Prognosis in patients with intra-Hisian conduction disturbances

449

International Journal of Cardiology, 5 (1984) 449-457 Elsevier

IJC 00114

Prognosis in patients with intra-Hisian conduction disturbances Bruce B. Lerman, Francis E. Marchlinski I, Francis C. Kempf *, Alfred E. Buxton 3, Harvey L. Waxman, Mark E. Josephson 4 Clinical ElecirophysiologV Laboratory, Hospital of the University of Pennsylvania, Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania (Received

29 June 1983; second revision received and accepted

19 October

1983)

Lerman BB, Marchlinski FE, Kempf FC, Buxton AE, Waxman HL, Josephson ME. Prognosis in patients with intra-Hisian conduction disturbances. Int J Cardiol 1984; 5 1449-457. Intra-Hisian delay is usually associated with fascicular conduction abnormalities. We report our experience in 23 patients who had i&a-Hisian delay as their only conduction defect. First-degree intra-Hisian delay (His bundle deflection 2 30 msec) was present in 17 patients, 5 of whom also had split His potentials. Three of these patients received permanent pacemakers, all of whom had a history of syncope. Higher degrees of intra-Hisian delay were observed either spontaneously or in response to atrial pacing in 6 patients. Five of these patients were treated with permanent pacing, 4 of whom had symptomatic bradyarrhythmias and/or syncope. No patient has had a recurrence of symptoms following pacemaker insertion during the mean 31-month follow-up. No patient with first-degree intra-Hisian delay not receiving a pacemaker developed symptomatic bradyarrhythmias or syncope during a mean follow-up of 21 months. ’ Supported by the University of Pennsylvania Department of Medicine Measey Foundation. * Supported by National Institutional Training Grant No. HL07346, National Heart, Lung, and Blood Institute, Bethesda, MD. 3 Recipient of Research Service Award No. HL07201, National Heart, Lung, and Blood Institute, Bethesda, MD. 4 Recipient of Research Career Development Award No. HLO0361, National Heart, Lung, and Blood Institute, Bethesda, MD. Dr. Josephson is the Robinette Foundation Associate Professor of Medicine (Cardiovascular Diseases). Supported in part by grants from the American Heart Association, Southeastern Pennsylvania Chapter, Philadelphia, Pennsylvania, and National Heart, Lung and Blood Institute, Bethesda, Maryland (No. ROl HL24278). Reprint requests to: Francis E. Marchlinski, M.D., Hospital of the University of Pennsylvania, Clinical Electrophysiology Laboratory, Ravdin Building, 6th Floor, 3400 Spruce Street, Philadelphia, PA 19104, U.S.A.

0167-5273/84/$03.00

0 1984 Elsevier Science Publishers

B.V.

450

We conclude that first-degree intra-Hisian delay has a favorable short-term prognosis and is not associated with progression of symptomatic conduction disease. Data, however, are insufficient to draw firm conclusions regarding the significance of higher degrees of intra-Hisian delay. Prior documentation of intermittent heart block or recurrent syncope in the majority of these patients, nevertheless, suggests that they may be at risk for developing symptomatic bradyarrhythmias.

