Crataegus extract is used in cardiology for the treatment of mild to moderate
heart failure (NYHA II) in Germany. However, little is known about the electrophysiological actions of
Crataegus extract in the heart. Recently, it was shown that
Crataegus extract prolongs the refractory period in isolated perfused hearts and increases action potential duration in guinea pig papillary muscle. It was the aim of this study to find out the mechanism of the increase in action potential duration caused by
Crataegus extract. Using the patch-clamp technique, we measured the effects of
Crataegus extract (10 mg/l;
flavonoid content: 2.25%, total
procyanidin content: 11.3 +/- 0.4%) on the inward rectifier and the delayed rectifier
potassium current in isolated guinea pig ventricular myocytes. To get some insight into the mechanism underlying the positive inotropic effect of
Crataegus extract, we also looked for effects on the L-type
calcium current.
Crataegus extract slightly blocked both the delayed and the inward rectifier
potassium current. The inhibition amounted to 25% and about 15%, respectively. This amount of inhibition of these repolarising currents is sufficient to explain the prolongation of action potential duration caused by
Crataegus extract. To our surprise we could not detect any influence of
Crataegus extract on the L-type
calcium current. In summary, our results show that
Crataegus extract blocks repolarising
potassium currents in ventricular myocytes. This effect is similar to the action of class III
antiarrhythmic drugs and might be the basis of the antiarrhythmic effects described for
Crataegus extract. Our measurements of the L-type
calcium current indicate that
Crataegus extract's positive inotropic effect is not caused by
phosphodiesterase inhibition or a beta-
sympathomimetic effect.