Vitamin K modulates cardiac action potential by blocking sodium and potassium ion channels
1Institut de cardiologie de Québec, Hôpital Laval et Université Laval, Sainte-Foy, Québec, Canada.
Background:
Cardiovascular collapses, syncopes, and sudden deaths have been observed following the rapid administration of intravenous vitamin K. Our objectives were to characterize the effects of vitamin K on cardiac action potentials and to evaluate effects of vitamin K on sodium and potassium currents, namely I(Na), I(Kr), and I(Ks).
Methods And Results:
Guinea pig hearts (n = 21) were paced at a cycle length of 250 msec and exposed to vitamin K at 1.15-4.6 micromol/L (2.5-10 mg/L). Monophasic action potential duration measured at 90% repolarization (MAPD(90)) was not significantly reduced (-1.6 +/- 0.3 msec; P >.05; N.S.) at 1.15 micromol/L, but increased by 6.5 +/- 0.4 msec (P <.05) at 2.3 micromol/L. MAPD(90) was not measurable at 4.6 micromol/L, as a result of inexcitability. Patch-clamp experiments in ventricular myocytes demonstrated a approximately 50% reduction in I(Na) by 10 micromol/L vitamin K and a concentration-dependent reduction of the K(+) current elicited by short depolarizations (250 msec; I(K250)). Estimated IC(50) for I(K250), mostly representing I(Kr), was 2.3 micromol/L. Vitamin K was less potent to block the K(+) current elicited by long depolarizations (5,000 msec; I(K5000)), mostly representing I(Ks), with an estimated IC(50) over 100 micromol/L.
Conclusions:
Therapeutic concentrations ( approximately 1.5 micromol/L) of intravenous vitamin K modulate cardiac action potential by blocking ionic currents involved in cardiac depolarization and repolarization.
Insights
Intravenous vitamin K can alter heart electrical activity by affecting sodium and potassium currents. This study shows vitamin K impacts cardiac action potentials, potentially explaining adverse cardiovascular events.
Area of Science:
- Cardiology
- Electrophysiology
- Pharmacology
Background:
- Rapid intravenous vitamin K administration has been linked to cardiovascular events like collapse and sudden death.
- Understanding vitamin K's cardiac effects is crucial for patient safety.
Purpose of the Study:
- To investigate the impact of vitamin K on cardiac action potentials.
- To assess vitamin K's effects on key sodium (I(Na)) and potassium currents (I(Kr), I(Ks)).
Main Methods:
- Guinea pig hearts were exposed to varying concentrations of vitamin K.
- Monophasic action potential duration (MAPD(90)) was measured.
- Patch-clamp electrophysiology was used to study ionic currents in ventricular myocytes.
Main Results:
- Vitamin K increased action potential duration at 2.3 micromol/L and caused inexcitability at higher concentrations.
- Vitamin K significantly reduced sodium current (I(Na)) by approximately 50% at 10 micromol/L.
- It concentration-dependently blocked rapid potassium current (I(Kr)) with an IC(50) of 2.3 micromol/L, while I(Ks) was less affected.
Conclusions:
- Therapeutic concentrations of intravenous vitamin K modulate cardiac action potentials.
- Vitamin K blocks ionic currents critical for cardiac depolarization and repolarization.
- These electrophysiological effects may underlie observed cardiovascular adverse events.
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