Introduction Electrophysiologic recognition of intra-Hisian conduction disturbances was first reported in 1970 [l]. Since then, several reports have discussed the significance and treatment of intra-Hisian delay [2-61. In many of these cases, however, intra-Hisian block was frequently associated with bundle branch block. Furthermore, recommendations regarding indications for pacemaker insertion have often been contradictory [4-61. This study examines the prognosis associated with various degrees of intra-Hisian delay unassociated with bundle branch block. In particular, the clinical significance of first-degree intra-Hisian conduction delay is addressed. Methods Patients (Table 1) Twenty-three patients undergoing electrophysiologic evaluation at the Hospital of the University of Pennsylvania demonstrated intra-Hisian conduction delay without associated bundle branch block. There were 13 men and 10 women with a mean age of 53 years (range 23 to 74 years). Fourteen patients had coronary artery disease, including 6 with ventricular aneurysm. Three patients had valvular disease, including one with mitral stenosis, one with mitral valve prolapse, and one patient was status post aortic valve replacement for aortic stenosis. Other cardiac diagnoses were idiopathic congestive cardiomyopathy in one patient, and non-obstructive asymmetric septal hypertrophy in another. Four patients had no clinical evidence of organic heart disease and had normal echocardiographic, radionuclide, and/or coronary arteriographic studies. Indications for electrophysiologic study included symptomatic ventricular tachycardia in 11 patients, documented intermittent heart block in three, syncope without an associated documented arrhythmia in five, refractory paroxysmal atrial fibrillation in two and recurrent palpitations in one patient. In addition, one patient was studied for evaluation of distal conduction disease after developing transient bifascicular block complicating an acute myocardial infarction. Definitions First-Degree Intra-Hisian Block. Intra-Hisian conduction duration 2 30 msec [7,8]. The onset of His bundle activity was measured from the initial fast or slow depolarization that deviated from the baseline recording. This appears as either a broad His spike or “split” (two or more) His potential.

451 TABLE Patient

1 characteristics.

Case No.

Age/Sex

Cardiac diagnosis

Indication

for EPS

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23

40F 72 F 67 F 51 M 63 M 61 M 65 F 68 M 14 F 38 M 34 F 61 M 43 M 55 M 39 M 67 M 50 M 50 F 23 M 21 F 48 M 65 F 59 F

MS ASH CAD CAD AS CAD, LVAN CAD, LVAN CAD, LVAN CAD CAD Normal CAD CAD CAD CAD, LVAN CAD, LVAN CAD Normal MVP CM Normal CAD, LVAN Normal

VT Syncope Syncope VT Bradyarrhythmia Syncope VT VT Bradyarrhythmia VT VEA and palpitations VT Syncope VT BFB with MI VT VT Syncope Paroxysmal AF VT Paroxysmal AF VT Bradyarrhythmia

AF = atria1 fibrillation; AS = aortic stenosis; ASH = asymmetric septal hypertrophy; BFB with MI = bifascicular block with myocardial infarction; CAD = coronary artery disease; CM = cardiomyopathy; EPS = electrophysiologic study; LVAN = left ventricular aneurysm; MS = mitral stenosis; MVP = mitral valve prolapse; VEA = ventricular ectopic activity; VT = ventricular tachycardia.

Second-Degree In&a-His&m Block. Block occurring between the proximal and distal His bundle potentials. Type I block is manifested by Wenckebach periodicity. Type II block is manifested by abrupt failure to conduct without prior progressive H-H’ prolongation. Third-Degree Intra-Hisian Block. Complete heart block occurring within the His bundle. The atria1 to proximal complexes are dissociated from the distal His-ventricular complexes. Electrophysiologic

Study

Electrophysiologic studies were performed in the nonsedated, postabsorptive state after informed consent had been obtained. All antiarrhythmic drugs were discontinued at least five half-lives prior to electrophysiologic study. Routinely, three quadripolar and one tripolar catheter were inserted percutaneously or by cutdown

