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Three important studies on acute exacerbations of chronic obstructive pulmonary disease (ECOPD)have been published in Thorax. Two of them, by Chang et al1(see page 764) and Hoiset et al2 (see page 775), 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 hospitalised because of ECOPD.1 2 The third, by Maclay et al3 (see page 769), provides evidence that patients with stable chronic obstructive pulmonary disease (COPD) have increased circulating platelet–monocyte aggregates—a potential specific pathogenic mechanism of atherosclerosis. These aggregates 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 hospitalisation must be considered very severe events in the natural course of the disease because 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 towards a more comprehensive definition, diagnostic approach and treatment.
Risk of death and exacerbations of COPD
Several previous studies have clearly established that episodes of ECOPD are a major driver of mortality in this disease, especially during and immediately after the acute event. (The long-term effects are discussed in next paragraph.) For instance, in a cohort of 1016 patients hospitalised because of ECOPD with hypercarbia (PaCO2≥50 mm Hg), Connors et al5 …