1222 BRIEF REPORTS

Verapamil-Induced Retrograde Conduction Block in a Concealed

Atrioventricular Bypass Tract

MARK ROSENTHAL, MD DANIEL S. OSERAN, MD

ELI GANG, MD ZHAOWEN DENG, MD

WILLIAM J. MANDEL, MD THOMAS PETER, MD

Reentrant supraventricular tachycardia (SVT) using a concealed bypass tract is a relatively common cause of narrow QRS complex tachycardia, accounting for 15 to 30% of cases in patients without evidence of preex- citation on the surface electrocardiogram.’ The slow channel-blocking agent, verapamil, has been effective in the termination of such tachyarrhythmias, primarily through its actions on the atrioventricular node, with little effect on accessory atrioventricular (AV) path- ways.24 This report describes a patient with refractory SVT and a left-sided concealed bypass tract, in whom intravenous verapamil caused retrograde conduction block in the bypass tract.

D.D., a 42-year-old white woman, was referred for evalu- ation of recurrent SVT refractory to pharmacologic sup-

From the Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048. Manuscript received October 1, 1984; revised manuscript received December 17, 1984. accepted December 31, 1984.

pression. Twelve-lead electrocardiograms obtained before admission revealed a normal PR interval and no evidence of ventricular preexcitation. The patient underwent electro- physiologic study using the standard catheter technique and stimulation protocol for evaluation of SVT. During posi- tioning of the coronary sinus catheter, right bundle branch block was induced and persisted for the remainder of the study, Baseline PA, AH and HV intervals were all normal, as were the atria1 and AV nodal effective refractory periods. There was no evidence for dual AV nodal pathways or ven- tricular preexcitation. Sustained episodes of SVT (cycle length 360 ms) ocurred after spontaneous premature ven- tricular depolarizations, as well as after premature atria1 and ventricular extrastimuli introduced during fixed-rate pacing of these respective chambers. During SVT, the pattern of retrograde atria1 activation demonstrated earliest activation in the distal coronary sinus with subsequent sequential ac- tivation of the mid- and proximal coronary sinus, the low right atrium and the high right atrium (Fig. IA). Retrograde preexcitation of the left atrium indicated the presence of a left-sided accessory AV connection capable of conduction only in the retrograde direction. After termination of SVT, right ventricular pacing demonstrated a similar retrograde atria1 activation as during SVT, with 1:l ventriculoatrial (VA) conduction over the accessory pathway (Fig. 1B). The VA conduction time was determined to be 85 ms with no decremental conduction in the bypass tract. The retrograde effective refractory period of the bypass tract was 265 ms.

Ten milligrams of intravenous verapamil were adminis- tered during sinus rhythm. After verapamil, the tachycardia could no longer be initiated with either premature atria1 or ventricular extrastimuli. Right ventricular pacing at mul- tiple cycle lengths revealed abolition of retrograde VA con- duction over the accessory pathway after administration of verapamil (Fig. 2). The patient tolerated the procedure without difficulty and was discharged with 120 mg of verap-

WI

HRA

HBE

CSm

CSd CSd

FIGURE 1. A, atrial activation sequence during supraventricular tachycardia. Simultaneous recordings are shown of surface electrocardiographic leads I, aVF and Vr and intracardiac electrograms from the high right atrium (HRA), His bundle region (HBE) and the mid- and distal coronary sinus (CSm, CSd) at a paper speed of 125 mm/s. SVT is shown with catheter-induced right bundle branch block at a cycle length of 360 ms. Note the sequence of atrial activation with initial activation in the distal coronary sinus followed by CSm, HBE and HRA. Left atrial retrograde preexcitation indicates the presence of a left-sided accessory pathway being used for retrograde conduction in the reentrant circuit. 8, atrial activation sequence during right ventricular pacing at a cycle length of 400 ms. Paper speed is 100 mm/s. Note the 1:l pattern of ventriculoatrlal conduction with the earliest atrial activation in the coronary sinus followed by the His bundle region and high right atrium. This is identical to the pattern of retrograde atrial activation that was seen during SVT and indicates retrograde ventriculoatrial conduction through a left-sided accessory pathway. A = atrial electrogram; H = His bundle electrogram; S, = pacing stimulus artifact; V = ventricular electrogram.

April 15. 1985 THE AMERICAN JOURNAL OF CARDIOLOGY Volume 55 1223

amil every 8 hours and pressure of 90 mm Hg.

