The QTc interval, autonomic neuropathy and mortality in hypoxaemic COPD

Abstract Patients with hypoxaemic chronic obstructive pulmonary disease (COPD) have a subclinical autonomic neuropathy. Autonomic neuropathy has been associated with a prolonged electrocardiograph Q Tc interval and risk of ventricular arrhythmias and death. We studied cardiovascular autonomic nerve function and Q Tc 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 ( P aO 2 7·3 ± 0·3 compared to 9·2 ± 1·8, P 1 and had a longer Q Tc at rest (0·43 ± 0·01 compared to 0·40 ± 0·01, P P When analysed after 2 yr, there were two deaths in group C and seven deaths in group AN. The Q Tc was abnormal >0·44 s at rest and at peak valsalva stress in five of group AN, three of these five patients died. Q Tc 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 Q Tc prolongation (>0·44 s) at rest was significantly associated ( P Q Tc prolongation at the peak of a valsalva stress was significantly associated with death at 2 yr follow-up ( P Patients with hypoxaemic COPD, particularly those with a parasympathetic autonomic neuropathy have evidence for a prolongation of the Q Tc interval which is associated with an increased mortality risk.