Transvenous catheter ablation of the His bundle in ventricular tachycardia

The usefulness of transvenous catheter ablation of the His bundle in three patients with recurrent ventricular tachycardia (VT), in which the initiating mechanism was recognized during a rapid atrial rhythm, is reported. Tachycardia was refractory to conventional treatment and required transthoracic direct-current shocks in all patients. In patient No. 1 double tachycardia (atrial flutter and VT) was documented and VT was easily induced by rapid atrial pacing. In patients Nos. 2 and 3 initiation of VT during junctional reciprocating and atrial tachycardia, respectively, was observed. Interruption of the His bundle was performed by means of fulguration. Stable atrioventricular (AV) block was observed in patient No. 1 after the ablative procedure; patient No. 2 showed anterograde conduction over a posterior septal accessory pathway with no evidence of conduction over the normal conduction system in both the anterograde and retrograde directions. In patient No. 3, transient AV block was observed; AV conduction resumed 2 days later and the cardiac rhythm showed persistent ectopic atrial tachycardia with second-degree AV block. Patients Nos. 1 and 2 underwent pacemaker implantation, but patient No. 2 was not pacemaker dependent. After the procedure, VT no longer occurred in any of the patients (follow-up: 2 years, 5 months, and 6 months). (AM HEART J 111:1106, 1986.)

Giuseppe Critelli, M.D., Marino Scherillo, M.D., Vittorio Monda, M.D., Cristoforo D’Ascia, M.D., Salvatore Musumeci, M.D. and Anita Antignano, M.D. Naples, Italy

The transvenous catheter technique was introduced for ablation of the atrioventricular (AV) junction in patients with drug-refractory supraventricular tachycardia. The original method involved delivery of one or more synchronized direct-current shocks through a catheter electrode positioned in the region of the His bundle,‘f2 thus providing a therapeutic alternative to open-heart surgery. Although the closed-chest ablative technique has also been used for nonsurgical division of both overt and concealed accessory pathways in the Wolff-Parkinson-White syndrome,3-8 as well as for ablation of arrhythmogen- ic tissue in patients with ventricular tachycardia (VT):-” atria1 fibrillation or flutter associated with rapid ventricular response represents the most fre- quent arrhythmias treated by this method.12 We report the usefulness of transvenous catheter abla- tion of the His bundle in three patients with VT in

From the Istituto di 1” Clinica Medica, 2’ Facolt~ di Medicina e Chirurgia, Universitd degli Studi di Napoli.

Supported in part by grant 81.017118.11 from the Consiglio Nazionale delle Ricerche.

Received for publication May 1, 1985; revision received Sept. 18, 1985; accepted Oct. 28, 1986.

Reprint requests: Giuseppe Critelli, M.D., Istituto di Clinica Medical, 2 Policlinico via Sergio Pansini 5, 80131-Napoli, Italia.

which the initiating mechanism was recognized dur- ing a rapid atrial rhythm.

METHODS AND RESULTS

Patient No. 1. A 68-year-old man with a previous myocardial infarction had had recurrent VT since 1979. Episodes of tachycardia occurred every 2 months and were associated with precordial heavy sensation. A pattern of right bundle branch block with left-axis deviation was present during tachycardia; the heart rate ranged from 160 to 180 bpm. An intravenous bolus of 100 mg lidocaine was effective in terminating arrhythmia in all but one instance, which required transthoracic DC shock. Attempts to prevent recurrences of tachycardia by con- ventional oral drugs were unsuccessful.

An electrophysiologic study was performed according to standard protocol. I3 Programmed stimulation from the right ventricular apex with single and double impulses did not induce VT. Ventricular pacing at a cycle length of 300 msec repeatedly initiated arrhythmia. During tachycardia ventriculoatrial dissociation and capture phenomena were present; no His bundle deflection was evident except for the capture beats. All induced tachycardia episodes were terminated by premature ventricular stimulation with double impulse. An antiarrhythmic radiofrequency scan- ning device was implanted. Tachycardia was controlled for 2 years by means of this antiarrhythmic system; a total of 13 spontaneous episodes were converted.

