Refractory paroxysmal sinus tachycardia: Management by subtotal right atrial exclusion

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Refractory Paroxysmal Sinus Tachycardia: Management by Subtotal Right Atrial Exclusion RAYMOND YEE, MD, GERARD M. GUIRAUDON, MD, FRCS(C), FACC, MARTIN J. GARDNER, MD, FRCP(C), SAJAD S. GULAMHUSEIN, MD, FRCP(C), GEORGE J. KLEIN, MD, FRCP(C), FACC London. Ontario and Halifax, Nova Scotia. Canada

A 27 year old woman presented with recurrent episodes of disabling paroxysmal sinus tachycardia (150 to 180 beats/min) in the absence of identifiable organic disease. Tachycardia was resistant to all drug therapy. Programmed stimulation could not induce the tachycardia but high dose propranolol therapy failed to suppress sinus tachycardia in response to isoproterenol infusion.

Sinus tachycardia is generally an appropriate response to altered physiologic and autonomic states (I). "Primary" or "paroxysmal" sinus tachycardia is uncommon and may be the result of enhanced automaticity or a reentrant circuit within the sinus node region. Differentiation of these two mechanisms is based on observations of the duration and behavior of the tachycardia and the response to programmed stimulation (2-4). Primary sinus tachycardia is associated with a normal sequence of atrial activation and normal P wave configuration on the standard electrocardiogram. Experience in the management of sinus node tachycardia, whether due to sinoatrial reentry or enhanced automaticity, has been limited owing to the small number of patients who require treatment. We describe a patient disabled by recurrent episodes of sinus tachycardia resistant to all medical therapy. We performed a new operative procedure that involved an incision encircling part of the right atrium including the sinus node

From the Clinical Electrophysiology Laboratories. University Hospital, London, Ontario and Victoria General Hospital, Halifax, Nova Scotia. Canada. Dr. Klein is a Senior Research Fellow of the Ontario Heart Foundation. Toronto, Ontario. Canada. Dr. Gardner is a recipient of a Research Grant-In-Aid from the Nova Scotia Heart Foundation. Halifax. Nova Scotia. Canada. Manuscript received June 27, 1983; revised manuscript received August 23, 1983, accepted September 20. 1983. Address for reprints; George J. Klein, MD, Cardiac Investigation Unit, University Hospital. P.O. Box 5339, Station 'A', London, Ontario, N6A 5A5 Canada.

© 1984 by the American College of Cardiology

Because of the disability resulting from refractory tachycardia, the patient underwent a new operative procedure to create exit block around the region of abnormal impulse formation. This resulted in the appearance of a stable junctional escape rhythm at 60 beats/min. No adverse effects occurred and the patient has remained free of symptoms after a follow-up period of 10 months.

region. This prevented manifest tachycardia by creating exit block around the region of abnormal impulse formation.

Case Report The patient was a 27 year old woman without prior history of cardiac disease or chronic medical illness. She presented in 1979 with sinus tachycardia lasting from hours to several days and associated dyspnea, aching inframammary chest discomfort, fatigue and malaise. Onset of episodes was characterized by gradual acceleration but was not related to activity, posture, emotional state, drug intake or any other identifiable factor. Frequency of attacks was I to 2 per week and nocturnal episodes were a frequent occurrence. Between episodes the patient was well, but during attacks she was disabled by symptoms. Physical examination was normal and no cause for the rhythm disturbance was identified. Treatment with sedatives and analgesics over the ensuing 2 years failed to diminish symptoms and she was referred to Victoria General Hospital (Halifax) for further evaluation. Subsequent investigations, including complete endocrinologic, neurologic and psychiatric assessments, were entirely normal. Cardiovascular examination was normal, as was a graded treadmill exercise test. Two-dimensional echocardiography and cardiac catheterization revealed no organic lesions. She was treated with several beta-adrenergic antagonists, including propranolol in high doses (1,200 mg/day)

