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Mechanisms of verapamil-induced conduction block in anomalous atrioventricular bypass tracts
Insights
Verapamil effectively terminates AV reciprocating tachycardia by blocking conduction in bypass tracts, not the AV node. This drug works through direct or indirect actions on the bypass tract, depending on its properties.
Area of Science:
- Cardiology
- Electrophysiology
- Pharmacology
Background:
- Atrioventricular (AV) reciprocating tachycardia is often treated with medications that affect AV nodal conduction.
- Verapamil, a calcium channel blocker, primarily affects the AV node but its impact on anomalous AV bypass tracts is less understood.
Purpose of the Study:
- To investigate the mechanisms by which verapamil terminates AV reciprocating tachycardia involving anomalous AV bypass tracts.
- To determine if verapamil's effect is on the AV node or the bypass tract itself.
Main Methods:
- Electrophysiologic studies were conducted in 39 patients with AV reciprocating tachycardia using left-sided bypass tracts.
- Intravenous verapamil (0.15 mg/kg) was administered to assess its effect on tachycardia termination and conduction properties.
Main Results:
- Verapamil terminated tachycardia in 31 of 39 patients.
- In 5 patients, verapamil induced retrograde conduction block in the bypass tract, not the AV node.
- Two distinct mechanisms were observed: Ashman phenomenon induction and prolongation of the bypass tract's effective refractory period.
Conclusions:
- Verapamil can interrupt AV reciprocating tachycardia by acting directly or indirectly on the bypass tract.
- The mechanism of action depends on the specific electrophysiologic properties of the anomalous bypass tract.
- These findings highlight verapamil's efficacy and versatile mechanisms in managing specific tachyarrhythmias.
Abstract:
Verapamil, a calcium channel blocking agent, has been demonstrated to have depressive effects on the atrioventricular (AV) node but not anomalous AV bypass tracts. Of 39 patients with AV reciprocating tachycardia utilizing left-sided bypass tracts for retrograde conduction, intravenous infusion of verapamil (0.15 mg/kg) terminated the tachycardia in 31 patients. Verapamil interrupted the tachycardia circuit by inducing retrograde conduction block in the bypass tract rather than the AV node in 5 of these 31 patients. Electrophysiologic studies in these five patients revealed that verapamil-induced conduction block in the bypass tract could be accounted for by two distinctly different mechanisms. In three patients, verapamil induced alternating slow and fast AV nodal conduction resulting in alternating long and short cycle lengths during the tachycardia; consequently, development of the Ashman phenomenon in the bypass tract terminated the tachycardia. In the remaining two patients, the bypass tract exhibited properties similar to those of the AV node; verapamil prolonged the effective refractory period of the bypass tract, thereby terminating the tachycardia. Thus, depending on the functional properties of the bypass tract, verapamil may interrupt an AV reciprocating tachycardia circuit by exerting either a direct or indirect depressive action on the bypass tract.