Refractory reentrant atrial tachycardia

Refractory Reentrant Atrial Tachycardia Successful Treatment with a Permanent Radio Frequency Triggered Atrial Pacemaker

This 66 year old man had recurrent episodes of paroxysmal atrial tachycardia, probably due to chronic pericarditis, persisting over a 7 year period. These episodes were resistant to all conventional medical therapy and at times produced ischemic chest pain. There was no evidence of Wolff-Parkinson-White syndrome either on the standard electrocardiogram or on the His bundle electrogram performed with atrial pacing. Rapid atrial pacing at a rate of 200/min was found to promptly terminate the tachycardia and restore normal sinus rhythm. Because of the refractoriness of the patient’s tachycardia, in addition to the presence of ischemic chest pain during these episodes, a permanent radio frequency triggered atrial pacemaker was inserted which enables him to initiate rapid atrial pacing by pressing an external control. The patient has been maintained on antiarrhythmic medications in an attempt to decrease the frequency of these episodes; during an 6 month follow-up period, he has done well with approximately one episode of tachycardia each month requiring radio frequency atrial pacing for termination.

SHIV L. GOYAL, M.D. EDGAR LICHSTEIN, M.D. PREM K. GUPTA, M.D. KUL D. CHADDA,

M.D.

Elmhurst, New York

Recurrent paroxysmal atrial tachycardia is a common arrhythmia which is usually promptly reverted by carotid sinus pressure or other vagal maneuvers. Occasional patients require the use of various antiarrhythmic drugs and in some instances, DC cardioversion. A more significant management problem may arise due to either difficulty in terminating the tachycardia itself or to the frequency of its occurrence. We describe a patient with recurrent atrial tachycardia who was resistant to all usual antiarrhythmic therapy, and required insertion of a radio frequency triggered rapid atrial pacemaker. The mechanism is discussed and the results described. CASE REPORT From the Department of Medicine, Division of Cardiology, Mount Sinai Hospital Services, City Hospital Center at Elmhurst, Mount Sinai School of Medicine of the City University of New York, Elmhurst, New York 11373. Requests for reprints should be addressed to Dr. Edgar Lichstein, Division of Cardiology, Mount Sinai Hospital Services, City Hospital Center at Elmhurst, 79-01 Broadway, Elmhurst, New York 11373. Manuscript accepted April 5, 1974.

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This was the 11th hospital admission of a 68 year old man, this time for elective implantation of a radio frequency triggered atrial pacemaker*. The patient’s first admission to this hospital 15 months earlier was for persistent palpitations. At that time, he gave a history of similar episodes of palpitation for the preceding 7 years. He denied any history of rheumatic fever, hypertension, tations of congestive

diabetes

mellitus, dizziness,

syncope

or any manifes-

heart failure. He denied having typical angina pecto-

* Specially designed and provided by Medtronic Inc., Minneapolis, Minn.

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ris but did note a “heavy sensation” in his precordium when episodes of palpitation lasted longer than 1 hour. He smokes 3 to 4 cigarettes daily and consumes alcoholic beverages only occasionally. During his first admission, many typical episodes of paroxysmal atrial tachycardia were documented. The episodes were sudden in onset and at a rate of 166/min. The QRS morphology was similar to that seen when he was in sinus rhythm and was consistent with incomplete bilateral bundle branch block manifested by left anterior hemiblock and complete right bundle branch block (Figure 1). The episodes promptly reverted to sinus rhythm with carotid sinus pressure after the patient was digitalized. In addition to digitalis, he was also maintained on 200 mg of quinidine four times daily. Work-up included normal thyroid and pulmonary function studies. On his 2nd admission 2 months later, cardiomegaly and a left pleural effusion were noted, and a pericardial rub was heard. The patient was treated with steroids, and isoniazid (INH) because of a positive reaction to purified protein derivative. With this therapy, the pleural effusion disappeared and, for a brief period, the episodes of paroxysmal atrial tachycardia were less frequent. On his 3rd hospital admission, a friction rub was again heard despite continuation of steroid therapy. A lung scan showed no evidence of pulmonary emboli. A pleural biopsy, performed because of reaccumulation of pleural fluid, showed chronic fibrosis. Culture for acid-base bacilli was negative as was the work-up for systemic lupus erythematosus. The patient’s subsequent admissions were all prompted by episodes of paroxysmal atrial tachycardia which lasted longer than 1 hour. He had many other episodes while at home which reverted either spontaneously, by Valsalva maneuver or by carotid sinus pressure applied by his wife. He came to the hospital only for episodes which could not be broken by these simple maneuvers. On admission, carotid sinus pressure was applied followed by administration of edrophonium, Neo-Synephrinee, Valium@, propranolol, diphenylhydantoin and occasionally lidoCaine. On some occasions, lidocaine was successful in reverting paroxysmal atrial tachycardia. The patient was treated with a maintenance dose of digoxin and initially with quinidine, 200 mg four times a day. Following an allergic reaction to quinidine, he was given pronestyl 500 mg four times a day. Atrial pacing studies were performed during the patient’s 10th hospital admission. Figure 2 shows initiation of an atrial reentrant tachycardia following a timed premature atrial stimulus. The His bundle electrogram recorded prior to atrial pacing was within normal limits. Episodes of paroxysmal atrial tachycardia were terminated with atrial pacing at a rate of 195/min (Figure 3). During atrial pacing, Mobitz type I atrioventricular block was noted. Due to the frequency of paroxysmal atrial tachycardia, the symptoms produced by prolonged episodes and the inability to suppress these episodes with medication, a radio frequency triggered permanent atrial pacemaker was inserted with electrodes attached to the right atrium (Figure 4). After an uneventful recovery, the patient was able to place the radio frequency antenna over .his chest and then by pushing a button on the external unit, induce atrial pacing for

