Cardiovascular disease is common in patients with COPD with the two conditions often being linked by the common aetiology of smoking.\u00a0 Moreover, dysfunction in one organ system can transmit to the other with severe hypoxemia, pulmonary hypertension, and systemic inflammation all potentially impacting on cardiac function.\u00a0 However, the interplay between lung and cardiac disease is still incompletely understood and little is known about the prognosis of patients whose presentation with acute exacerbations of COPD also suggests involvement of the cardiac system.<\/p>\n
In these two studies the authors investigated patients with biochemical evidence of cardiac involvement when presenting with symptoms of COPD.\u00a0 In the first prospective study, patients presenting with COPD to a single centre had both troponin T and NT-proBNP measured with the primary outcome measure being 30-day mortality. Elevated NT-proBNP was present in 65\/244 patients (27.5%) and significantly predicted 30-day mortality (OR 9.0, 95% CI 3.1 to 26.2, p<0.001). Elevated troponin T was found in 40\/241 patients (16.6%) and also predicted 30-day mortality (OR 6.3, 95% CI 2.4 to 16.5, p<0.001). Moreover, NT-proBNP and troponin T levels appeared to have additive associations with 30-day mortality among patients with abnormalities of both being 15-fold higher than among patients with normal values.<\/p>\n
In a second similar prospective study the authors measured high-sensitivity troponin T (hs-cTnT) in patients presenting acutely with COPD and then followed them up for a median period of 1.9 years.\u00a0 97 of 99 patients (98%) had measurable levels of hs-cTnT and 73 (74%) had hs-cTnT above the normal range. During follow-up, 57 patients (58%) died with crude mortality rates in patients having hs-cTnT levels <14.0, 14.0-39.9 and \u226540 ng\/l being 4.6, 30.2 and 58.3 per 100 patient-years respectively, thus demonstrating a strong increase in risk with higher values of hs-cTnT.<\/p>\n
Therefore, while neither study is able to provide information about the pathophysiological basis for the increases in mortality, both show a convincing link\u00a0 between increased risk and the presence of raised cardiac biomarkers in patients with COPD.<\/p>\n
Conclusions: <\/strong><\/p>\n The presence of even mildly increased cardiac specific biomarkers in patients presenting with exacerbations of COPD identifies a group with a much poorer prognosis and substantially increased mortality.\u00a0 Further work is required to ascertain the pathophysiology underlying this phenomenon and what interventions if any might be beneficial in mitigating this risk.<\/p>\n