Cardiovascular injury and repair in chronic obstructive pulmonary disease

Abstract

Cardiovascular disease represents a considerable burden in terms of both morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD). For 20 years, forced expiratory volume in 1 second (FEV(1)) has been an established predictor of cardiovascular mortality among smokers, never-smokers, and patients with COPD. We review evidence for increased cardiovascular risk in COPD. In addition, we assess the emerging evidence which suggests that hypoxia, systemic inflammation, and oxidative stress in patients with COPD may cause cardiovascular disease. We also discuss alternative hypotheses that the endothelium and connective tissues in the arteries and lungs of patients with COPD and cardiovascular disease have a shared susceptibility to these factors.

Figures

Figure 1.

Pathophysiology in chronic obstructive pulmonary disease and coronary heart disease.

Figure 2.

Putative mechanisms linking coronary heart disease and chronic obstructive pulmonary disease. hsCRP = high-sensitivity C-reactive protein; IL-6 = interleukin-6; MMPs = matrix metalloproteases; NO = nitric oxide; ROS = reactive oxygen species; TNF-α = tumor necrosis factor α; tPA = tissue plasminogen activator.