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The effects of diltiazem hydrochloride on the cardiac conduction: a clinical study of His bundle electrogram
Insights
Diltiazem hydrochloride, a calcium channel blocker, selectively slows cardiac conduction in the atrioventricular node. This effect on atrioventricular nodal action potential is independent of vagus tone changes.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Atherosclerotic heart disease poses significant risks.
- Calcium channel blockers are crucial antianginal agents.
Purpose of the Study:
- To evaluate the effects of diltiazem hydrochloride on cardiac conductivity.
- To understand the mechanism of diltiazem's action on the atrioventricular node.
Main Methods:
- Conducted His bundle electrograms in 10 patients with atherosclerotic heart disease.
- Measured R-R, A-H, and H-V intervals before and after intravenous diltiazem administration.
- Assessed diltiazem's interaction with atropine's cardiac effects.
Main Results:
- Diltiazem significantly prolonged the A-H interval.
- R-R and H-V intervals remained unaffected by diltiazem.
- Diltiazem's A-H prolongation persisted despite atropine pretreatment.
Conclusions:
- Diltiazem selectively depresses atrioventricular node conductivity.
- The mechanism is not mediated by vagus tone alteration.
- Calcium influx likely contributes to atrioventricular nodal action potential generation in humans.
Abstract:
The effects of diltiazem hydrochloride, a new Ca++ antagonistic antianginal drug, on the cardiac conductivity were evaluted in 10 patients with atherosclerotic heart disease. His bundle electrograms were obtained by catheter technique. R-R, A-H and H-V intervals were measured before and after intravenous administration of diltiazem. Diltiazem acted towards significant prolongation in A-H interval. R-R and H-V intervals were insensitive to diltiazem. Diltiazem did not interrupt the cardiac effects of atropine when A-H prolongation was still observed in the subject pretreated with atropine. In short, diltiazem depresses the conductivity of the atrioventricular node selectively and this is not mediated through vagus tone change. This Ca++ antagonist induced A-H prolongation strongly suggests the contribution of Ca++ current on the generation of atrioventricular nodal action potential in humans.