452

and advanced under fluoroscopic guidance into the high right atrium, coronary sinus, right ventricular apex and atrioventricular junction, respectively. Split His potentials were sought by recording from the distal and proximal pair of electrodes of the tripolar catheter and by recording electrograms at various positions across the tricuspid valve. In ambiguous cases, a proximal His potential was distinguished from the terminal portion of an atria1 defection by altering atrioventricular nodal conduction (AH interval) with either atria1 pacing and/or vagal stimulation. A distal His potential (H’), when observed, was distinguished from a right bundle branch potential by requiring it to precede the onset of the surface QRS activation by at least 30 msec. The pair of electrodes (10 mm interelectrode distance) of the tripolar catheter that provided the most consistent and stable proximal His potential was used to record His bundle activation throughout the study. Intracardiac recordings were filtered at 30 to 500 Hz and simultaneously displayed with three electrocardiographic leads on a multi-channel oscilloscope (Electronics for Medicine VR-16, White Plains, NY). The data were stored on magnetic tape (Honeywell 1Cchannel analog tape recorder) and later retrieved on photographic paper at speeds of 100 to 250 mm/set for illustrative purposes. Real-time recordings were made with an ink jet recorder (Siemens Elema Mingograph). Programmed stimulation was performed from several atria1 and ventricular sites using a stimulation protocol previously reported and included the introduction of extrastimuli during sinus rhythm and at multiple paced cycle lengths [8]. Stimuli were delivered as rectangular pulses, 1 msec in duration at twice diastolic threshold. Stimulation was performed using a specially designed programmable stimulator with an optically isolated constant current source (Bloom Associates Ltd, Narberth, PA). Follow-up and Data Analysis Follow-up information was obtained at the time of revisit to the Arrhythmia Evaluation Center at the Hospital of the University of Pennsylvania or by telephone contact with the patient and the patient’s private physician. All numerical values are expressed as mean k SD unless otherwise specified. Results Surface Electrocardiography

(Table 2)

The mean PR interval was 174 f 44 msec. Only two patients (Cases 5, 16) had prolonged PR intervals, 350 msec and 210 msec, respectively. The mean QRS duration was 90 k 13 msec. No patient demonstrated evidence of right or left bundle branch block or intraventricular conduction delay. Results of Electrophysiologic Testing (Table 2) The mean AH interval was 86 k 23 msec (normal, 60-125 msec). In all patients the AH interval was the normal except for one in whom the AH interval was 140 msec (Case 3). The mean HV interval was 68 k 35 msec (range 35 to 205 msec). The

2

A flutter = atria1 flutter; A pacing VT = ventricular tachycardia.

80 90 140 65 120 115 80 90 120 108 90 67 75 75 80 90 60 60 90 74 50 60 95

loo 80 80 110 90 100 95 110 80 85 105 95 95 85 75 85 105 60 95 85 70 90 100

180 160 170 160 350 190 160 140 170 180 155 180 135 190 180 210 140 140 180 130 135 180 190

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23

AF = atria1 fibrillation; ventricular tachycardia;

AH (60-125 msec)

QRS (msec)

PR

(mW

features.

and electrophysiologic

Case No.

Electrocardiographic

TABLE

= atrial pacing;

50 52 60 55 205 62 45 100 35 55 48 70 53 65 68 120 58 55 35 46 50 85 70

HV (35-55 (msec)

EPS = electrophysiologic

30 15 40 30 165 30 20 70 20 30 30 30 30 30 30 70 30 30 30 30 30 45 35

Intra-Hisian duration (lo-29 msec)

study;

No No No No No No Yes No No No No No No Yes

No

Yes Yes Yes No No Yes

IHB = intra-Hisian

block;

Type 1

Type 1

Type 1 Type 2

2’ IHB 2” IHB No No 2” IHB No 2’ IHB No 3” IHB No No No No No No No No No No No No No No

No No

IHB with A pacing

Split His

NSVT = non-sustained

VT None None None None None VT VT None VT A flutter VT VT None None NSVT VT None A flutter VT AF VT Spontaneous 2’ IHB Type 2

Other EPS findings

R w

454

three patients (Cases 5, 8, 16) who had HV intervals > 100 msec demonstrated split His potentials with intra-Hisian conduction intervals 2 70 msec. In each of these three patients, the H’V duration was 2 50 msec, indicating that the major contribution to HV prolongation was due to intra-Hisian conduction delay. Of note, both patients with PR prolongation recorded on surface electrocardiograms had normal AV nodal conduction times (Cases 5, 16). HV prolongation confined to intra-Hisian conduction delay accounted for the prolonged PR intervals in these two patients. First-degree intra-Hisian block was the highest degree of intra-Hisian conduction delay in 17 patients. The mean intra-Hisian duration in this group was 36 + 13 msec (range 30-70 msec). Five of these patients also demonstrated split His potentials, one of which was pacing induced. Five patients developed second- or third-degree intra-Hisian block in response to atria1 pacing. Second-degree intra-Hisian block (Type 1) was induced in three patients (Cases 1, 5, 7), second-degree intra-Hisian block (Type 2) in one patient (Case 2), and third-degree intra-Hisian block in one patient (Case 9). In addition, spontaneous 2 : 1 intra-Hisian block occurred in one individual (Case 23) (Fig. 1). A normal PR interval and narrow QRS complex were present during conducted beats in this patient. 1

