Shimon Rosenheck

Diagnosis and cure of the Wolff-Parkinson-White syndrome or paroxysmal supraventricular tachycardias during a single electrophysiologic test

BACKGROUND We conducted this study to determine the feasibility of an abbreviated therapeutic approach to the Wolff-Parkinson-White syndrome or paroxysmal supraventricular tachycardia, in which the diagnosis is established and radiofrequency ablation carried out during a single electrophysiologic test. METHODS One hundred six consecutive patients were referred for the management of documented, symptomatic paroxysmal supraventricular tachycardias (66 patients) or the Wolff-Parkinson-White syndrome (40 patients). All agreed to undergo a diagnostic electrophysiologic test and catheter ablation with radiofrequency current. No patient had had such a test previously. RESULTS Among the 66 patients with paroxysmal supraventricular tachycardias, the mechanism was found to be atrioventricular nodal reentry in 46 (70 percent) (typical in 44 and atypical in 2), atrioventricular reciprocating tachycardia involving a concealed accessory pathway in 16 (24 percent), atrial tachycardia in 2 (3 percent), and noninducible paroxysmal supraventricular tachycardia in 2 (3 percent). A successful long-term outcome was achieved in 57 of 62 patients (92 percent) with paroxysmal supraventricular tachycardia in whom ablation was attempted and in 37 of 40 patients (93 percent) with the Wolff-Parkinson-White syndrome. The only complications were one instance of occlusion of the left circumflex coronary artery, leading to acute myocardial infarction, and one instance of complete atrioventricular block. The mean (+/- SD) duration of the electrophysiologic procedures was 114 +/- 55 minutes. CONCLUSIONS The diagnosis and cure of paroxysmal supraventricular tachycardia or the Wolff-Parkinson-White syndrome during a single electrophysiologic test are feasible and practical and have a favorable risk-benefit ratio. This abbreviated therapeutic approach may eliminate the need for serial electropharmacologic testing, long-term drug therapy, antitachycardia pacemakers, and surgical ablation.

Long-term results of catheter ablation of idiopathic right ventricular tachycardia.

Ten consecutive patients with recurrent episodes of symptomatic, idiopathic, sustained monomorphic ventricular tachycardia (VT) originating in the right ventricle underwent an attempt at catheter ablation of the ventricular tachycardia. There were seven women and three men, with a mean age of 39 +/- 14 years (+/- SD). None of the patients had any evidence of structural heart disease. The VT had a left bundle branch block configuration and an inferior axis in each patient, and the mean cycle length was 313 +/- 75 msec. Based on the methods of induction of the VT and the response of the VT to verapamil, the VT mechanism was presumed to be reentry in six patients, triggered activity in three patients, and catecholamine-sensitive automaticity in one patient. Sites for ablation were guided by pace mapping, and an appropriate target site was identified in the right ventricular outflow tract in each patient. From one to three shocks of 100-360 J (mean total, 336 +/- 195 J) were delivered from a defibrillator between the tip of the ablation catheter (cathode) and a patch electrode on the anterior chest (anode). An electrophysiology test 7-9 days after ablation demonstrated that VT was still inducible in only one patient, who was treated with amiodarone. One other patient had a recurrence of VT 3 weeks after ablation and was treated with verapamil. Eight of 10 patients were not treated with antiarrhythmic medications and have had no episodes of symptomatic VT during 15-68 months of follow-up (mean follow-up, 33 +/- 18 months). There were no acute or long-term complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Concealed entrainment as a guide for catheter ablation of ventricular tachycardia in patients with prior myocardial infarction

Fifteen consecutive patients with drug-refractory, recurrent, sustained, monomorphic ventricular tachycardia and a history of remote myocardial infarction underwent catheter ablation of ventricular tachycardia. Shocks of 100 to 300 J were delivered to sites at which pacing during ventricular tachycardia resulted in concealed entrainment, in which the ventricular tachycardia accelerated to the pacing rate, there was a long stimulus to QRS interval and there was no change in the configuration of the QRS complex during pacing at several rates compared with the configuration during ventricular tachycardia, thus identifying a zone of slow conduction in the reentrant circuit. Concealed entrainment was demonstrated in nine (60%) of 15 patients, and the stimulus to QRS intervals were 90 to 400 ms. At sites of concealed entrainment, the endocardial activation time relative to the QRS complex during ventricular tachycardia ranged from -125 to +50 ms, the timing of the local electrogram relative to the QRS complex was the same during entrainment as during ventricular tachycardia and the pace map during sinus rhythm was discordant with that of the ventricular tachycardia in seven patients. In the six patients in whom a site of concealed entrainment could not be identified, the target site for ablation was selected on the basis of identification of an isolated mid-diastolic potential, activation mapping and pace mapping. The mean (+/- SD) cumulative number of joules delivered to the target site was 306 +/- 140. A successful long-term clinical outcome was achieved in 9 of the 15 patients (mean follow-up 20 +/- 7 months). The clinical success rate was the same whether the target site was selected on the basis of concealed entrainment (five of nine, 56%) or on the basis of the other mapping techniques (four of six, 67%). In conclusion, the responses to pacing suggest that sites at which there is concealed entrainment may be located within a zone of slow conduction in the ventricular tachycardia reentry circuit, although not necessarily in an area critical for the maintenance of reentry. The long-term clinical efficacy of catheter ablation targeted to sites of concealed entrainment is about 60%, similar to the results achieved when conventional mapping techniques are used.

