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Normalization of acquired QT prolongation in humans by intravenous potassium
A M Choy1, C C Lang, D M Chomsky
1Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn 37232-6602, USA.
Insights
Increasing serum potassium levels can correct dangerous QT abnormalities in patients with congestive heart failure (CHF) and those taking quinidine. This finding suggests a potential therapeutic strategy for managing these cardiac conditions.
Area of Science:
- Cardiology
- Electrophysiology
- Pharmacology
Background:
- QT interval prolongation and dispersion are linked to arrhythmias in congestive heart failure (CHF) and long-QT syndromes (LQTS).
- Potassium (K+) can correct QT abnormalities in some LQTS cases by increasing outward currents.
- Increased extracellular potassium ([K+]o) reduces the blocking effect of drugs like quinidine on I(Kr) channels in vitro.
Purpose of the Study:
- To investigate if increasing extracellular potassium ([K+]o) can correct QT abnormalities in patients with CHF and those treated with quinidine.
Main Methods:
- Potassium chloride (KCl) was infused into healthy subjects on quinidine or placebo, and into CHF patients and age-matched controls.
- Serum potassium levels were monitored during infusion.
- QT interval, QT dispersion, and QT morphology were assessed before and after potassium infusion.
Main Results:
- Potassium infusion significantly reversed QTUc prolongation in quinidine-treated subjects and CHF patients.
- Potassium infusion decreased QTUc dispersion in both quinidine-treated subjects and CHF patients.
- No significant effects on QT parameters were observed in control subjects.
Conclusions:
- Modest elevation of serum potassium can nearly normalize potentially arrhythmogenic QT abnormalities in quinidine-treated individuals and CHF patients.
- This suggests a potential therapeutic role for potassium in managing these conditions.
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(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 QTUc 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 QTUc 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.