hh

1

.L

Fig. 1. Intracardiac recording of spontaneous 2 :l intra-Hisian block. Block occurs between the proximal His bundle deflection (H) and the distal His deflection (H’). Surface electrocardiographic leads 1, aVF and V, and intracardiac recordings from the high right atrium (HRA), mid-right atrium (MRA) and His bundle region (HBE) are shown. See text for discussion.

455

Other electrophysiologic findings (Table 2) included induction of sustained ventricular tachycardia in nine patients, eight of whom had clinical ventricular tachycardia; the other had a history of syncope. Nonsustained ventricular tachycardia was induced in one patient, while atria1 flutter/fibrillation was induced in three patients. Ten patients had no other significant electrophysiologic findings other than intra-Hisian conduction delay. Treatment and Follow-up First-Degree Intra-Hisian Block. Three of 17 patients (Cases 3, 13, 18) who had first-degree intra-Hisian block, each of whom had a history of recurrent syncope, received permanent pacemakers. The follow-up period for these three patients has been 11, 26, and 5 months, respectively. One of these patients (Case 13) was also discharged on amiodarone for treatment of recurrent sustained ventricular tachycardia. All three patients have been asymptomatic. The remaining 14 patients with first-degree intra-Hisian block who did not receive pacemaker therapy have been followed for 21 months. (range 1 to 59 months). One patient with recurrent ventricular tachycardia who was treated with quinidine died suddenly one month after discharge. The remaining 13 patients have had no symptomatic bradyarrhythmias or syncope. Only one of these patients experienced syncope prior to study. Second- and Third-Degree Intra-Hisian Block. Five of 6 patients with either spontaneous or pacing induced second- or third-degree intra-Hisian block received permanent pacemakers. Three of these patients demonstrated symptomatic intermittent heart block prior to implantation; one had recurrent syncope and the remaining two were studied for ventricular tachycardia. The mean follow-up has been 31 months (range 18 to 54 months). All patients with second-degree intra-Hisian block receiving pacemaker therapy have remained asymptomatic during this period except one (Case 1). This patient had inducible sustained ventricular tachycardia and was discharged on disopyramide at a dose which had prevented induction. Twenty-two months following discharge the patient died suddenly. One patient with pacing induced second-degree intra-Hisian block did not receive a permanent pacemaker. Inducible sustained ventricular tachycardia was treated with procainamide. This patient had been asymptomatic and arrhythmia free during the 33-month follow-up period.

Discussion Pathological studies in humans have shown that intra-Hisian disease can be caused by fibrotic changes in the distal His bundle and by calcium deposition within the His bundle in association with calcific aortic stenosis [9,10]. Complete atrioventricular block complicating an inferior wall myocardial infarction has been shown to occur within the bundle of His [ll]. In this study the majority of patients had underlying coronary artery disease as the possible pathological substrate for their intra-Hisian conduction delay.