ET AL.

several seconds. On each occasion, atrial pacing has been successful in immediately reverting the paroxysmal atrial tachycardia to sinus rhythm. The patient has been followed as an outpatient for 8 months and is maintained on digoxin, pronestyl and propranolol in an attempt to decrease the frequency of the episodes. With this therapy, the patient has approximately one episode of paroxysmal atrial tachycardia each month for which he requires radio frequency atrial pacing for termination. COMMENTS Wolff-Parkinson-White syndrome is commonly associated with recurrent paroxysmal atrial tachycardia. The diagnosis of Wolff-Parkinson-White syndrome may be difficult to establish in a patient with recurrent paroxysmal atrial tachycardia since the characteristic short P-R interval and delta wave may alternate with a normal electrocardiogram [ 11. Numerous electrocardiograms taken during our patient’s many hospitalizations and outpatient visits showed no evidence of this pattern. In addition, the His bundle electrogram recorded during sinus rhythm and again during atrial pacing showed no evidence of anomalous conduction. Work-up was negative for other causes of recurrent paroxysmal atrial tachycardia including coronary heart disease, acute rheumatic activity and collagen disease.

m&ion showing normal sinus rh*hm and pattern of left anterior hemiblock and complete right bundle branch block. A lead II rhythm strip taken on the same day shows a typical episode of paroxysmal atrial tachycardia at a rate of 165/min.

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Figure 2. Initiation of an atria/ reentrant tachycardia following a timed premature atria/ impulse (I). The A-H and the H-V interval prior to the premature stimulus are within normal limits. The A-H interval immedia{ely following the premature impulse increases to 260 msec thus allowing for initiation of the reentrant atrial tachycardia. As the tachycardb continues, the A-H interval stabilizes at 205 msec whereas the H-V interval remains fixed at 50 msec. A = atria/ depolarization; H = His bundle depolarization; V = ventricular depolarization.

During two of the patient’s hospital admissions, a pericardial friction rub was heard by several observers. Following this, steroid therapy was started with dramatic improvement which was manifested by a marked decrease in the number of tachycardias. The etiology of the pericardial disease in this patient remains unclear. During implantation of the right atrial epicardial electrodes, a pericardial biopsy specimen was taken and revealed chronic nonspecific inflammation. An increased incidence of paroxysmal atrial

tachycardia in patients with pericarditis is recognized. James [2] postulates that several mechanisms are involved and these include direct involvement of the sinus node by pericarditis, damage to epicardial Purkinje tracts leaving the region of the sinus node, involvement of the atrial wall and inflammatory involvement of the autonomic fibers in the region of the sinus node. This patient had recurrent episodes of paroxysmal atrial tachycardia which frequently responded to ca-

A.F!= 195/MIH Figure 3. Termination of atrial tachycardia with atria/ pacing at a rate of 195/min. The atria/ impulse (I) causes 1: 1 atria1 capture with a brief period of Wenckebach type second degree atrioventricular block. On cessation of atria/ pacing, normal sinus rhythm returns.