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alone or in various combinations with digoxin, quinidine, verapamil and amiodarone. All drug regimens were ineffective. Indeed, high serum propranolol levels (> 1,000 ng/ml) combined with verapamil caused episodic sinus bradycardiawith a slowjunctional escape rhythm with resultant near syncope and profound fatigue. This necessitated the implantation of a permanentventriculardemand pacemaker, but the patientcontinuedto have paroxysmal attacksof sinus tachycardia. Electrocardiograms. Electrocardiograms during sinus rhythm showed a P wave axis of + 30°, normal P wave configuration and no other abnormalities. During attacks, the heart rate reached ISO to 180 beats/min. The P wave axis and configuration were unchanged, but the QRS complex showed right bundle branch block aberration (Fig. I). Ambulatory recordings revealed gradual acceleration of heart rate at onset of attacks and slow deceleration when attacks abated. Propranolol, 10 to 12 mg intravenously, administered during episodes caused gradual slowing of the rate without change in P wave configuration. Electrophysiologic studies. Electrophysiologic evaluation was performedin the nonsedated state using multipolar catheters for intracardiac recording and stimulation from right atrium, right ventricle and His bundle. Programmed stimulation was performed using standard methodsto assess sinus node function and properties of atrioventricular (AV) conduction (5,6). The initial control studies demonstrated normal sinoatrial conductiontime (90 rns), normalcorrected sinus node recovery time (220 ms), a normal sequence of atrial activation and no evidence of preexcitation. Tachycardia was not inducible so the patient was then given an isoproterenol infusion (2 fLg/min) to decrease sinus cycle length by 25% and programmed stimulation was repeated.

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Symptoms were reproduced by rapid atrial pacing and isoproterenol infusion, but no other tachyarrhythmias were induced. The atrial activation sequenceremainedunchanged during isoproterenol-induced sinus tachycardia and could not be terminated by overdrive pacing or premature atrial extrastimuli. After several days oforal propranolol therapy to achieve serum levels all ,041 nglml, programmed stimulation was

repeatedbeforeand after isoproterenol infusion. Propranolol slightly increased sinus cycle length (980 ms), corrected sinus node recovery time (440 ms) and sinoatrial conduction time (100ms). However, isoproterenol infusionat 2 fLg/min restored corrected sinus node recovery time and sinoatrial conduction time values to control levels despite high serum levels of propranolol, The patientcould no longerworkbecauseof her disability and she was referred to University Hospital (London, Ontario) for an operative intervention aimed at prevention of further attacks. Surgical procedure. The heart was exposed through a median sternotomy. Right atrial and ventricular reference electrodes were appliedto the epicardium and a rovingquadripolar probe electrode was used for epicardial atrial mapping under normothermic conditions. Because tachycardia could not be induced, atrial mapping was performed during sinus rhythm. The earliest atrial epicardial activation occurred at the anterolateral aspect of the junction between the superior vena cava and right atrium (Fig. 2) corresponding to the region of the sinus node. Cardiopulmonary bypass was established and the heart was fibrillated electrically. A transverse right atrial transmural incision was made parallel to the tricuspid anulus and extended medially. avoiding the AV node region (Fig. 2).

Figure 1. Standard 12 lead electrocardiogram during an episode of tachycardia (140 beats/min). The P wave axis is + 30° and the QRS complex shows right bundle branch block aberration. _ I _ III

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YEE ET AL. ATRIAL EXCLUSION FOR REFRACTORY SINUSTACHYCARDIA

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Figure 2. Schematic diagram (right anterior oblique view) illustrating thesurgical technique employed. The hatchedlinedenotes the circumferential line of incision dividing the right atrium into a superior cuff (excluded right atrium) and inferior segment (nonexcluded right atrium). The star and shaded area mark theregion of earliest epicardial atrial activation. AO = aorta; RV = right ventricle.

Following the superior limit of the fossa ovalis, the incision continued until it joined the inferior end of the incision in the right atrial free wall. The resulting superior cuff of the right atrium was then freed from surrounding structures, particularly the left atrium. In the course of dissection, the sinus node artery was severed. The net result of this circumscribed incision was a division of the right atrium into