Radiofrequency catheter ablation of the atrioventricular junction from the left ventricle.

BackgroundThe purpose of this study was to describe a new technique for catheter ablation of the atrioventricular junction using radiofrequency energy delivered in the left ventricle. Methods and ResultsCatheter ablation of the atrioventricular (AV) junction using a catheter positioned across the tricuspid annulus was unsuccessful in eight patients with a mean+ SD age of 51 ± 19 years who had AV nodal reentry tachycardia (three patients), orthodromic tachycardia using a concealed midseptal accessory pathway, atrial tachycardia, atrial flutter (two patients), or atrial fibrillation. Before attempts at catheter ablation of the AV junction, each patient had been refractory to pharmacological therapy, and four had failed attempts at either catheter modification of the AV node using radiofrequency energy or surgical and catheter ablation of the accessory pathway. Conventional right-sided catheter ablation of the AV junction using radiofrequency energy in six patients and both radiofrequency energy and direct current shocks in two patients was ineffective. The mean amplitude of the His bundle potential recorded at the tricuspid annulus at the sites of unsuccessful AVjunction ablation was 0.1 ± 0.08 mV, with a maximum His amplitude of 0.03–0.28 mV. A 7F deflectable-tip quadripolar electrode catheter with a 4-mm distal electrode was positioned against the upper left ventricular septum using a retrograde aortic approach from the femoral artery. Third-degree AV block was induced in each of the eight patients with 20–36 W applied for 15–30 seconds. The His bundle potential at the sites of successful AV junction ablation ranged from 0.06 to 0.99 mV, with a mean of 0.27 ± 0.32 mV. There was no rise in the creatine kinase-MB fraction and no complications occurred. An intrinsic escape rhythm of 30–60 beats/min was present in seven of the eight patients. Each patient received a permanent pacemaker and has been asymptomatic during 3–13 months of follow-up. ConclusionsCatheter ablation of the AVjunction can be achieved effectively and safely using radiofrequency energy delivered in the left ventricle when the conventional right-sided approach is unsuccessful.

Comparison of responses to isoproterenol and epinephrine during head-up tilt in suspected vasodepressor syncope

Abstract Head-up tilt is known to play an important role in establishing the diagnosis of vasodepressor syncope in patients with syncope of unknown etiology. 1–5 Although passive head-up tilt alone may trigger a vasodepressor response, recent studies show that an infusion of isoproterenol significantly increases the sensitivity of head-up tilt in reproducing vasodepressor syncope. 1–5 However, isoproterenol is not endogenously produced and the role of endogenous catecholamines, such as epinephrine, in provoking vasodepressor syncope is unknown. Therefore, we compared the responses to isoproterenol and epinephrine during head-up tilt in patients suspected of having vasodepressor syncope.

Effects of resting vagal tone on accessory atrioventricular connections.

The purpose of this study was to determine the effects of resting vagal tone on accessory atrioventricular (AV) connections. Atropine (0.04 mg/kg) was administered to 13 patients with the Wolff-Parkinson-White syndrome and was found to have the following effects on the accessory AV connection: the anterograde block cycle length shortened from 305 +/- 51 to 279 +/- 54 msec (mean +/- SD; p less than 0.001); the retrograde block cycle length shortened from 288 +/- 57 to 251 +/- 50 msec (p less than 0.001); and the effective refractory period measured at a basic drive cycle length of 400 msec shortened from 295 +/- 45 to 265 +/- 47 msec in the anterograde direction (p less than 0.001) and from 283 +/- 18 to 261 +/- 12 msec in the retrograde direction (p less than 0.01). During atrial fibrillation, the mean ventricular cycle length decreased from 434 +/- 88 to 352 +/- 56 msec (p less than 0.001), and the shortest preexcited RR interval decreased from 302 +/- 56 to 256 +/- 43 msec (p less than 0.01). In another seven patients, propranolol (0.2 mg/kg) was administered before atropine, and atropine lengthened the anterograde block cycle length and the effective refractory period of the accessory AV connection; the magnitude of these effects was similar to that in the patients who did not receive propranolol. In conclusion, these data demonstrate that resting vagal tone exerts a direct depressant effect on accessory AV connections that does not require background sympathetic activity to be manifest.

Prospective comparison of a conventional and an accelerated protocol for programmed ventricular stimulation in patients with coronary artery disease.