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rotid sinus pressure but on occasion required digitalis, pronestyl, quinidine, propranolol, diphenylhydantoin, edrophonlum or Neo-Synephrine. On several occasions, DC conversion was necessary. The number of hospitalizations and the degree of disability, despite the extensive therapy he received, justify use of the term refractory paroxysmal atrial tachycardia in this patient. In this situation, rapid atrial pacing has been used either with a permanent implanted pacemaker [3,4] or with a temporary catheter which may convert the arrhythmia or control the ventricular rate [5-101. Rapid atrial pacing may terminate atrial tachycardia by various mechanisms. Overdrive and suppression of the ectopic pacemaker [6] may have been the mechanism in our patient since a pacing rate slightly faster than the tachycardia rate was necessary for conversion. Atrial pacing may cause atrial fibrillation [ 1 l] which is often unstable and may spontaneously revert to normal sinus rhythm [6]. Interruption of reciprocating circus pathways [7] or interruption of a re-entry pathway [4,12] may also occur. Temporary rapid atrial pacing may be used in the treatment of supraventricular tachycardia associated with digitalis toxicity when there is evidence of clinical deterioration and contraindication to the use of DC conversion. Rapid atrial pacing is also used with supraventricular tachycardia resistant to antiarrhythmic drugs, following open heart surgery and during cardiac catheterization [9]. Although rapid atrial pacing has been used successfully to terminate tachycardias associated with the Wolff-Parkinson-White syndrome, the procedure is thought by some to be contraindicated in patients with anomalous atrioventricular conduction. The initiation of atrial fibrillation in these patients may result in ventricular rates in excess of 300/min because of preferential conduction through the bypass [ 91. During temporary rapid atrial pacing, the catheter is inserted transvenously and is constantly under fluoroscopic control. The constant fluoroscopic observation is necessary to avoid the potential hazard of the catheter slipping into the ventricle and inducing ventricular tachycardia or possibly ventricular fibrillation. Successlul conversion of supraventricular tachycardia by temporary rapid atrial stimulation has varied from 71 to 90 per cent [ 7, lo]. Permanent rapid atrial pacing is usually achieved with implanted right atrial epicardial electrodes [ 131. A pervenous electrode which can be attached to the intra-atrial septum by an extra thoracic maneuver has also been described [ 141. Long-term atrial pacing via the coronary sinus [IS] which may be used with slow pacing rates is not used because of the potential danger of catheter dislodgement and stimulation of the ventricle.

FREOUENCY

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ATRIAL

I

PACING

FOR

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ET AL.

TRANSMlTTER

F&e 4. Schema tic diagram showing the position of the attached atria/ electrodes, the implanted receiver, the external antenna ring and the externally worn transmitter.

The radio frequency triggered permanent atrial pacemaker we describe has also been used by others with favorable results [3,4]. Atrial electrodes are sutured directly to the right atrial wall and a receiver is implanted subcutaneocrsly. The transmitter, which includes an on-off button and a dial for changing the pacing rate, is kept externally. The unit is activated by simply placing the external antenna ring over the subcutaneously implanted receiver and briefly pressing the “on” button. Major advantages of this device are that the rate control dial and the battery source are external and therefore can be changed with ease. The subcutaneously implanted receiver is small and produces no discomfort or inconvenience to the patient. This technic represents a practical application of rapid atrial stimulation which may be offered to patients with recurrent paroxysmal atrial tachycardia which is refractory to medical therapy. ACKNOWLEDGMENT We thank Fred Lajam, M.D. for performing the surgical implantation.

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REFERENCES 1.

2. 3.

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7.

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Newman BJ, Donoso E. Freidberg CK: Arrhythmias in Wolff-Parkinson-White syndrome. Progr Cardiovasc Dis 9: 147, 1966. James TN: Pericarditis and the sinus node. Arch Intern Med 1 f0: 305, 1962. Davidson RM. Wallace AG, Sealy WC, Gordon MS: Electrically induced atrial tachycardia with block: a therapeutic application of permanent radiofrequency atrial pacing. Circulation 44: 1014, 1971. Dreifus LS, Arriaga J, Watanabe Y, Downing D, Haiat R, Morse D: Recurrent Wolff+Parkinson-White tachycardia in an infant. Successful treatment by a radio-frequency pacemaker. Am J Cardiol 28: 586, 197 1. Haft JI, Kosowsky BD, Lau SH, Stein E. Damato AN: Termination of atrial flutter by rapid electrical pacing of the atrium. Am J Cardiol 20: 239, 1967. Lister JW, Cohen LS, Bernstein WH, Samet P: Treatment of supraventricular tachycardia by rapid atrial stimulation. Circulation 38: 1044, 1968. Vergara GS. Hildner FJ, Schoenfeld CB, Javier RP, Cohen LS, Samet P: Conversion of supraventricular tachycardias with rapid atrial stimulation. Circulation 46: 788, 1972.

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Cheng TO: Atrial pacing: its diagnostic and therapeutic applications. Progr Cardiovasc Dis 14: 230, 1971. Lister JW, Gosselin AJ, Nathan DA, Barold SS: Rapid atrial stimulation in the treatment of supraventricular tachycardia. Chest 63: 995, 1973. Pitmann DE. Makar JS, Kooros KS, Joyner CR: Rapid atrial stimulation: successful method of conversion of atrial flutter and atrial tachycardia. Am J Cardiol 32: 700, 1973. Haft JI, Kosowsky BD, Lau SH. Stein E, Damato AN: Vulnerable period of the human atrium. Circulation 34: (suppl Ill): Ill 119, 1966. Massumi RA, Kiston AD, Tawakkol AA: Termination of reciprocating tachycardia by atrial stimulation. Circulation 36: 637, 1967. Perryman RA, Sealy WC: Permanent atrial pacing: improved methods of electrode implantation and current therapeutic uses. Ann Thorac Surg 15: 16. 1973. Udall JA: Pervenous atrial pacing by fixed electrode (letter to editor). JAMA 222: 702, 1972. De Sanctis RW: Diagnostic and therapeutic uses of atrial pacing. Circulation 43: 748, 197 1.