During the subsequent course, double tachycardia was

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observed. Atria1 flutter and VT were simultaneously present (Fig. 1, A), the cycle length of the independent rhythms being 200 and 390 msec, respectively. This finding suggested the possibility that atrial flutter could be the initiating mechanism of VT. In order to verify this hypothesis, a second electrophysiologic study was per- formed. In addition to findings previously obtained, easy inducibility of VT by atrial pacing at a cycle length of 280 msec after atropine administration (1 mg intravenously) was demonstrated (Fig. 1, B). Thus we were encouraged to perform interruption of the His bundle by means of fulguration.1,2 The patient was sedated with intravenous diazepam, and the electrode that showed the largest His bundle deflection was connected to the cathodal output of a standard cardioversion unit, while the anodal output was linked to a back paddle placed adjacent to the left scapula. After delivery of two synchronized shocks (280 J), com- plete AV block resulted and temporary pacing was insti- tuted. The procedure was well tolerated by the patient, and 72 hours later a DVI pacemaker was implanted. During a 2-year follow-up period the patient remained free of tachycardia without any antiarrhythmic medica- tion. However, repeat electrophysiologic evaluation per- formed 6 months after discharge confirmed the inducibil- ity of VT by rapid ventricular pacing.

Patient No. 2. A 52-year-old man had a 15-year history of supraventricular tachycardia which was unresponsive to pharmacologic treatment. He was referred because of recurrent sustained VT. Standard ECG showed “long RP’ tachycardia” with a pattern of previous myocardial infarc- tion (Fig. 2, A). The rate of VT ranged from 160 to 190/min. The arrhythmia was refractory to conventional treatment and had required transthoracic direct-current shock in several instances. Burst ventricular pacing resulted in acceleration of tachycardia (Fig, 2, B). Fre- quent premature ventricular beats and occasional cou- plets were present during sinus rhythm, but initiation of VT was documented only during supraventricular tachy- cardia (Fig. 3).

The endocavitary electrophysiologic study demonstrat- ed that reentry utilizing a concealed posterior accessory pathway with a long conduction time was the underlying mechanism of supraventricular tachycardia. Ventricular arrhythmia could not be evaluated because of the easy inducibility of reciprocating tachycardia by programmed stimulation. Details of electrophysiologic findings con- cerning “long RP’ tachycardia” are reported elsewhere.14

Interruption of the His bundle was accomplished by means of a previously described technique and was direct- ed to prevent supraventricular tachycardia. After a single discharge of 280 J, AV block with junctional escape rhythm at a rate of 62/min was observed and temporary pacing was instituted. Sinus rhythm with Wenckebach type and 2~1 AV block appeared 24 hours after the procedure (Fig. 4, A). Two days later, stable AV conduc- tion with a long PR interval (320 msec) was observed (Fig. 4, B), the QRS configuration (Fig. 4, C) being consistent with posterior septal preexcitation.14 A permanent VVI pacemaker was implanted. After the procedure, neither

Fig. 1. Patient No. 1. A, Coexistence of VT and atrial flutter. Atria1 electrogram (RA) demonstrates that the two rhythms are dissociated (dashed lines). B, Induction of VT by atria1 pacing at a cycle length of 280 msec. HB = His bundle electrogram; RV = right ventricle elec- trogram; ES0 = transesophageal atrial electrogram; St = stimulus artifact; numbers are in milliseconds.

supraventricular nor ventricular tachycardia occurred, in spite of inducibility of VT by rapid ventricular pacing. The patient developed a ventricular aneurysm as a result of the myocardial infarction and died suddenly 5 months after His bundle ablation. Postmortem examination of the heart was performed. The left anterior descending coro- nary artery showed atherosclerotic obstruction 1.5 cm from its origin; there was a healed anterior myocardial infarction with aneurysmatic dilatation. A recent throm- botic occlusion of the distal right coronary artery with subacute posterior apical myocardial infarction was also found. Serial sections of the AV junctional tissue demon- strated a scar process replacing the AV node and the penetrating His bundle. I5 The presence of a posterior septal accessory pathway, as documented during the patient’s life, was confirmed by histologic studies.ls

