Abstract

See related article, p 459–467 Cardiovascular complications, such as cor pulmonale, have been well characterized in severe chronic obstructive pulmonary disease (COPD).1 However, although this is a direct hemodynamic consequence of lung disease, cardiovascular involvement in COPD is much more complex. The majority of patients experiencing COPD die because of cardiovascular disease (CVD) rather than respiratory failure, with coronary artery disease and heart failure being the prominent specific cardiac causes of death.1 Cross-sectional analyses of >1.2 million patient records showed that COPD was associated with increased risk of CVD (odds ratio, 4.98; 95% confidence interval, 4.85–5.81) and of stroke (odds ratio, 3.34; 95% confidence interval, 3.21–3.48) and this risk persisted after controlling for confounding by sex and smoking status and stratifying for age.2 Indeed, reduced pulmonary function, no matter what the cause, is associated with increased cardiovascular mortality or myocardial infarction. Each 10% of reduction in forced expiratory volume in 1 second (FEV1; which is a measure of obstructive lung dysfunction) increases the risk of cardiovascular death by 28% and of a nonfatal cardiovascular event by 20%.3 This ranks decreased FEV1 only second to smoking as a cardiovascular risk factor, placing it ahead of dyslipidemia or hypertension in patients with COPD.1 The mechanisms of the relationship between CVD and COPD remain unclear. Initially increased cardiovascular morbidity and mortality has been attributed to smoking being a common major risk factor for both diseases; however, even in subjects who have never smoked in their life, FEV1 reduction persists as a major cardiovascular event predictor.3 Obviously other common risk factors such as air pollution or shared genetic susceptibility (matrix metalloproteinase or oxidative stress genes such as epoxide hydrolase and glutathione-s-transferase) may play a role in linking COPD to CVD. The major hypothesis linking the 2 conditions is, …

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