Ajmaline and its derivatives

Cardiovascular

Ajmaline occasionally causes cardiac dysrhythmias [ ]. Of 1995 patients who were given ajmaline 1 mg/kg intravenously during an electrophysiological study, 63 developed a supraventricular tachydysrhythmia (atrial flutter, fibrillation, or tachycardia), and seven an atrioventricular re-entrant tachycardia [ ]. Those most at risk were older patients, those with underlying cardiac disease, and those with a history of dysrhythmias or sinus node dysfunction.

Two cases of torsade de pointes have been reported in association with prolongation of the QT interval [ ]. Polymorphous ventricular tachycardia has been reported in three cases [ ].

• A 13-year-old boy with Brugada syndrome (right bundle branch block with persistent ST segment elevation) was given an injection of ajmaline 1 mg/kg and developed greater ST segment elevation and more marked right bundle branch block morphology [ ]. This was followed by short runs of non-sustained polymorphic ventricular tachycardia, gradually increasing until monomorphic ventricular tachycardia occurred. The dysrhythmia eventually resolved without further treatment.

It is unwise to give antidysrhythmic drugs to patients with Brugada syndrome.

The diagnostic electrocardiographic pattern in Brugada syndrome can be absent and can be unmasked by sodium channel blockers, such as ajmaline. The risks of a standardized ajmaline challenge test have been studied in 158 patients, who were given intravenous ajmaline 10 mg every 2 minutes up to a target dose of 1 mg/kg [ ]. In 37 patients (23%) the typical coved ST pattern of the Brugada syndrome was unmasked. During the test, symptomatic ventricular tachycardia occurred in two patients. In all other patients, the drug challenge did not induce ventricular tachycardia if the endpoints of the test were the administration of the target dose, QRS prolongation over 30%, the presence of the typical electrocardiogram, or the occurrence of ventricular extra beats. There was a positive response to ajmaline in two of 94 patients with a normal baseline electrocardiogram, who underwent evaluation solely for syncope of unknown origin.

Ajmaline challenge was positive in 48 of 103 patients with Brugada syndrome [ ]. J wave elevation in V2 and a reduced T wave amplitude in V3 at baseline were independent predictors of a positive response.