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Sustained ventricular tachycardia due to bundle branch reentry

Elwyn A. Lloyd, Douglas P. Zipes, James J. Heger, and Eric N. Prystowsky. Indianapolis, Ind.

Repetitive ventricular responses thought to be due to bundle branch reentry are induced commonly during programmed ventricular stimulation and are considered to be a physiologic response.’ However, sustained ventric- ular tachycardia due to bundle branch reentry rarely occurs. We have found only one well-documented case report in the English literature.2 The purpose of this report is to present data from a patient in whom we induced ventricular tachycardia that appeared to be due to bundle branch reentry.

A 54-year-old man was referred for further management of recurrent ventricular tachycardia. The diagnosis of congestive cardiomyopathy of unknown origin was first

From the Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine; and the Veterans Administration Medical Center.

Supported by part by the Herman C. Krannert Fund; by Grants HL-06308, HL-07182, and HL-18795 from the National Heart, Lung and Blood Institute of the National Institutes of Health, Bethesda, Md.; by the Attorney General of Indiana Public Health Trust; by the Veterans Administration; and by a Grant-in-Aid from the American Heart Associa- tion, Indiana Affiliate, Inc.

Received for publication June 23, 1982; accepted July 1, 1982.

Reprint requests: Eric N. Prystowsky, M.D., Krannert Institute of Cardi- ology, 1001 W. Tenth St., Indianapolis, IN 46202.

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made 4 years earlier following cardiac catheterization which revealed global left ventricular hypokinesis, left ventricular end-diastolic pressure of 37 mm Hg, cardiac index of 1.7 L/m2, and normal coronary arteries. Antiar- rhythmic therapy was instituted following a syncopal episode due to documented ventricular tachycardia requiring direct current countershock. The patient could not tolerate quinidine, and despite therapy with procain- amide at a dose of 500 mg every 3 hours he continued to have episodes of ventricular tachycardia. Disopyramide was not administered because of poor myocardial func- tion. The patient then was referred for evaluation. Physi- cal examination revealed atria1 fibrillation, cardiomegaly, a third heart sound, and a grade III/VI murmur of mitral regurgitation.

After all antiarrhythmic therapy had been withdrawn for 3 days, the patient underwent an electrophysiologic study using standard techniques.3 Fig. 1 confirms atria1 fibrillation with a ventricular response of approximately 66/min and an HV interval of 50 msec. Fig. 2, A illustrates the response to right ventricular pacing at a cycle length of 600 msec; two premature stimuli (S&S,) are introduced at intervals of 250 (S,S,) and 340 (S,S,) msec and result in retrograde His bundle depolarizations (H,H,) at intervals of 230 msec (S,H,) and 180 msec (S,H,). When S, is introduced with increasing prematurity (Figs. 2, B, and C), it further delays retrograde His bundle depolarization until a critical S,H, interval of 220 msec is reached. Sustained bundle branch reentry ventricular tachycardia then results at a cycle length of 250 msec (240/min) (Fig. 2, panel C; Fig. 3). Of note, each ventricular complex is preceded by a His bundle depolarization with an HV

HBE

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Fig. 1. Scalar electrocardiogram (ECG) and intracardiac electrograms. Atria1 fibrillation is present and the HV interval is 50 msec. Leads 1,11,111, V, = scalar ECG; HBE = His bundle electrogram; RV = right ventricular electrogram.

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1096 Brief Communications November, 1982

Amartcan Heart Journal

Fig. 2. The effect of introducing S, with increasing prematurity (see text). Abbreviations as in Fig. 1.

Fig. 3. Induction of sustained ventricular tachycardia due to bundle branch reentry. Note the His potential before each ventricular complex with an HV interval of 50 msec (compare to Fig. 1). Abbreviations as in Fig. 1.

interval of 50 msec, which is identical to the HV interval of the supraventricular conducted complexes. Ventricular tachytardia lasted for 34 seconds when it was finally terminated by two pacing-induced ventricular extrastimu- li.

Although bundle branch reentry has been clearly dem- onstrated to occur in animaW5 and probably in humans as well,1*6-8 sustained ventricular tachycardia due to bundle branch reentry is a rare event. Of the last 235 patients in

whom ventricular tachycardia has been induced during electrophysiologic studies in our laboratory, only the episode described in this report was considered to be due to bundle branch reentry. The criteria for bundle branch reentry in humans previously described1z7 require that: (1) bundle branch reentrant complexes occur only after a critical S,H, (V,H,) or S,H, (V,H,) delay; (2) the HV interval of the bundle branch reentrant complex equals or exceeds the HV interval of the spontaneous rhythm; and

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Fig. 4. Diagramatic representation of the proposed mechanism of bundle branch reentry. Stimuli introduced with increasing prematurity block retrograde in the right bundle branch and encounter increased conduction delay in the left bundle branch, until finally the delay is long enough for the right bundle branch to have recovered excitability. It is then able to conduct the impulse in an antegrade direction to complete the circuit. AVN = atrioventricular node; RB = right bundle branch; LB 2 left bundle branch.

