Normalization of acquired QT prolongation in humans by intravenous potassium
Choy, A.M.; Lang, C.C.; Chomsky, D.M.; Rayos, G.H.; Wilson, J.R.; Roden, D.M.
Circulation 96(7): 2149-2154
1997
ISSN/ISBN: 0009-7322 PMID: 9337183 Document Number: 470105
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 LOTS, infusion of potassium can correct QT abnormalities, consistent with in vitro increases in outward currents such as I-Kr or I-Kl 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, 59+-79 to 479+-35 (+-SD) ms-1/2, P lt .001; CHF, 521+-110 to 431+-47 ms-1/2, P lt .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 lt .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.