Abstract. Sudden cardiac death is common in patients on hemodialysis, and may occur in the immediate postdialysis period, when ventricular premature complexes are common. Elevated QT dispersion (Maximum — Minimum QT interval on standard 12-lead electrocardiogram) is associated with increased risk of ventricular arrhythmias following myocardial infarction, but has not previously been assessed in patients with chronic renal failure. We studied electrocardiograms recorded in 50 patients before and after a single hemodialysis session, and in 20 control subjects. QT dispersion was significantly higher in patients (63.1 ± 20.6 ms) compared with control subjects (36.0 ± 13.7 ms; P < 0.001) and rose significantly after hemodialysis to levels comparable to those seen following myocardial infarction (76.6 ± 27.0 ms; P < 0.01). Because QT dispersion reflects nonhomogeneous recovery of ventricular excitability, hemodialysis patients may be at significantly greater risk of reentrant arrhythmias and sudden death in the postdialysis period.

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The endopeptidase EC 3.4.24.11 (atriopeptidase) degrades atrial natriuretic factor (ANF). Intravenous administration of UK 69,578 (0.025 to 10.0 mg/kg), a new specific atriopeptidase inhibitor, in 16 normal volunteers produced a two- to three-fold rise in endogenous ANF. Peak levels were reached within 2 h declining to control values by 8 h. The rise in ANF was associated with an increase in urine volume and mean urinary sodium excretion rose from 64.9 mmoles/8 h after placebo to 116.1 mmoles/8 h after 10 mg/kg UK 69,578. Despite the natriuresis, plasma active renin concentration was suppressed for up to 8 h. We conclude that inhibition of the endopeptidase EC 3.4.24.11 in humans elevates endogenous ANF and causes a natriuresis and may offer a novel therapeutic approach to the treatment of hypertension and cardiac failure.

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