Stephen Denker

Sustained bundle branch reentry as a mechanism of clinical tachycardia

The incidence of sustained bundle branch reentrant (BBR) tachycardia as a clinical or induced arrhythmia or both continues to be underreported. At our institution, BBR has been the underlying mechanism of sustained monomorphic ventricular tachycardia in approximately 6% of patients, whereas mechanisms unrelated to BBR were the cause in the rest. Data gathered from 20 consecutive patients showed electrophysiologic characteristics that suggest this possibility. These include induction of sustained monomorphic tachycardia with typical left or right bundle branch block morphology or both and atrioventricular dissociation or ventriculoatrial block. On intracardiac electrograms, all previously published criteria for BBR were fulfilled, and in addition, whenever there was a change in the cycle length of tachycardia, the His to His cycle length variation produced similar changes in ventricular activation during subsequent complexes with no relation to the preceding ventricular activation cycles. Compared with patients with ventricular tachycardia due to mechanisms unrelated to BBR, patients with BBR had frequent combination of nonspecific intraventricular conduction defects and prolonged HV intervals (100% vs. 11%, p less than 0.001). When this combination was associated with a tachycardia showing a left bundle branch block pattern, BBR accounted for the majority compared with mechanisms unrelated to BBR (73% vs. 27%, p less than 0.01). The above finding in patients with dilated cardiomyopathy should raise the suspicion of sustained BBR because dilated cardiomyopathy was observed in 95% of the patients with BBR. Twelve of the 20 patients were treated with antiarrhythmic agents, and the other eight were managed by selective catheter ablation of the right bundle branch with electrical energy. Our data suggest that sustained BBR is not an uncommon mechanism of tachycardia; it can be induced readily in the laboratory and is amendable to catheter ablation by the very nature of its circuit. The clinical and electrophysiologic features outlined in this study should enable one to correctly diagnose this important arrhythmia.

Transcatheter electrical ablation of right bundle branch. A method of treating macroreentrant ventricular tachycardia attributed to bundle branch reentry.

The present study describes the clinical and electrophysiological characteristics of sustained bundle branch reentrant ventricular tachycardia treated with electrical ablation of the right bundle branch. Seven patients presented with syncopal episodes, and six of the seven had documented episodes of ventricular tachycardia. All patients had depressed left ventricular ejection fraction with cardiomegaly. Six of the seven had dilated cardiomyopathy in the absence of significant coronary disease. Twelve-lead electrocardiograms in all seven patients during sinus rhythm were remarkably similar; six demonstrated intraventricular conduction defect resembling left bundle branch block, and one showed left anterior fascicular block. All patients showed prolonged His-to-ventricle intervals during sinus rhythm. Sustained ventricular tachycardia (with atrioventricular dissociation) because of bundle branch reentry was induced in all patients during baseline electrophysiological study. The His-to-ventricle intervals during tachycardia were similar to those seen during sinus rhythm. Electrical ablation of the right bundle branch was accomplished in each patient with delivery of two electrical shocks (170-310 J) through electrode catheters. Right bundle branch block developed on their surface electrocardiogram immediately after the ablation. Follow-up electrophysiological studies showed no inducible ventricular tachycardia. Clinical follow-up showed no recurrence of syncope or ventricular tachycardia. From the data presented, the following can be concluded. First, right bundle branch ablation is a safe and promising means of treating ventricular tachycardia because of bundle branch reentry and can obviate the need for antiarrhythmic drug therapy and its frequent undesirable side effects. Second, there are common clinical and electrophysiological characteristics that are frequently seen in patients with this tachycardia, and the recognition of these common characteristics should alert the physician to a bundle branch reentrant mechanism of ventricular tachycardia.

Role of Cardiac Electrophysiologic Studies in Patients with Unexplained Recurrent Syncope

