Cardiovascular mechanisms of death in severe COPD exacerbation: time to think and act beyond guidelines

This issue of Thorax includes three important studies on acute exacerbations of chronic obstructive pulmonary disease (ECOPD). Two of them, by Chang et al. (1) and Hoiset et al. (2), show the importance of the cardiac biomarkers troponin T and NT-BNP (N-terminal pro-B-type natriuretic peptide) as strong predictors of the increased risk of death of patients hospitalized because of ECOPD (1, 2). The third, by Maclay et al. (3), provides evidence that patients with stable COPD have increased circulating platelet-monocyte aggregates—a potential specific pathogenic mechanism of atherosclerosis—and that they further increase during exacerbations, suggesting a plausible biological mechanism to explain the increased cardiovascular risk seen in ECOPD. Taken together, these studies confirm the view that ECOPD episodes requiring hospitalization must be considered very severe events in the natural course of the disease, since they are associated with such important outcomes as increased risk of mortality, reduced health status, impaired lung function, muscle weakness, and cardiopulmonary complications (4). The studies also suggest that the increased risk of death is often due to acute cardiovascular involvement, and they highlight the limitations of the current definition of ECOPD and the need to move toward a more comprehensive definition, diagnostic approach and treatment.