456

ECG Identification Scalar electrocardiography provides few clues as to the presence of intra-Hisian block. Patients with first-degree intra-Hisian block may have either normal or prolonged PR intervals [5]. Only two patients in our study with first-degree intra-HiSian block demonstrated prolonged PR intervals. Intracardiac recordings showed the site of block to be intra-Hisian as both AV nodal and H’V conduction times were normal. Second-degree intra-Hisian block is usually associated with a narrow QRS complex. The one patient in our study with spontaneous second-degree 2 : 1 intraHisian block had a PR interval of 190 msec and a narrow QRS complex during conducted beats (Case 23). All patients with pacing induced high-degree intra-Hisian block maintained a narrow QRS complex. First-Degree Block Second- and third-degree intra-Hisian block is relatively common, occurring in approximately 15% to 20% of all cases of second- or third-degree heart block [3,8,12]. However, experience with isolated first-degree intra-Hisian block is limited and only one study has examined its prognostic significance [6]. Most patients included in that study had other conduction disease abnormalities. The current study includes 17 patients with first-degree intra-Hisian block as their only conduction defect. The data suggest that asymptomatic first-degree intra-Hisian block is not associated with the development of symptomatic bradyarrhythmias during the mean follow-up period of 21 months. Therefore, prophylactic treatment with permanent pacing is not indicated in this group of patients. Pacemaker Treatment Treatment with permanent pacing may be of benefit in those patients in whom higher degrees of intra-Hisian block are uncovered by atria1 pacing, although the data are insufficient to draw firm conclusions. These patients may have either normal or prolonged intra-Hisian conduction intervals during sinus rhythm. Three of the five patients who developed second- or third-degree intra-Hisian block in response to atria1 pacing had a documented history of symptomatic intermittent heart block or recurrent syncope. Most studies have examined only those patients with spontaneous second- or third-degree intra-Hisian block and have recommended pacemaker implantation because of the observation that second-degree block progresses to third-degree block and the frequent association of higher degrees of block with symptoms of syncope and dizziness [4,5]. Conclusions The finding of isolated first-degree prognosis. Therefore, asymptomatic

intra-Hisian delay is associated with a benign patients do not require permanent pacing.

457

Atria1 pacing may uncover latent second- or third-degree intra-Hisian block. The prognostic significance of this finding is uncertain. However, documentation of intermittent heart block or recurrent syncope in three of five patients demonstrating this finding suggests that these patients may be at high risk for developing symptomatic bradyarrhythmias.

References 1 Narula OS, Samet P. Wenckebach and Mobitz type II A-V block due to block within the His bundle and bundle branches. Circulation 1970;41:947-965. 2 Schuilenburg RM, Durrer D. Problems in the recognition of conduction disturbances in the His bundle. Circulation 197S;S1:68-74. 3 Rosen KM, Dhingra RC, Loeb HS, Rahimtoola SH. Chronic heart block in adults. Arch Intern Med 1973;131:663-672. 4 Gupta PK, Lichstein E, Chadda KD. Chronic His bundle block. Clinical, electrocardiographic, electrophysiological and follow-up studies on 16 patients. Br Heart J 1976;38:1343-1349. 5 Amat-y-Leon F, Dhingra R, Denes P, et al. The clinical spectrum of chronic His bundle block. Chest 1976;70:747-754. 6 McAnuIty JH, Murphy E, Rahimtoola SH. A prospective evaluation of intrahisian conduction delay. Circulation 1979;59:103S-1039. 7 Narula OS, Scherlag BJ, Samet P, Javier RP. Atrioventricular block: localization and classification by His bundle recordings. Am J Med 1971;50:146-152. 8 Josephson ME, &ides SR. Clinical cardiac electrophysiology. Techniques and interpretations. Philadelphia: Lea & Febiger, 1979;1Sl-155, 217-229, 251-252. 9 Rosen KM, Rahimtoola SH, Gunnar RH, Lev M. Transient and persistent atria1 standstill with His bundle lesions: electrophysiologic and pathologic correlations. Circulation 1971;44:220-236. 10 Bharati S, Lev M, Wu D, Denes P, Dhingra R, Rosen KM. Pathophysiologic correlations in two cases of split His bundle potentials. Circulation 1974;49:615-623. 11 Rosen KM, Loeb HS, Chuquimia R, Sinno MZ, Rabimtoola SH, Gunnar RM. Site of heart block in acute myocardial infarction. Circulation 1970;42:925-933. 12 Puech D. Atrioventricular block: the value of intracardiac recordings. In: Krikler KM, Goodwin JF, eds. Cardiac arrhythmias. London: W.B. Saunders, 1975;88.