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two segments: an excluded superior right atrial cuff containing the sinoatrial node region, and an inferior segment in continuity with the rest of the heart. The endocardial and epicardial surfaces of the entire right atrium were inspected and no gross lesion was identified. The two atrial segments were then reunited by a continuous suture. Temporary pacing wires were sutured to the epicardial surfaces of both right atrial segments in addition to the leftatriumand ventricle. When the heart was defibrillated, a junctional rhythm (Fig. 3) with retrograde activation of the nonexcluded inferior right atrial segment and left atrium was recorded. The surgically excluded superior right atrial segment displayed independent electrical activity best observed during pacing of left atrial and inferior right atrial segments. Postoperative course. One week postoperatively, the heart was still in junctional rhythm with intermittent ventricular demand pacing. Intrinsic heart rate was determined with complete autonomic blockade (atropine, 2.4 mg, and propranolol, 12 mg, intravenously) and with chest wall stimulation to suppress the implanted pacemaker. The intrinsic rate of the excluded right atrial segment was 95 beats/min (normal = 102.8 beats/min [7]) and 60 beats/min for the junctional pacemaker. A symptom-limited treadmill exercise test was performed before discharge; it demonstrated acceleration of the junctional rate from 70 to 105 beats/min. Response to incremental doses of isoproterenol was also assessed (8). The dose required to increase the rate of the excluded right atrial segment by 25% was 4.7 J-tg and that of the junctional pacemaker was 4.3 J-tg. At discharge, no antiarrhythmic medication was prescribed. Follow-up. After a 10 month follow-up period, the patient remains well with no further symptoms. She remains in stable junctional rhythm.

Discussion Sinus tachycardia is generally of a physiologic origin and mediated primarily by the autonomic nervous system (I). Its occurrence as a primary disorder of the sinus node apparatus is an infrequent cause of supraventricular tachy-

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Figure 3. Simultaneous recordings of surface electrocardiographic leads I, II, III and epicardial electrograms from theexcluded right atrium (RAE)' nonexcluded right atrium (RAN)' left atrium (LA) and left ventricle (LV). The patient exhibited junctional rhythm (65 beats/min) with intact ventriculoatrial conduction (A with arrow) and dissociation of atrial activity from theexcluded right atrium.

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cardia (2). Sinus tachycardia would be expected to have a normal P wave configuration and axis. In addition, the onset of the high right atrial electrogram should coincide with the onset of the P wave. Despite these strictly applied criteria, it may be difficult to distinguish sinus tachycardia from an automatic atrial focus located in the vicinity of the sinoatrial node. Mechanisms of paroxysmal sinus tach ycardia. Two mechanisms have been described to explain paroxysmal sinus tachycardia. Sinus tachycardia as the result of a rnicroreentrant circuit in the sinus node region has been demonstrated in human beings (3,4). Episodes due to sinus node reentry are usually brief paroxysms that can be induced and terminated by programmed electrical stimulation. Individuals may be asymptomatic or complain of palpitation. Digoxin, verapamil, quinidine and propranolol have been reported to be effective for sinus node reentrant tachycardia (2.9). Recently, Bauernfeindet al. (10) described seven patients with idiopathic chronic sustained sinus tachycardia that could be neither induced nor terminated by critically timed atrial extrastimuli or atrial pacing. These features distinguished this group of patients from those with sinus node reentry. These authors postulated that the increased sinus node automaticity observed was due to altered autonomic modulation with or without an intrinsic disturbance of sinus node function. A beta-adrenergic antagonist was the recommended first choice drug for symptomatic patients. Our patient suffered disabling recurrent attacks of tachycardia during which the P wave configuration was unchanged from those of normal sinus beats. Attacks were prolonged and characterized by gradual acceleration and deceleration. They could not be induced by programmed stimulation, although an isoproterenol infusion did induce sinus tachycardia with a P wave identical to that which occurs during spontaneous episodes. It is remarkable that the atrial rate responded to isoproterenol infusion despite maximal beta-adrenergic blockade. We believe that the features exhibited by our patient suggest enhanced automaticity of the sinoatrial node or possibly an ectopic focus situated in close proximity to the sinoatrial node. However, we cannot exclude a possible role for altered autonomic modulation of a normal sinus node in the genesis of the patient's arrhythmia. Rationale for subtotal right atrial exclusion. The decision to use a surgical approach for this patient was based on considerations of the disability imparted by the tachycardia, its refractoriness to aggressive medical management and the relatively low risk of cardiac surgery directed at the right atrium. Several procedures could have been applied in the management of this problem. Ablation of the AV node-His bundle by catheter techniques ( I I) or cryoablati ve surgery (\ 2) were possible, but may have rendered the patient pacemaker-dependent. The inability to accurately IDealize a discrete focus obviated a limited surgical procedure aimed at excluding or ablating the arrhythmogenic focus.

