A prospective comparison of triple extrastimuli and left ventricular stimulation in studies of ventricular tachycardia induction.

Abstract

One hundred and one patients with sustained unimorphic ventricular tachycardia underwent programmed ventricular stimulation with one of two protocols. Fifty patients underwent programmed stimulation with protocol A, which consisted of burst overdrive pacing, single, double, and triple extrastimuli at the right ventricular apex, right ventricular outflow tract, or septum, and then at the left ventricular apex. Fifty-one patients underwent programmed stimulation with protocol B, which consisted of burst overdrive pacing, single and double extrastimuli at the right ventricular apex, right ventricular outflow tract or septum, and at the left ventricular apex, followed by triple extrastimuli at these sites. The stimulation protocol was continued until sustained ventricular tachycardia or rapid, polymorphic ventricular tachycardia greater than 10 sec in duration was induced. With protocol A, clinical and nonclinical ventricular tachycardia was induced in 76% and 36% of patients, respectively; with protocol B, clinical and nonclinical ventricular tachycardia was induced in 85% and 38% of patients, respectively. Direct-current countershock for sustained polymorphic ventricular tachycardia was required in 10% of patients studied under protocol A, compared with in 2% of patients studied under protocol B. With protocol A, near-maximal yield of induced clinical (72%) and nonclinical ventricular tachycardia (30%) was attained after the use of triple extrastimuli at the first stimulation site. The yield of stimulation at a second right ventricular site and of left ventricular stimulation was only an additional 2% each. With protocol B, triple extrastimuli increased the yield of induced clinical ventricular tachycardia from 61% to 85%. In patients with sustained unimorphic ventricular tachycardia undergoing programmed ventricular stimulation, the use of triple extrastimuli at the first stimulation site (protocol A) resulted in a high yield of induced clinical ventricular tachycardia early in the protocol, but at the cost of a significant yield of nonclinical ventricular tachycardia. In the patient who has documented ventricular tachycardia, protocol A may be suitable since the nonclinical arrhythmias that are induced will be readily identifiable as such. The initial use of burst overdrive pacing and single and double extrastimuli in the right ventricle (protocol B) will obviate the need for triple extrastimuli and left ventricular stimulation in 53% of patients and result in a low yield of nonclinical arrhythmias, especially those that are polymorphic (4%). Protocol B may therefore be preferable in patients with sustained but undocumented ventricular tachycardia, to minimize uncertainty regarding the clinical significance of induced tachycardia. However, triple extrastimuli will still be required to induce clinical ventricular tachycardia in 24% of patients, and the overall yield of nonclinical ventricular tachycardia is similar with protocols A and B. Circulation 70, No. 1, 52-57, 1984.THE USE of triple extrastimuli...

Programmed electrical stimulation of the heart in patients with life-threatening ventricular arrhythmias: what is the significance of induced arrhythmias and what is the correct stimulation protocol?

“…In accordance with the findings with regard to monomorphic ventricular tachycardia that we discussed above, we believe that to reproduce the arrhythmia in patients with documented sustained monomorphic ventricular tachycardia, right ventricular apical stimulation using one site, three basic pacing 4 rates, and a maximum of three extrastimuli is usually sufficient. Stimulation from another right ventricular site or the left ventricle is indicated only in the rare patient in whom this stimulation protocol does not result in initiation of the clinical arrhythmia and in whom endocavitary mapping is essential for subsequent surgical treatment.…”

“…3' 14 This suggests that polymorphic ventricular tachycardia is a "non-specific response to aggressive stimulation protocols."' 4 Sustained polymorphic ventricular tachycardia is induced more frequently in patients resuscitated from sudden death than in those presenting with sustained ventricular tachycardia without cardiac arrest, suggesting that it may be a precursor of ventricular fibrillation. The initiation of nonsustained polymorphic ventricular tachycardia has also been interpreted to be indicative of a greater risk of ventricular fibrillation and sudden death.…”

“…figure), (2) recognition of stimulation steps that were ineffective (for instance, pacing with 140/min and one extrastimulus in both groups of patients) (3) log-rank test recognition of programmed stimulation steps that contributed significant differences in the results of the stimulation protocol between the two groups (for example, pacing at 120/min with two extrastimuli). (4) determination of the relative efficacy or lack thereof of the program by studying the area under the curve and comparing it with the total area, and (5) determination of the mean number of extrastimuli and stimulation steps required to induce a sustained ventricular tachycardia that can be calculated and compared between the two groups.…”

ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death

“…This test may be repeated during isoproterenol infusion (187)(188)(189). The prematurity of extrastimuli is increased until refractoriness or induction of sustained ventricular tachyarrhythmia is achieved.…”

“…Because premature ventricular stimulation with a very short coupling interval is more likely to induce VF as opposed to monomorphic VT, it may be reasonable to limit the prematurity of the extrastimuli to a minimum of 180 ms when studying patients for whom only inducible sustained monomorphic VT would be considered a positive endpoint (190). EP testing may be repeated at the RV outflow tract (RVOT) or LV (189). In some patients with ratedependent induction of VT, rapid atrial or ventricular stimulation may induce VT (191 Drug testing for assessing antiarrhythmic drug efficacy has largely been abandoned.…”