Verapamil, a calcium _ _

a well-tolerated systolic blood

channel antagonist, has been reported by several investigators to be efficacious in the termination of reentrant SVTs when administered acutely.2-4 In all reported cases of SVT using an AV bypass tract, whether concealed or with overt Wolff- Parkinson-White syndrome, termination of the ar- rhythmia by verapamil occurred by way of a direct effect on the AV node by increasing the AV node effective refractory period and prolonging AV node conduction time.2-4 In no instance was a significant effect on either anterograde or retrograde conduction properties of the accessory AV pathway noted after acute administration of verapamil. Recently, Horio et al5 described 2 patients with catecholamine-induced ventricular preexcitation, in whom verapamil blocked anterograde conduction in the accessory pathway after catecholamine adminis- tration. Our patient was not given isoproterenol during the study, and therefore, we cannot comment on the relevance of these findings to our case.

This case constitutes the only report of verapamil- induced conduction block in a concealed AV bypass tract. Histologic studies have found anomalous AV connections to be composed of either myocardial fibers or Purkinje cells.6 These cells primarily depend on the fast sodium channel for action potential initiation and propagation and are usually not affected by calcium channel blockade. This case illustrates that concealed bypass tracts may rarely be composed of tissue, either normal or diseased, that uses slow channel conduction for impulse propagation. The exact nature of this tissue remains to be defined. Because most patients with SVT and no evidence of preexcitation never come to elec- trophysiologic study, the findings in this patient may be more widespread among the subset of patients with SVT and a concealed bypass tract, in whom empiric calcium channel antagonist therapy is successful.

Acknowledgment: We thank Brenda Williams, Carol Ginyard and Elizabeth Rose Isidro for assistance in preparing this manuscript and Lance LaForteza for preparation of art- work.

HFIA ““A

HBE

+6oomsec ---cI

FIGURE 2. Loss of retrograde accessory pathway conduction during right ventricular pacing after the administration of intravenous verapamil. Simultaneous recordings from surface electrocardiographic leads I, aVF and VI and intracardiac electrograms from the high right atrium (HRA), His bundle region (HBE), and the mid- and distal coronary sinus (CSm and CSd) at a paper speed of 100 mm/s. This figure demonstrates a loss of ventrlculoatrial conduction during right ventricular pacing at a cycle Ien& of 600 ms. Note the normal anterograds atrial activation sequence of spontaneous sinus beats. Abbreviations as in Figure 1.

References 1. Josephson ME? Sektes S. Clinical Cardiac Electrophysiology. Techniques

and Interpretations. Philadelphia: Lea 8 Febiger. 1979:163. 2. Hamef A, Peter T, Platt M, Yandel WJ. Effects of verapamil on supraven-

tricular tachycardia in patients with overt and concealed Wolff-Parkinson- White syndrome. Am Heart J 1981;101:600-612.

3. Spurrell RAJ, Krlkler DY, Sowton E. Effects of verapamil on electrophysi- ological properties of anomolous atrioventricular connection in Wolff-Par- kinson-White s

f ndrome. Br Heari J 1974;36:256-264.

4. Wellens HJJ, an SL, Frits WHS, Duren DR, Lie KL, Dohmen HM. Effect of verapamil studies by programmed electrical stimulation of the heart in patients with paroxysmal re-entrant supraventricular tachycardia. Br Heart J 1977;39:1056-1066.

5. Horlo Y, Maisuyame K, Morlkaml Y, Rokutanda M, Hirata A, Okumura K, Takaoka A, Uchlda H, Kuglyama K, Arakl S. Blocking effect of verapamil on conduction over a catecholamine-sensitive bypass tract in exercise- induced Wolff-Parkinson-White syndrome. JACC 1984;4:166-191.

6. Anderson RH, Becker AE. Gross anatomy and microscopy of the conducting system. In: Mandel WJ, ed. Cardiac Arrhythmia-Their Mechanisms, Diag- nosis and Management. Philadelphia: J.B. Lippincott, 1960;12-54.

Paradoxical Delay in Accessory Pathway Conduction During Long R-P’

Tachycardia After Interpolated Ventricular Premature Complexes

From the Department of Medicine, Division of Cardiology, Duke Uni- versity Medical Center, Durham, North Carolina. This study was sup ported in part by Research Training Grant HL-07101, SCOR HL-17670, RCDA HL-00546, and HL-15190 from the National lnstiiutes of Health, Bethesda, Maryland. Manuscript received June 4, 1984; revised man- uscript received January 4, 1985, accepted January 5, 1985.

GUST H. BARDY, MD DOUGLAS L. PACKER, MD

LAWRENCE D. GERMAN, MD FERNANDO COLTORTI, MD JOHN J. GALLAGHER, MD

The introduction of a ventricular premature complex (VPC) into reciprocating tachycardia is a technique used to confirm the presence of an accessory ptrioven- tricular (AV) pathway.1-3 Retrograde atria1 preexcita- tion after a VPC introduced during reciprocating tachycardia when the His bundle is refractory to ret- rograde conduction is evidence that an accessory pathway is present.3 The failure of an appropriately