BackgroundThis study compared the sensitivity, specificity, and efficiency of a “conventional” and “accelerated” programmed stimulation protocol in 293 patients with coronary artery disease who had a history of sustained or nonsustained monomorphic ventricular tachycardia (VT). Methods and ResultsIn the conventional protocol, one and two extrastimuli were introduced during sinus rhythm and during basic drive trains at cycle lengths of 600 and 400 msec at the right ventricular apex and then at the outflow tract or septum. In the accelerated protocol, one, two, and then three extrastimuli were introduced at each of three basic drive train cycle lengths (350, 400, and 600 msec) at the right ventricular apex; the procedure was repeated at a second right ventricular site. Six hundred thirty-four electrophysiological tests were performed using one of these two protocols either in the baseline state (293 tests) or during drug testing (341 tests). The yield of sustained, monomorphic VT was 89%1 with the conventional protocol and 92% with the accelerated protocol during baseline tests in patients who had a history of sustained VT (p = 0.5); 20% and 34%, respectively, during baseline tests in patients with a history of nonsustained VT (p = 0.06); and 701% and 77%, respectively, during drug testing (p = 0.2). To induce sustained, monomorphic VT, 10.1 ± 5.0 (mean ± SD) protocol steps and 14.4 ± 8.7 minutes were required with the conventional protocol, compared with 4.0 ± 3.7 steps and 5.6 ± 6.1 minutes with the accelerated protocol (p<0.001 for each comparison). Among the tests in which sustained, monomorphic VT was induced, sustained polymorphic VT or ventricular fibrillation was induced more often with the conventional protocol (3.6%) than with the accelerated protocol (O.9%, p = 0.05). ConclusionsThe efficiency of programmed stimulation can be improved by the early use of a basic drive train cycle length of 350 msec and three extrastimuli. Compared with a conventional stimulation protocol, the accelerated protocol used in this study reduces the number of protocol steps and duration of time required to induce monomorphic VT by an average of more than 50% and improves the specificity of programmed stimulation without impairing the yield of monomorphic VT. (Circulation 1991;83:764–773)

Effect of basic drive cycle length on the yield of ventricular tachycardia during programmed ventricular stimulation

The yield of sustained, monomorphic ventricular tachycardia (VT) induced by programmed ventricular stimulation was compared, using basic drive trains of 400 ms, 600 ms and sinus rhythm, to identify the most efficient sequence of basic drive trains to use during programmed stimulation. Fifty-five patients with coronary artery disease and inducible sustained monomorphic VT not requiring countershock to terminate underwent 81 electrophysiology tests in which 1 to 3 extrastimuli were introduced during sinus rhythm and after basic drive trains of 600 and 400 ms. In 72 electrophysiology tests, sustained, monomorphic VT was induced at the right ventricular apex. The yield of VT using a drive cycle length of 400 ms was 63 of 72 (88%), compared to 46 of 72 (64%) when the drive cycle length was 600 ms, and 23 of 72 (32%) when the extrastimuli were introduced during sinus rhythm (p less than 0.001 for all pairwise comparisons). In 14 electrophysiology tests in which VT was not induced using a 400 ms basic drive cycle length at the apex, the yield of VT was higher using a 400 ms drive cycle length at a second right ventricular site (12 of 14) than with a 600 ms drive cycle length (3 of 12) or sinus rhythm (4 of 12) at the apex (p less than 0.05). The yield of sustained, monomorphic VT induced by 1 to 3 extrastimuli increases as the basic drive cycle length shortens. Whereas programmed stimulation is conventionally started during sinus rhythm or with a drive cycle length of 600 ms, the present results suggest that starting with a drive cycle length of 400 ms may be more efficient.

Effect of the Intertrain Pause on the Ventricular Effective Refractory Period Measured by the Extrastimulus Technique

This study determined the effect of the duration of the intertrain pause on the ventricular elective refractory period (VERP) measured by the extrastimulus technique using conventional eight‐beat basic drive trains. In 50 subjects, the VERP was measured using a basic drive train cycle length of 500 msec, 2‐msec steps in the extrastimulus coupling interval, and intertrain pauses of 0, 1, 4, 8, 20, 40, 60, or 380 seconds. The VERP increased significantly with each stepwise increment in the intertrain pause up to 20 seconds, then reached a plateau. The VERP measured with an intertrain pause of 20 seconds was a mean of 13 msec longer than when measured with a conventional 4‐second pause. The results of this study demonstrate a direct relationship between the VERP and the duration of the pause separating the eight‐beat basic drive trains used to measure the VERP. When the cycle length of the basic drive train is 500 msec, the VERP lengthens as the duration of the intertrain pause increases from 1 to 20 seconds, demonstrating that the basic drive trains exert a cumulative effect on the VERP when the intertrain pause is shorter than 20 seconds. A cumulative effect of the basic drive trains on the VERP is lost when the intertrain pause is 20 seconds or more.

Effect of rate augmentation and isoproterenol on the amplitude of atrial and ventricular electrograms.

Abstract Recent studies have shown a decrease in the amplitude of intracardiac electrograms during exercise in patients with permanent pacemakers. 1–3 However, the mechanism by which exercise decreases the amplitude of the intracardiac electrograms has not been investigated. Because exercise is associated with both an increase in heart rate and an increase in circulating catecholamines, 4,5 the purpose of this study was to determine how these factors influence the amplitude of the atrial and ventricular electrograms.