Apex-to-base dispersion of refractoriness underlies the proarrhythmic effect of hypokalaemia/hypomagnesaemia in the rabbit heart.

Apex-to-base differences in the density of potassium currents have been recently described in isolated rabbit myocytes. The significance of those findings for arrhythmogenesis in the whole heart is not known. We aimed to examine electrophysiological effects of hypokalaemia/hypomagnesaemia in isolated working rabbit hearts. Monophasic action potential duration (MAPD(90)), effective refractory period (ERP) and conduction delay were measured at 3 left ventricular sites (basal epicardium, apical epicardium, apical endocardium) in control (K(+) = 4mmol/L, Mg(2+) = 1mmol/L) and hypokalaemia/hypomagnesaemia (K(+) = 2mmol/L, Mg(2+) = 0.5mmol/L) groups. It was found that hypokalaemia/hypomagnesaemia shortened ERP in the apical epicardial region (by 22 +/- 6ms), without any significant effect in the basal area. Consequently, hypokalaemia/hypomagnesaemia increased transepicardial dispersion of refractoriness (from 10 +/- 3 to 25 +/- 7ms, P <.05) and increased inducibility of ventricular fibrillation (from 10% to 100%, P <.05). Similar effects were seen in hearts with left ventricular hypertrophy secondary to perinephritis-induced hypertension. These results suggest that hypokalaemia/hypomagnesaemia is pro-arrhythmic in normal or hypertrophied hearts due to an increase in apex-to-base dispersion of refractoriness.