Cardiac electrophysiologic studies (EPS) with programmed electrical stimulation (PES) were performed in 30 patients with recurrent syncope to uncover possible arrhythmic etiology. All patients had undergone thorough medical and neurologic evaluation prior to EPS without finding a definitive cause for syncope. In the majority of patients an arrhythmic etiology for syncope was suspected but could not be documented utilizing the 12‐lead surface ECG, extended in‐hospital and/or ambulatory monitoring (for ≥ 48 hours) and exercise testing prior to the EPS. The studies provided a clue to the possible underlying rhythm disturbance which could have caused syncope in 16/30 patients. Sustained or nonsustained ventricular tachycardia and/or ventricular fibrillation was induced in 11/30, sinus node dysfunction in 4/30 and intra‐His block in the remaining one. Fourteen of the 16 have remained free of symptoms following therapy based on results of EPS during a follow‐up period ranging from 6–30 months (mean 16.5 ± 7.8). In 2/16 syncope recurred (one arrhythmic and one non‐arrhythmic) despite pacemaker therapy for sinus node dysfunction detected during EPS. In the remaining 14/30 patients, EPS and PES did not induce arrhythmia which could account for patient symptomatology and therefore no specific therapy could be recommended. Eleven of these 14 patients experienced a recurrence of symptoms within a 6–25 month period (mean 16.2 ± 6.8). Of the 16 patients with inducible arrhythmias considered clinically significant, 15 had associated structural heart disease. On the other hand, of the 14 patients without clinically significant arrhythmias, structural heart disease could be detected in only three. It is concluded that cardiac arrhythmias constitute a common cause of unexplained syncope, particularly in patients with structural heart disease, and that EPS with PES can uncover the type of arrhythmic disturbance in a significant number of cases.

Facilitation of ventricular tachycardia induction with abrupt changes in ventricular cycle length

The effect of abrupt short-to-long changes in cycle length (CL) on the postulated reentrant circuit of ventricular tachycardia (VT) was evaluated. This was performed using single and double ventricular extrastimuli in a group of 21 patients clinically suspected of having VT in whom VT could not be induced at comparable or shorter constant CLs. A second group of 10 patients without suspected VT was similarly studied. Compared with constant CLs of equal or shorter duration preceding the single or double ventricular extrastimuli, abrupt short-to-long CL changes resulted in (1) initiation of sustained VT in 13 of 21 patients in whom VT could not be induced at constant CLs despite the use of shorter S1S3 by 66 +/- 17 ms; (2) increased incidence of initiation of sustained VT after the V3 phenomenon resulting from macroreentry within the His-Purkinje system (Re-HPS); (3) a small but higher incidence of sustained VT due to sustained Re-HPS; and (4) no induction of sustained or nonsustained VT with either method in the second group of patients. These results provide additional support for reentry as the basis for sustained ventricular tachyarrhythmias. Abrupt short-to-long CL changes may be effective for initiating sustained VT in patients at risk for these arrhythmias.

Useful clinical criteria for the diagnosis of ventricular tachycardia

Misdiagnosis occurs upon initial presentation to medical attention in a considerable number of patients referred for evaluation of wide QRS tachycardia. In order to improve diagnostic accuracy (ventricular versus supraventricular tachycardia), the answers to two key bedside questions were prospectively evaluated: (1) Had the patient experienced a prior myocardial infarction? (2) Did symptoms of tachyarrhythmia start only after the infarction? A patient presenting with a wide QRS tachycardia was considered to have ventricular tachycardia if he or she answered in the affirmative to both of these questions. Of 31 consecutive patients referred with electrocardiographically documented sustained wide QRS tachycardia that was reproduced in the electrophysiology laboratory, the diagnoses made when the patients first presented to medical attention were ventricular tachycardias in 17 patients and supraventricular tachycardias in 14 patients. Following electrophysiologic evaluation, 29 were diagnosed as having ventricular tachycardia and two as supraventricular tachycardia. If the diagnoses were made solely on the basis of responses to the bedside questions mentioned earlier, 28 of the 29 patients having a final diagnosis of ventricular tachycardia would have been correctly identified. It is concluded that the use of these two questions can be very helpful in improving the clinical diagnosis of ventricular tachycardia.

Effects of abrupt changes in cycle length on refractoriness of the His-Purkinje system in man.

