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.

Airflow Limitation and Endothelial Dysfunction. Unrelated and Independent Predictors of Atherosclerosis

“…These have been the subject of multiple review articles and a detailed discussion is beyond the scope of this report (5,33). Among these increased arterial stiffness and systemic inflammation are worthy of brief mention here.…”

Association of Airflow Limitation With Carotid Atherosclerosis in a Japanese Community ― The Hisayama Study ―

“…In addition, there may be other underlying mechanisms, such as oxidative stress. 25 Clinical and experimental studies have shown that the production of reactive oxygen species (ROS) is increased in COPD patients by inhalation of toxic substances, [26][27][28] and that the antioxidative system in these patients is impaired, 29 leading to a state of high oxidative stress. After such an increase in ROS production, the spillover of ROS from the lung could lead to systemically increased levels of oxidative stress.…”

Thrombocytopenia as a Marker of Outcome in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease

“…COPD is currently considered as a systemic disorder that is associated with an increased risk of diabetes mellitus, hypertension, and cardiovascular disease [an independent risk factor] [2,3]. The suggested mechanisms for these associations include hypoxia, oxidative stress, and systemic inflammation in COPD [4,5].…”