Patient No. 3. A 74-year-old woman with a previous myocardial infarction had had frequent episodes of VT with syncope. She had also experienced paroxysmal supra- ventricular tachyarrhythmias for many years. At the time of admission to the hospital, ECG monitoring showed atria1 flutter with 2:l AV conduction. During the subse- quent course, ectopic atrial tachycardia was frequently observed. Decrease in cycle length to 280 msec repeatedly initiated VT (Fig. 5, A) with severe hemodynamic imbal- ance requiring external direct-current shock. All pharma-

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B BURST PACING

CL 200 . -

Fig. 2. Patient No. 2. A, Long RP’ tachycardia with QRS pattern of anterior myocardial infarction. B, Burst ventricular pacing at a cycle length of 200 msec resulting in acceleration of VT.

Fig. 3. Patient No. 2. In spite of frequent premature ventricular beats, VT starts during supraventricular tachycardia. (See text for discussion.)

cologic attempts to restore sinus rhythm and reduce ventricular rate were unsuccessful.

Transesophageal electrogram recorded during VT allowed recognition of the presence of two independent ‘tachyarrhythmias, atria1 and ventricular tachycardias, with cycle lengths of 240 and 400 msec, respectively, being evident (Fig. 5, B). Transthoracic direct-current shock was administered resulting in termination of VT with persis- tance of atria1 tachycardia.

Two electrode catheters were positioned in the right ventricular apex and in the region of the His bundle. Complete AV block was obtained after delivery of three shocks (320 J each) through the catheter positioned in the AV junctional area (Fig. 5, C). The rate of the escape rhythm was 32/min, the QRS configuration showing a pattern of right bundle branch block. Atria1 tachycardia was still present. Temporary ventricular pacing was insti- tuted. Two days later, AV conduction resumed and the cardiac rhythm showed persistent ectopic atria1 tachycar- dia with Wenckebach-type AV block. Sudden increase in atria1 rate, as observed before the shock, frequently occurred but P waves were blocked when the atria1 cycle length was equal to or less than 340 msec (Fig. 6). Mean ventricular rate was lOO/min. VT no longer occurred and the patient was discharged on no antiarrhythmic medica- tion; during the follow-up (6 months) she remained free of VT. The patient refused a repeat electrophysiologic study,

so that the inducibility of VT after the ablative procedure was not evaluated. Transtelephonic ECG recordings con- firmed chronic atria1 tachycardia with moderate ventricu- lar response due to AV block at faster atria1 rates.

DISCUSSION

Direct surgical techniques are the most rational therapeutic approach in VT refractory to pharmaco- logic treatment. l6 However, such procedures are not advisable in patients with severe hemodynamic imbalance because of the morbidity associated with thoracotomy and heart-lung bypass. Catheter abla- tion of the arrhythmogenic zone was recently devised:-I’ but the safety and efficacy of this tech- nique need to be defined.

This report demonstrates that closed-chest abla- tion of the His bundle might be useful in patients with chronic recurrent VT, provided that a rapid atrial rhythm is recognized as the initiating mecha- nism. In the first patient, this was suggested by the occasional finding of simultaneous atrial flutter and VT, and was subsequently demonstrated by the easy inducibility of the latter arrhythmia by atrial pac- ing, while premature ventricular stimulation was ineffective. In patients Nos. 2 and 3, initiation of VT

Volume 111 Number 6 Catheter ablation of His bundle in VT 1109

Fig. 4. Patient No. 2. ECG recordings obtained after closed-chest ablation of His bundle. A, Wenckebach type and 2: 1 AV block is present 24 hours after the procedure. B, Stable sinus rhythm with a long PR interval is observed 2 days later, the QRS configuration being consistent with posterior septal preexcitation (C).