(3) the QRS morphology of the bundle branch reentrant complex is similar to that of the QRS complex stimulated from the right ventricular apex.

The case described here meets these three require- ments, as does the only other case in the English language literature that we could find.2 Fig. 2 confirms the critical timing of the programmed stimuli required to produce sufficient delay in the retrograde His bundle depolariza- tion. This delay allows adequate time for the right bundle branch to repolarize, so that the retrograde impulse from the left bundle branch can be conducted in an antegrade direction over the right bundle branch and thus establish the reentrant circuit in the left and right bundle branches (Fig. 4). Although the S, produced less retrograde conduc- tion delay than did the SZ, the S, was required to start tachycardia, possibly to shorten the refractory period of the His-Purkinje system. The long refractory period and rapid conduction velocity of the His-Purkinje system probably prevent sustained circuits of bundle branch reentry from occurring and therefore make bundle branch reentry a rare mechanism of ventricular tachycardia in humans and unlikely to be of any great clinical signifi- cance?~ lo REFERENCES

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Farshidi A, Michelson EL, Greenspan AM, Spielman SR, Horowitz LN, Josephson ME: Repetitive responses to ven- tricular extrastimuli: Incidence, mechanism and significance. AM HEART J lOOz59, 1980. Reddy CP, Slack JD: Recurrent ventricular tachycardia: Report of a case with His-bundle branches reentry as the mechanism. Eur J Cardiol 11:23, 1980. Rinkenberger RL, Prystowsky EN, Jackman WM, Naccarelli GV, Heger JJ, Zipes DP: Drug conversion of nonsustained ventricular tachycardia to sustained ventricular tachycardia during serial electrophysiologic studies: Identification of drugs that exacerbate tachycardia and potential mechanisms. AM HEART J 103:177, 1982. Moe GK, Mendez C, Han J: Aberrant AV impulse propaga- tion in the dog heart: A study of functional bundle branch block. Circ Res 16:261, 1965. Glassman RD, Zipes DP: Site of antegrade and retrograde functional right bundle branch block in the intact canine heart. Circulation 64:1277, 1981. Zipes DP, DeJoseph RL, Rothbaum DA: Unusual properties of accessory pathways. Circulation 49:1200, 1974. Akhtar M, Damato AN, Batsford WP, Ruskin JN, Ogunkelu JB, Vargas G: Demonstration of reentry within the His-

Purkinje system in man. Circulation 50:1150, 1974. 8. Naccarelli GV, Prystowsky EN, Jackman WM, Heger JJ,

Rinkenberger RL, Zipes DP: Repetitive ventricular response. Prevalence and prognostic significance. Br Heart J 46:152, 1981.

9. Josephson ME, Horowitz LN, Farshidi A, Kastor JA: Recur- rent sustained ventricular tachycardia. I. Mechanisms. Circu- lation 57:431, 1978.

10. Zipes DP, Foster PR, Troup PJ, Pedersen DH: Atria1 induc- tion of ventricular tachycardia: Reentry versus triggered automaticity. Am J Cardiol 44:1, 1979.

Supraventricular tachycardia associated with nodoventricular and concealed atrioventricular bypass tracts

Bruce B. Lerman, M.D., Harvey L. Waxman, M.D., Alessandro Proclemer, M.D., and Mark E. Josephson, M.D. Philadelphia, Pa.

Anatomically, two types of Mahaim fibers have been described.’ Fasciculoventricular fibers originate from the His bundle or bundle branches while nodoventricular fibers originate from the atrioventricular node. Nodoven- tricular fibers are thought to actively participate in tachyarrhythmias while fasciculoventricular tracts are not.* The true prevalence of nodoventricular accessory connections and their role in tachyarrhythmias may be greater than is generally recognized. This, in part, is related to the fact that the arrhythmias associated with nodoventricular bypass tracts are regular wide complex tachycardias that can be confused with ventricular tachy- cardia. Electrophysiologic differentiation between these

From the Clinical Electrophysiology Laboratory, Hospital of the Universi- ty of Pennsylvania, Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine.

Supported in part by grants from the American Heart Association, Southeastern Pennsylvania Chapter, Philadelphia; and by grants from the National Heart, Lung and Blood Institute, Bethesda, Md.

Received for publication June 24, 1982; accepted July 1, 1982.

Reprint requests: Mark E. Josephson, M.D., Box 683, 656 Ravdin Bldg., Hospital of the University of Pennsylvania, 3400 Spruce St., Philadelphia, PA 19104.

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