THE QTC INTERVAL, AUTONOMIC NEUROPATHY AND MORTALITY IN HYPOXEMIC COPD

Patients with hypoxaemic chronic obstructive pulmonary disease (COPD) have a subclinical autonomic neuropathy. Autonomic neuropathy has been associated with a prolonged electrocardiograph QTc interval and risk of ventricular arrhythmias and death. We studied cardiovascular autonomic nerve function and QTc interval at rest and during stress (a valsalva manoeuvre) in 34 patients with hypoxaemic COPD who were followed up after 2 yr. Seventeen patients had a subclinical autonomic neuropathy (group AN) and the remaining 17 were normal (group C). Group AN were significantly more hypoxaemic (PaO2 7.3 +/- 0.3 compared to 9.2 +/- 1.8, P<0.05), had a lower FEV(1) and had a longer QTc at rest (0.43 +/- 0.01 compared to 0.40 +/- 0.01, P<0.01) and at peak valsalva (0.44 +/- 0.01 compared to 0.41 +/- 0.01, P<0.05). When analysed after 2 yr, there were two deaths in group C and seven deaths in group AN. The QTc was abnormal >0.44 s at rest and at peak valsalva stress in five of group AN, three of these five patients died. QTc was normal at rest but abnormal at peak valsalva stress in eight further patients. This included three further patients from group AN of whom two had died and five group C patients which included both the group C deaths. The presence of autonomic neuropathy and QTc prolongation (>0.44 s) at rest was significantly associated (P<0.05). Likewise QTc prolongation at the peak of a valsalva stress was significantly associated with death at 2 yr follow-up (P<0.01) with an odds ratio of 11.1. Patients with hypoxaemic COPD, particularly those with a parasympathetic autonomic neuropathy have evidence for a prolongation of the QTc interval which is associated with an increased mortality risk.