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Because we were confi dent that the arrhythmia was originating from within or near the sinus region, we elected to perform subtotal right atrial exclusion. This procedure is analogous to the left atrial isolation technique initially described by Williams et al. (13). Subsidiary pacemaker. Postoperatively, a junctional escape pacemaker rhythm emerged and to date the patient has remained in stable junctional rhythm. This initial sequence of events is similar to that observed by Sealy et al. (\ 4) and other investigators (15,16) in the canine model after excision of the sinoatrial node. However, neither an ectopic atrial rhythm nor periods of asystole occurred postoperatively as was noted in manyof the animal experiments, suggesting that the intrinsic automaticity of the AV junctional region exceeds that of atrial septal or left atrial tissue in human patients. Our patient has returned to an active life without restriction on physical activity. We thank Suzanne Stewart for preparing the manuscript.

References I. Damato AN. Cardiac arrhythmias. tn: Beeson B. ed. Cecil Textbook of Medicine. Philadelphia: WB Saunders. 1979:1243- 4. 2. Narula O. Paroxysmal supraventricular tachycardia due to sinus node and intra-atrial reentry. In: Narula OS. ed. Cardiac Arrhythmias: Electrophysiology. Diagnosis and Management. Philadelphia: Lea & Febiger, t979:272-93. 3. Wu D. Amat-Y-Leon F. Denes P. Dhingra R. Pietras RJ. Rosen KM. Demonstration of sustained sinus and atrial reentry as a mechanism of paroxysmal supraventricular tachycardia. Circulation 1975;51 :234- 43. 4. Narula OS. Sinus node reentry: a mechanism for supraventricular tachycardia. Circulation 1974:50:1114-28. 5. Josephson ME. Seides SF. Elcctrophysiologic investigation: general concepts. In: Josephson ME. Seides S. eds. Clinical Cardiac Electrophysiology: Techniques and Interpretations. Philadelphia: Lea & Febiger, 1979:23- 55. 6. Svenson RH. Miller He. Gallagher JJ. Wallace AG. Electrophysiological evaluation of the WPW syndrome: problems in assessing anregrade and retrograde conduction over the accessory pathway. Circulation 1975:52:552- 62. 7. Jose AD. Effect of combined sympathetic and parasympathetic blockade on heart rate and cardiac function in man. Am J Cardiol 1966:18:476-8 . 8. Cleaveland CR. Rango RE. Shand DG. A standardized isoproterenol sensitivity test. Arch Intern Med 1972:130:47- 52. 9. Curry PVL Shenasa M. Atrial arrhythmias: clinical concepts. In: Mandel WJ. cd. Cardiac Arrhythmias. Philadelphia: 18 Lippincott. 1982:175. 10. Bauernfeind RA. Amat-Y-Leon F. Dhingra Re. Kehoe R. Wyndham C. Rosen KM. Chronic paroxysmal sinus tachycardia in otherwise healthy persons. Ann Intern Med 1979:91:702- 10. II. Gallagher JJ. Svenson RH. Kasell JH. et al. Catheter technique for closed-chest ablation of the atrioventricular conduction system. N Engl J Med 1982;306:194- 200. 12. Harrison L. Gallagher JJ. Kasell J. et al. Cryosurgical ablation of the AV node-His bundle: a new method for producing AV block. Circulation 1977:55:463- 70.

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13. Williams 1M. Ungerleider RM. Lofland GK. Cox lL. Left atrial isolation: new technique for the treatment of supraventricular arrhythmias. 1 Thorac Cardiovasc Surg 1980;80:373-80.

15. Eyster l AE, Meek Wl. Experiments on the origin and conduction of the cardiac impulse. Arch Intern Med 1916;18:775-99.

14. Sealy WC. Bache Rl, Seaber AV. The atrial pacemaking site after

We. Cardiac arrhythmias in the conscious dog after excision of the sinoatrial node and crista terminalis. Circulation 1979;59:468-75 .

surgical exclusion of the sinoatrial node. 1 Thorac Cardiovasc Surg 1973;65:841- 50.

16. Euler DE, lones 5B. Gunnar WP. Loeb 1M. Merlock OK. Randall