Atherosclerosis, COPD and chronic inflammation

Abstract

The prevalence of ischemic heart disease is approximately twofold higher in chronic obstructive pulmonary disease (COPD) cohorts compared to the general population. Likewise, cardiac patients with COPD have a reduced short- and long-term survival. This co-morbidity of COPD with atherosclerotic vessel disease is associated with common risk factors, such as smoking. However, atherosclerosis, in addition, shares many of the inflammatory mechanisms with those found in COPD. Atherosclerotsic lesions, as well as the COPD lung, are sites of local inflammation. Furthermore, a systemic inflammatory response, measured as increased CRP, has been reported in both patient populations. There are a number of inflammatory mediators produced in both the vessel wall and in the lungs, which potentially induce common pathological processes. For example, leukotriene B 4, which induces chemotaxis of neutrophils, monocytes, T-lymphocytes and smooth muscle cells, has been suggested as a therapeutic target in both diseases. Furthermore, activation of smooth muscle cells may lead to a narrowing of the lumen in both airways and vessels. Finally, proteolytic activities of matrix metalloproteinases may be involved both in emphysema formation and in atherosclerotic plaque rupture, leading to myocardial infarction and stroke. Taken together, the associated co-morbidity of COPD with atherosclerosis and their potential common pathophysiological mechanisms support a notion of these, and other inflammatory diseases, as manifestations of chronic inflammation.