Publication by Izbicki G, et al (Respiratory Medicine. 2009;103:1346-1349.)

Commentary by Steven A. Sahn, MD, of the Medical University of South Carolina

Article Summary
The prevalence of coronary artery disease in end-stage pulmonary disease: Is pulmonary fibrosis a risk factor?

Izbicki G, Ben-Dor I, Shitrit D, et al. Respiratory Medicine. 2009;103:1346-1349.

Introduction:
A 2004 study suggested a higher rate of coronary artery disease (CAD) in patients with IPF than COPD.1 Izbicki and colleagues evaluated for CAD in a group of lung transplantation candidates with IPF or emphysema.2

Methods:

  • 100 lung transplant candidates (49 with pulmonary fibrosis and 51 with emphysema) were evaluated for the presence of CAD risk factors, including hypertension, hypercholesterolemia, diabetes mellitus, obesity, and smoking status. Glucocorticosteroid use was recorded.
  • Patients were evaluated for CAD by coronary angiography. Significant CAD was defined as ≥ 50% stenosis in at least one coronary artery

Results:

  • CAD was found in 14/49 (29%) of patients with pulmonary fibrosis and 5/51 (10%) of patients with emphysema (P = 0.019)
  • 98% of patients with emphysema, but only 31% of those with pulmonary fibrosis were smokers (P < 0.0001)
  • The emphysema and pulmonary fibrosis groups did not differ in age, gender, or presence of CAD risk factors
  • Emphysema patients were more likely to have received corticosteroids (P < 0.0001)

Conclusions and Expert Opinion:

The authors concluded that CAD was significantly more likely to occur in lung transplant candidates with pulmonary fibrosis compared to those with emphysema despite the increased prevalence of smoking in the emphysema group.

Systemic inflammation may play a role in the development of pulmonary fibrosis as well as CAD. Pathogenesis models of both diseases involve fibroblastic proliferation, angiogenesis, and excessive collagen deposition, which may be a result of injury or an anti-inflammatory cellular response that releases pro-inflammatory and pro-fibrotic cytokines. Alternatively, both diseases might entail reparative processes at the epithelial and endothelial surfaces. While markers of the atherosclerotic process, such as C-reactive protein, serum amyloid A, and interleukin-6 have been found to be increased in patients with coronary artery disease, these markers fail to correlate with the severity of CAD. They may reflect the diffuse pro-atherosclerotic environment rather than the degree of localized obstruction in coronary artery lesions.

Others have shown that baseline plasma concentrations of C-reactive protein predict the risk of myocardial infarction and stroke.3 Aspirin, which has both anti-inflammatory and antiplatelet properties, reduces the risk of a first myocardial infarction in subjects with elevated concentrations of C-reactive protein.4

These findings support the clinical benefit of anti-inflammatory agents for cardiovascular disease. However, a different mechanism may be operative in patients with idiopathic pulmonary fibrosis, whose lung disease is not responsive to anti-inflammatory agents. Nevertheless, in managing the comorbidities of patients with idiopathic pulmonary fibrosis, evaluation and treatment of coronary disease should be the standard of care.

References:

  1. Kizer JR, Zisman DA, Blumenthal NP, et al. Association between pulmonary fibrosis and coronary artery disease. Arch Intern Med. 2004;164:551-556.
  2. Izbicki G, Ben-Dor I, Shitrit D, et al. The prevalence of coronary artery disease in end-stage pulmonary disease: Is pulmonary fibrosis a risk factor? Respir Med. 2009;103:1346-1349.
  3. Elkind MS. Inflammation, atherosclerosis, and stroke. Neurologist. 2006;12(3):140-148.
  4. Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Eng J Med. 1997;336:973-979.

Abstract

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