found in hospitalized patients compared with outpatients.2

The strongest risk factor for CV complications in patients with pneumonia is pre-existing CVD, which is present in more than half of elderly patients hospitalized for CAP.3,4 The risk of developing CAP is up to 3 times greater in individuals with chronic CVD, especially heart failure, and those individuals with cerebrovascular disease have twice the risk for CAP.5

Although the precise mechanisms by which CAP may trigger CV complications have not been identified, it has been proposed that many CV complications result from the "interactions between demographic characteristics of the patients (eg, age, comorbid conditions, obesity, etc.), pneumonia severity and host reactions to the infection of the lower respiratory tract," wrote the authors of a recent review published in Respirology.2,6 "Once pneumonia is established, the host remains in a relative hypoxaemic state secondary to alveolar consolidation that affects the normal ventilation/perfusion...homeostasis."

The investigators described other processes that may influence the CAP-CV complications relationship, as follows:

  • Pneumonia is a proinflammatory disease characterized by elevated levels of circulating cytokines and chemokines that, in excess, may increase tissue damage.
  • Circulating endotoxin and bacterial pathogens can activate platelets, which may lead to a procoagulant state, and ultimately acute coronary syndrome (ACS).
  • The upregulation of the sympathetic nervous system during infection "leads to increased heart rate and vascular resistances that drop cardiac output and coronary perfusion of the heart." 

The review further highlighted the following specific CV conditions and their roles in CV complications of pneumonia.

ACS

Studies have linked CAP with an elevated risk for ACS, with some findings showing twice the risk for myocardial infarction (MI) in the 7 days after respiratory infection.7 Researchers have hypothesized that "CAP patients could develop ACS secondary to atherosclerotic plaque destabilization."[6] Animal studies have demonstrated associations between Streptococcus pneumoniae infection and higher levels of local inflammation and activated macrophages, which indicate plaque instability.8

Chlamydophila pneumoniae, which is often found in patients with CAP and atypical pneumonia, has been implicated in the development of plaque instability, atheromas, and cardiotoxicity.9 In addition, thrombosis formation may induce CV complications in patients with pneumonia.10 "Thrombus could be generated locally due to a mechanical stimuli and exposure to tissue factors (eg, secondary to plaque rupture) or spontaneously in the bloodstream during procoagulant states," the authors of the Respirology article explained.

Arrhythmias

New or worsening heart arrhythmias represent the third most common CV complication in patients with CAP, with a reported incidence of 4.7%.2 Among other proposed mechanisms, recent findings suggest the possibility of a pathogen-specific pathway. In mice, S. pneumoniae reached the heart and generated microscopic lesions that were linked to high levels of troponin I and rhythm abnormalities.11

Heart Failure

The risk for heart failure in patients with pneumonia is elevated after hospital admission and for up to 10 years postdischarge.2 Possible underlying mechanisms include persistent inflammation, with Mycoplasma pneumoniae as a potential mediator.

Antibiotics

Although macrolide antibiotics may reduce overall mortality in patients with CAP, they may also pose a significant CV risk, as these agents have been associated with an increased risk for MI, sudden cardiac death, and ventricular tachyarrhythmias.12,13 The authors of the Respirology article recommended that "the use of fluoroquinolones or macrolides should be individualized and a careful assessment of the risks and benefits is crucial...for the appropriate antibiotic therapies in patients with CAP."[6]

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