Objective: Fatal arrhythmias are a common cause of death in chronic obstructive pulmonary disease (COPD). Two major hypotheses for arrhythmogenesis in COPD have been proposed: arrhythmias are a consequence of hypoxaemia, hypercapnia or (tissue localised) acid-base disturbances, or arrhythmias are the result of the autonomic neuropathy that characterises COPD. Our objective was to verify these two hypotheses.
Methods: A total of 29 consecutive COPD patients (seven men and 22 women, mean age 63.75 +/- 10.50 years) were included in the study. Pulmonary function tests were performed and arterial blood gases were obtained simultaneously. Twelve-lead electrocardiograms were recorded from all patients. QT dispersion, which is a measure of myocardial repolarisation heterogeneity, and the coefficient of variation of the RR interval, which is a measure of heart rate variability, were calculated.
Results: Of the parameters measured, only the coefficient of variation of the RR interval appeared to be related to arrhythmias, since it correlated positively with arterial oxygen pressure (r = 0.418, statistical significance set at P < 0.05).
Conclusions: Our results rule out the electropathy hypothesis and underline the role of autonomic neuropathy as the most probable arrhythmogenic mechanism in hypoxaemic COPD patients. Our interpretation is based on the fact that hypoxaemia decreases heart rate variability and on the strong association between the reduction in heart rate variability and arrhythmogenesis.