Fig. 5. Patient No. 3. A, Decrease in cycle length (280 msec) during atria1 tachycardia repeatedly induces VT. B, Transesophageal atria1 electrogram demonstrates the presence of double tachycardia. C, After His bundle ablation complete AV block with persistence of atria1 tachycardia is evident. C = capture beat. Numbers are in milliseconds.

during junctional reciprocating and atria1 tachycar- dia, respectively, was observed. Two mechanisms could be invoked in order to explain precipitation of VT during supraventricular tachyarrhythmias in our patients: (1) triggered automaticity as a result of increased afterdepolarizations or (2) ventricular reentry initiated by inhomogeneity of electrophysio- logic properties induced by rapid atria1 rhythm. Once the initiating mechanism was neutralized by means of the ablative procedure, VT no longer occurred in any of the three patients.

In patients Nos. 2 and 3 the procedure did not result in pacemaker dependence. In one of them activation of the ventricles occurred by anterograde conduction over the accessory pathway with decre- mental properties; in the other one, only partial damage of the AV junctional area resulted and conduction remained unimpaired, except for the shortest atria1 cycles.

Concerning the sudden death that occurred in patient No. 2, we believe that postinfarction aneu- rysm could have constituted the substrate of a

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mean ventricular rate: 100bpm

Fig. 6. Patient No. 3. ECG recordings obtained 20 days after His bundle ablation. Atria1 tachycardia with different degrees of AV block and occasional junctional escape rhythm (first four beats) is present. Decrease in atria1 cycle length to 340 msec or less results in block of the P wave. (See text for discussion.)

Fig. 7. EGG recording obtained from a patient who died suddenly during Holter monitoring. In spite of the pres- ence of frequent premature ventricular beats, initiation of ventricular flutter is observed during sinus tachycardia. (See text for discussion.)

catastrophic arrhythmia. Indeed, electrical instabili- ty has been observed with rapid ventricular pacing performed in an attempt to terminate VT. On the other hand, asystole caused by pacemaker failure should be considered unlikely in this patient. In fact, during transient AV block recorded just after the shock, the QRS structure of the escape rhythm was similar to that seen before the procedure (heart rate 62 bpm). This suggested the proximal location in the His bundle of a subsidiary pacemaker. No lesion of the branching His bundle, as shown by pathologic examination, confirmed the proximal location of the potential escape rhythm. In addition, during follow- up, the ECG showed stable sinus rhythm with 1: 1 AV conduction, although the PR interval was long.

A growing body of literature suggests that rapid atria1 rhythms might be responsible for precipita-

tion of VT more frequently than is currently believed, as discussed in the following three situa- tions.

Double tachycardia. The occurrence of simulta- neous atria1 and ventricular tachycardia, either in the presence of digitalis toxicity or in patients with coronary artery disease,17-20 is reported and regarded as rare and fortuitous. Nevertheless, the low inci- dence of double tachycardia could be the result of difficulty in recognizing atria1 activity during rapid ventricular rate. In the absence of an endocavitary atrial electrogram, the atrial arrhythmia can be obscured by VT; indeed, the exisistence of indepen- dent rhythms is often diagnosed after conversion of one of the two.17 In addition, as observed in our patients, a causal relationship may exist in double tachycardia, the high atrial rate being likely respon- sible for initiation of VT. Triggered automaticity might be the mechanism in the presence of digitalis toxicityzl; in our patients who had coronary artery disease the same mechanism as well as ventricular reentry induced by atria1 tachycardia could be invoked.

Induction of VT by atrial pacing, exercise, and isopro- terenol. Atrially induced VT by premature or rapid pacing133 22-27 and exercise-triggered VT27*28-30 are not infrequent in patients either with or without demon- strable heart disease. Furthermore, a high incidence of VT induction by isoproterenol-provoked sinus tachycardia was recently reported in both catego- ries.27g30 Notably, the absence of chest pain or repo- larization changes suggests that VT induced by provocative tests is rate dependent rather than ischemic in origin. Therefore, an increase in atrial rate-either induced or occurring spontaneously- may precipitate VT when the refractory period of the ventricles exceeds that of the AV conduction system. According to the data of Buxton et a1.,27 the incidence of VT induction in patients with and