Abrupt changes in cycle length (CL) occur frequently in the clinical setting of atrial fibrillation. However, the effects of such changes on the His-Purkinje system (HPS) have not previously been considered during aberrant ventricular conduction (VAb). In 12 patients who manifested VAb with atrial premature stimulation (A2) during sinus rhythm, the relative refractory period (RRP) of the HPS was evaluated during a constant atrial CL (method I) and during abrupt changes in the CL (method II), wherein the A2 was coupled to an atrial CL (last A1A1) comparable to method I. This last A1A1 during method II was preceded by a series of constant atrial CLs 100–200 msec longer (method IIA) in 11 of 12 patients, or 100–300 msec shorter (method IIB) in all 12 patients. Although abrupt changes in the atrial CL using method IIA resulted in a longer HH interval (by 0–30 msec; mean 13.2 ± 9.2 msec) preceding the A2, the RRP-HPS was 5–20 msec shorter (mean 9.3 ± 5.3 msec) compared with method I in eight patients. The effect of abrupt changes was further evaluated in nine patients using method III, with a constant atrial CL, with a duration equal to the last HIH1 interval of method IIA. The VAb that occurred with method III was not manifested with method IIA in seven of nine patients, and in two patients the RRP-HPS was the same or less. Conversely, method IIB resulted in a shorter HH interval (by 0–110 msec; mean 28.9 ± 21.1 msec) preceding A2, but in 10 patients, RRP-HPS was 5–40 msec longer (mean 20.7 ± 10.5 msec) than that of method I and in two, VAb was only manifested using method IB. Further scanning with method III, derived from the HH interval immediately preceding A2 of method IIB, was performed in seven patients and compared with method IIB. Prolongation in the RRP-HPS was shown using the latter method. The results indicate that abrupt changes in CL influence the functional behavior of the HPS in a manner not anticipated. Such changes may have important implications in determining the occurrence of VAb during atrial fibrillation.

Value of preexisting bundle branch block in the electrocardiographic differentiation of supraventricular from ventricular origin of wide QRS tachycardia

The relation between the morphologic configuration of QRS complexes during wide QRS tachycardia induced during electrophysiologic studies and sinus rhythm was examined in 18 patients who had preexisting left or right bundle branch block. Representative QRS complexes during sinus rhythm and during tachycardia were isolated from each patient and juxtaposed for comparison. The QRS complexes that constituted each pair were judged by 4 observers as being identical, different or, if the decision was equivocal, similar. Nine patients had supraventricular tachycardia (SVT). In 8 of the 9 patients, all 4 observers found the QRS complexes during sinus rhythm and SVT identical in morphologic configuration. In the other patient, 2 observers found the QRS complexes identical and 2 found them similar. In 12 patients ventricular tachycardia (VT) was induced. In 11 of these 12, all 4 observers found the QRS complexes during VT different from their respective sinus beats. In the other patient, 3 observers found the QRS complexes different, whereas the fourth found them similar. During SVT, the QRS duration was unchanged from the corresponding value during sinus rhythm, whereas in patients with VT, QRS width increased by a mean of 56 +/- 20 ms (p less than 0.001). The results of our study suggest that the electrocardiographic differentiation of wide QRS tachycardia in patients with preexisting bundle branch block can be accomplished easily and accurately by comparing the QRS complexes during tachycardia with those during sinus rhythm: If the complexes are identical, the tachycardia is supraventricular, but if they are different, the arrhythmia is ventricular in origin.

Divergence between refractoriness of His-Purkinje system and ventricular muscle with abrupt changes in cycle length.

The concept that refractoriness of the His-Purkinje system (HPS) and ventricular muscle both vary directly with cycle length is based on observations during the use of constant cycle length. During abrupt changes in ventricular cycle length, refractoriness of the ventricular muscle is known to reflect the cumulative durations of preceding cycle lengths. The effect of such changes on retrograde refractoriness of the HPS is not known. In this study refractoriness of ventricular muscle and of the HPS was evaluated in 30 patients with normal intraventricular conduction by the ventricular extrastimulus (V2) technique during constant cycle length (method I) and during abrupt cycle length changes (method II). During method II the cycle length immediately before V2 was identical to the constant cycle length of method I and therefore was designated as the reference cycle length (CLR); however, the cycle length preceding (CLP) CLR was either longer than CLR (method IIA) by 100 to 300 msec in 11 patients or shorter than CLR (method IIB) by 100 to 300 msec in 30 patients. Results showed that compared with method I, method IIA shortened the relative refractory period (RRP) of the HPS from 350 +/- 29 to 344 +/- 29 msec (p less than .04), whereas the effective refractory period (ERP) of the ventricular muscle increased from 225 +/- 21 to 233 +/- 20 msec (p less than .0001). In contrast, compared with method I, method IIB lengthened the RRP of the HPS from 335 +/- 30 to 351 +/- 35 msec (p less than .0001), whereas ERP of the ventricular muscle decreased from 223 +/- 23 to 213 +/- 22 msec (p less than .0001). Similar to the inverse relationship between CLP and RRP of the HPS, ERP of the HPS was prolonged with short CLP (method IIB) compared with long CLP (method IIA). The results indicate a marked divergence between refractoriness of the HPS and of ventricular muscle during abrupt cycle length changes; these results were not previously anticipated. Whereas ventricular muscle responded to cumulative effects of preceding cycle lengths and varied directly with CLP, the HPS appeared to respond to directional and/or dynamic changes in cycle length and varied inversely with CLP. Moreover, in contrast to ventricular muscle, the HPS appeared to be responsive to rate of change in cycle length whereby short-to-long change in cycle length had a greater effect than long-to-short change in cycle length.

