Cardiovascular death is the most important cause of mortality in alcoh
olics, yet alcohol may protect against ischaemic heart disease. This c
ould be explained if deaths were a consequence of alcohol-related arrh
ythmias rather than of coronary atheroma. In many conditions, abnormal
ities of the QT interval are markers of arrhythmia and for risk of sud
den death. We examined the relation between QT intervals and mortality
in patients with alcoholic liver disease. Simultaneous 12-lead electr
ocardiographic recordings were obtained from 69 patients with histolog
ically proven alcoholic liver disease (without evidence of structural
heart disease), and from 40 healthy non-drinking controls matched for
age and sex. Patients were abstinent for at least 7 days before invest
igation to exclude acute effects of alcohol. QT intervals were correct
ed for rate with Bazett's and cube root formulae to define QT(c) and Q
T(cub), respectively. Unlike QT(c), QT(cub) was independent of rate. P
atients were followed for up to four years. For those who died, the ca
use was determined from case records and postmortem reports. Maximum Q
T intervals were longer in alcoholics than in controls (QT(cub) 450 vs
439, p = 0.016). This difference was not explained by variations in e
lectrolytes. QT intervals were prolonged in the 14 patients who died c
ompared with survivors (QT(cub) 471 vs 446, p = 0.007). This differenc
e was mainly due to the long QT intervals in the 6 patients with sudde
n cardiac deaths (QT(cub) 493). The only other factor independently as
sociated with death was sex. QT interval prolongation occurs in some p
atients with alcoholic liver disease and is associated with an adverse
prognosis, especially sudden cardiac death. QT measurement should be
included in the initial assessment of alcoholic patients, particularly
in those considered for liver transplantation.