General concepts and mechanisms of ventricular tachycardia

The predominant mechanism of ventricular tachycardia is thought to be reentry, although this has been proved to exist in definitely a minority of patients studied owing to technical limitations. Other mechanisms, such as spontaneous triggered automaticity, undoubtedly also cause clinical ventricular tachycardia. During electrophysiologic testing, sustained unimorphic ventricular tachycardia can be induced in the majority of patients who have this arrhythmia clinically. It is extremely rare to induce this rhythm in a patient who has not had ventricular tachyarrhythmias. Nonsustained ventricular tachycardia, repetitive ventricular responses, and pleomorphic ventricular tachycardia and ventricular fibrillation are all nonspecific responses to electrical stimulation and thus are not suitable end points for either the baseline study or serial drug testing. Although an optimal pacing protocol for all subjects does not exist, an adequate test should include pacing with multiple drive rates, at least two (and in some cases, three) extrastimuli, and more than one pacing site in the right ventricle. Isoproterenol infusion and left ventricular pacing may also be necessary in selected patients. During serial drug testing, a drug should not be considered effective if more than 15 repetitive beats are induced unless an extremely aggressive pacing protocol is used. Patients treated with drugs predicted to be effective at electrophysiologic study have a better prognosis than those treated with drugs predicted to be ineffective or those treated with drugs selected empirically.