Atrioventricular nodal conduction and refractoriness after intranodal collision from antegrade and retrograde impulses.

Animal studies have suggested that spontaneous or programmed ventricular beats that occur simultaneously with atrial activation may facilitate atrioventricular (AV) nodal conduction during subsequent atrial impulses. However, this possibility has not been systematically studied in the human heart. In the present study the AV nodal conduction during a programmed atrial premature beat (S2) was analyzed. The S2 was delivered after a series of atrial drive beats (SjSj) of constant duration; this was termed stimulation method I. The results were compared with stimulation method II, which was similar to method I except that a single ventricular beat (Vs) was introduced simultaneously with the last Sl. The longest and shortest possible paced atrial cycle lengths (CLs) were scanned during both methods. Twenty-six patients were studied: 14 with a normal PR and normal intraventricular conduction (NIVC), four with first-degree AV nodal block and NIVC, three with a complete left bundle branch block (LBBB) pattern, three with a complete right bundle branch block (RBBB) pattern, and two with an incomplete RBBB pattern.At the same SlS2 intervals, the AV nodal conduction times (S2112 intervals) were consistently shorter with method II than with method I except in three patients, two with complete RBBB and one with complete LBBB. The magnitude of S2H2 shortening with method II was more pronounced at the shorter basic CLs and shorter SlS2 intervals. During method I, the effective refractory period (ERP) of the AV node was measured in 13 patients, eight with NIVC and five with preexisting bundle branch block. With method II, the ERP of the AV node shortened in all but three patients (one with complete RBBB, one with incomplete RBBB and one with complete LBBB pattern), in whom this variable did not change. The findings suggest that intranodal collison from antegrade and retrograde impulses facilitates AV nodal conduction and shortens the ERP. The magnitude of this change is greater at shorter atrial CLs and is probably related to deeper intranodal penetration of a Vs. The shortening in AV nodal conduction and refractoriness is not noted in patients with bundle branch block when retrograde conduction delay or block in the bundle branches coexists with the antegrade counterpart producing delayed or ineffective input of Vs into the AVnode.

Effect of amiodarone on conduction and refractoriness of the His-Purkinje system in the human heart

Although the antiarrhythmic aspect of amiodarone has been extensively studied, its effects on His-Purkinje system conduction and refractoriness have not been systematically investigated in human beings. In 24 patients, anterograde His-Purkinje system conduction (HV intervals) and variables of His-Purkinje system refractoriness using the ventricular extrastimulus (V2) technique were analyzed before and after long-term therapy with amiodarone. The mean duration of amiodarone therapy at the time of repeat study was 16.2 +/- 7.7 weeks (range 11 to 42). The anterograde His-Purkinje system conduction time (HV interval) measured 49.6 +/- 9.5 ms (range 40 to 80) before and 60.6 +/- 10.7 ms (range 45 to 90) after amiodarone (p less than 0.005). During retrograde refractory period studies, the longest V1V2 interval at which a retrograde His bundle potential (H2) emerged from the V2 electrogram (relative refractory period of the His-Purkinje system) was consistently longer after amiodarone as compared with the control period (376.4 +/- 46.6 versus 318.8 +/- 33.1 ms, p less than 0.005). Similarly, the shortest and longest His-Purkinje system conduction times ( V2H2 interval) at comparable V1V2 intervals were uniformly and significantly prolonged after administration of the drug. Amiodarone also abolished macroreentry in the His-Purkinje system in six of the nine patients who showed such reentry during the control period. The effective refractory period of the ventricular myocardium was also increased from a mean of 227.1 +/- 13.9 to 259.2 +/- 20.2 ms (p less than 0.005) in this series of patients.(ABSTRACT TRUNCATED AT 250 WORDS)