Volume 111 Number 6 Catheter ablation of His bundle in VT 1111

without coronary artery disease is higher with iso- proterenol (83 % and 63%) respectively) than with exercise (50% and 61% ) or atria1 pacing (20% and 18%). The remarkable difference between the effec- tiveness of isoproterenol and atria1 pacing might be explained on the basis of their opposite effects on the refractoriness and conduction velocity of the AV node. The efficacy of isoproterenol in reproducing arrhythmias in patients with exercise-triggered VT-both tests resulting in an increase in sinus rate with enhancement of AV conduction-has also been reported.2s,31*32 Although such findings are usually observed in the absence of organic heart disease, it is conceivable that in patients with coronary artery disease and chronic recurrent VT an ectopic atrial rhythm as well as a critical increase of sinus rate may precipitate a clinical arrhythmia if some physi- ologic condition involving an increment of adrener- gic tone occurs. It is difficult to know the incidence of such a mechanism because of the impossibility of documenting the onset of arrhythmia in free-living subjects; thus our hypothesis is quite speculative. However, one may presume that rapid atrial rhythms occur more frequently than two or more premature ventricular beats (with proper coupling interval), which should replicate the most effective pacing mode for initiation of VT.32 In Fig. 7 an ECG recording taken from a patient who died suddenly during Holter monitoring is reported; in spite of frequent premature ventricular beats, ventricular flutter is precipitated by sinus rate increase.

Prevention of exercise-triggered VT in patients without obvious heart disease can be obtained by verapami1,2s a potent inhibitor of the inward calcium current. Nevertheless, in patients with coronary artery disease, spontaneous or exercise-induced VT can be prevented by using either verapamil or other drugs (type 1A agents, propranolol, amioda- rone).27~30,34~35 This suggests that the effectiveness of pharmacologic therapy in preventing VT might result from disparate nonspecific electrophysiologic effects, possibly including prevention of high sinus rates, suppression of ectopic atria1 activity, and depression of AV conduction. Indeed, a high respon- siveness to different antiarrhythmic drugs was recently observed in patients with a high incidence of VT induction by rapid atrial pacing, exercise, and isoproterenol.27

Pharmacologic therapy as assessed by programmed ventricular stimulation. An effective drug regimen in chronic recurrent VT is usually defined by pro- grammed ventricular stimulation. However, in spite of the general agreement about the clinical relevance of the induced arrhythmia, the specificity of the

method has been questioned, and discordant results of pharmacologic therapy, as assessed by means of stimulation protocol, are reported. In fact, it is well known that during a given treatment patients can be protected from recurrence of clinical tachycardia in spite of the inducibility of the arrhythmia,27,34s35 while suppression of the inducibility during phar- macologic therapy does not exclude clinical recur- rence.35 Thus, programmed ventricular stimulation is a means of inducing tachycardia but does not necessarily reproduce the natural mechanism which precipitates arrhythmia in individual patients. Since discordant electropharmacologic results have been observed during amiodarone treatment,34z 35 rapid atrial rate may be suspected of being the initiating mechanism in some instances. In some cases, it could be possible to ascribe the therapeutic results to prevention of sinus tachycardia or ectopic atria1 rhythms and/or inhibition of AV conduction. Indeed, all of these effects can potentially prevent VT due to either reentry or triggered activity. This hypothesis could be verified by retrospectively eval- uating, in a single patient, the inducibility of VT by atrial pacing, exercise, and isoproterenol before treatment. Conversely, in patients with clinical recurrences despite suppression of inducibility after treatment, the possible initiating role of atrial mech- anism should be investigated. In this connection, there are no available data. Actually, atria1 induc- tion of VT in patients with ischemic heart disease is not systematically performed and the inducibility of the arrhythmia in a single case is usually stated without taking into account the site and modality of stimulation.

Clinical implications. Recognition of rapid atria1 rhythm as the predominant precipitating mecha- nism for VT is advisable. In such instances, drug therapy could be helpfully addressed against fast atrial rates and AV conduction rather than toward premature ventricular beats or tachycardia induc- ibility by programmed ventricular stimulation. In some cases, closed-chest ablation of the His bundle could be considered in order to avoid pharmacologic side effects, including the arrhythmogenic ones.

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