Normalization of Acquired QT Prolongation in Humans by Intravenous Potassium

Abstract

Background QT interval prolongation and dispersion have been implicated in serious arrhythmias in congestive heart failure (CHF) and the congenital and drug-induced long-QT syndromes (LQTS). In a subset of the congenital LQTS, infusion of potassium can correct QT abnormalities, consistent with in vitro increases in outward currents such as I Kr or I K1 when extracellular potassium concentration ([K + ] o ) is increased. Furthermore, increasing [K + ] o decreases the potency of I Kr -blocking drugs in vitro. The purpose of this study was to test the hypothesis that increasing [K + ] o corrects QT abnormalities in CHF and in subjects treated with quinidine. Methods and Results KCl (maximum, 40 mEq) was infused into (1) 12 healthy subjects treated with quinidine sulfate (5 doses of 300 mg/5 h) or placebo and (2) 8 CHF patients and age-matched normal control subjects. Mean [K + ] increased from 4 to 4.2 mEq/L to 4.7 to 5.2 mEq/L. Potassium infusion significantly reversed QTU c prolongation, especially in the precordial leads (quinidine, 590±79 to 479±35 [±SD] ms 1/2 , P <.001; CHF, 521±110 to 431±47 ms 1/2 , P <.05). There was no effect in either control group. Similarly, potassium decreased QTU c dispersion (quinidine, 210±62 to 130±75 ms 1/2 , P <.01; CHF, 132±68 to 84±35 ms 1/2 , P =.07) and was without effect in the control subjects. QT morphological abnormalities, including U waves and bifid T waves, were reversed by potassium. Conclusions Potentially arrhythmogenic QT abnormalities during quinidine treatment and in CHF can be nearly normalized by modest elevation of serum potassium.