Effect of ajmaline on sustained ventricular tachycardia induced by programmed electrical stimulation in conscious dogs after myocardial infarction

Summary

As yet the antiarrhythmic efficacy of ajmaline with regard to suppressing the induction of sustained ventricular tachycardia after myocardial infarction has not been determined. Therefore, programmed electrical stimulation was performed in 8 conscious, chronically instrumented mongrel dogs 8–20 days after a 4-hour occlusion of the left anterior descending coronary artery. At baseline all animals responded with sustained ventricular tachycardia. Thereafter, ajmaline was administered at two consecutive ix. doses: a bolus of 0.7 mg kg⁻¹ followed by infusion of 2 mg kg⁻¹ h⁻¹ and infusion of 4 mg kg⁻¹ h⁻¹. The induction of sustained ventricular tachycardia was prevented in 2/8 animals by 2 mg kg⁻¹ h⁻¹ ajmaline and in 1/8 animals by 4 mg kg⁻¹ h⁻¹ ajmaline. During sinus rhythm only 4 mg kg⁻¹ h⁻¹ ajmaline significantly increased QRS-duration and intraventricular activation times, but during rapid right ventricular pacing (cycle length = 330 ms) both doses of ajmaline increased QRS duration and intraventricular conduction times. 4 mg kg⁻¹ h⁻¹ ajmaline also increased the cycle length of induced sustained ventricular tachycardia. In 3 animals induction of sustained ventricular tachycardia during infusion of 4 mg kg⁻¹ h⁻¹ ajmaline was achieved by introduction of less extrastimuli than at baseline. Furthermore the coupling intervals of extrastimuli that induced sustained ventricular tachycardia were substantially prolonged by this dose. Inhomogeneity of conduction between left ventricular normal zone and left ventricular infarct zone was significantly increased by 4 mg kg⁻¹ h⁻¹ ajmaline during rapid right ventricular pacing, but not during sinus rhythm.

We conclude that ajmaline has only limited efficacy with regard to the prevention of induction of sustained ventricular tachycardia after myocardial infarction. Drug-induced increases in tachycardia cycle lengths, as observed under the higher dose of ajmaline, were associated with a rate-dependent rise in cardiac electrical instability.