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Chin Med J (Taipei) 1997;60:117-23.
1Division of Cardiology, Department of Medicine; 2Division of Cardiovascular Surgery, Department of Surgery, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan, R.O.C.
We present here, the case of a 22-year-old male suffering from persistent tachycardia for the past 3 years. His resting pulse rate was rarely below 100 beats/min, and it frequently increased to as high as 150 beats/min even after a minimal of activity. Associated symptoms included palpitation, chest tightness, dyspnea and presyncope, either during rest or with exercise. Propranolol and verapamil could not control the tachycardia. The application of radiofrequency energy to an area in the superior right atrium that demonstrated a discrete electrogram with earliest endocardial activation during tachycardia resulted in a decrease in sinus rate from 120 beats/min to 70 beats/min. Follow-up on Holter monitor, performed one month later, demonstrated an average heart rate of 84 beats/min (range 60-125). In exercise tolerance test, the patient exercised for 9 minutes, achieving a maximum heart rate of 140 beats/min. This patient remained asymptomatic without any antiarrhythmic drug during the 3-month follow-up period.
Medical management in case of patients showing disabling inappropriate sinus tachycardia refractory, sinus node modification could be considered as an suitable alternative to complete atrioventricular junctional ablation.
[Chin Med J (Taipei) 1997;60:117-23.]
Keywords: catheter ablation, inappropriate sinus tachycardia, sinus node
Received: August 23, 1996.
Accepted: May 7, 1997.
Address reprint requests to: Shih-Huang Lee, M.D., Division of Cardiology, Shin Kong Wu Ho-Su Memorial Hospital, No. 95, Wen Chang Road, Shih-Lin, Taipei, Taiwan, R.O.C.
Radiofrequency catheter ablation has become a safe and accepted form of therapy for reentrant tachycardias due to an accessory atrioventricular (AV) pathway or dual AV nodal pathway physiology. Recently, this technique has also been used to treat atrial flutter, sinus node reentry and atrial tachycardia [1-3]. Patients with inappropriate sinus tachycardia exhibit an abnormally high resting heart rate and a disproportionate increase in heart rate in response to even minimal activity [4-8]. The P wave morphology suggests the origin of tachycardia to be either inside or very close to the sinus node, and beta receptor blockade is considered to be the initial treatment of choice. For medically refracted patients with inappropriate sinus tachycardia, His bundle ablation and permanent pacemaker implantation or subtotal right atrial exclusion have been used [9]. We report herein a patient suffering from inappropriate sinus tachycardia, in whom radiofrequency modification of the superior posterolateral right atrium resulted in dramatic slowing of the heat rate, thereby obviating the need for a pacemaker.
The patient was a 22-year-old male with a history of persistent tachycardia for the past 3 years. He noted that his resting pulse rate was rarely below 100 beats/min, and it frequently increased to as high as 150 beats/min even after a minimal activity. Associated symptoms included palpitation, chest tightness, dyspnea and presyncope, either during rest or with exercise. In out-patient clinic, the patient's 12-lead electrogram demonstrated sinus tachycardia (120 beats/min) with an inferior P wave axis and a PR interval of 0.15 second (Figure 1A). Twenty-four hour examination by Holter monitor showed that the average heart rate was 121 beats/min, with a maximum rate of 160 beats/min, and a minimum rate of 84 beats/min (which occurred only during sleep). He refused to perform treadmill exercise test because of severe dyspnea after minimal activity. Echocardiogram revealed mild dilatation of left ventricle (left ventricular end diastolic dimension = 54 mm) with normal wall motion (ejection fraction = 70%). Moreover, propranolol and verapamil together could not control the tachycardia. The patient did not have orthostatic hypotension, diabetes mellitus, hyperthyroidism, drug abuse or coffee consumption.
Prior to the electrophysiological study, the patient signed an informed consent form for the attempted modification of sinus node. During the electrophysiological study, the patient remained in sinus tachycardia after intravenous sedation with diazepam. Three multipolar electrode catheters (Mansfield Scientific, Mansfield, Mass., USA) were positioned in the higher right atrium, His-bundle area and right ventricle via bilateral femoral veins. An orthogonal electrode catheter (Mansfield Scientific) was inserted into the coronary sinus via right internal jugular vein. Rapid atrial pacing resulted in transient overdrive suppression of the rhythm with normal sinus node recovery time (the maximal corrected sinus node recovery time was 480 msec). A single atrial premature stimulus was applied to reset the tachycardia. Neither incremental atrial pacing nor atrial premature stimulus initiated or terminated the tachycardia. After autonomic denervation was performed pharmacologically (propranolol 0.2 mg/kg and atropine 0.04 mg/kg), the observed intrinsic heart rate was 125 beats/min, while the predicted intrinsic heart rate for this patient was 106 beats/min.
Following the diagnostic evaluation, a 7 French deflectable quadripolar catheter with a 4-mm tip (Mansfield Scientific) was used to map and deliver the radiofrequency energy (Radionics, Radionic-3C, Boston, MA) through the distal electrode. A large electrosurgical paddle (Valleylab, Boulder, Co) positioned on the posterior chest wall served as the indifferent electrode. Earliest endocardial atrial activation during tachycardia was sought, and it occurred in the right atrium near the junction of the superior vena cava and the superior posterolateral wall of right atrium. A total of seven pulses of radiofrequency energy were delivered at 25 watts for a duration of 20-30 seconds in this region of the right atrium. The seventh pulse resulted in abrupt termination of the tachycardia with an atrial rhythm of 70 beats/min, and a significant change in the appearance of surface P wave also occurred. The atrial electrogram recorded at this site revealed a discrete, but multicomponent appearance, with an onset 25 msec before the surface P wave (Figure 2). The catheter position with successful ablation is shown in Figure 3. One additional pulse of radiofrequency energy was delivered for 60 seconds (25 watts) at this site to ensure the success of ablation. Subsequent atrial pacing, with and without isoproterenol, failed to initiate the tachycardia. After ablation, the earliest endocardial atrial electrogram was identified in a more caudal location along the posterolateral wall of right atrium. The distance between the sites with earliest endocardial atrial activation before and after ablation was 1 cm. The heart rate remained at around 70 beats/min 30 minutes after the conclusion of the procedure (Figure 1B). The intrinsic heart rate was 99 beats/min after autonomic denervation was performed pharmacologically. The heart rate increased to 168 beats/min during infusion of 4 micron g/min isoproterenol. A 24-hour Holter monitor recorded one month after the ablation procedure demonstrated sinus rhythm with an average rate of 84 beats/min, with a maximum rate of 125 beats/min, and a minimum rate of 60 beats/min. A comparison of 24-hour heart rate trends before and after the ablation is presented in Figure 4. During the treadmill exercise test, performed 1 month after the procedure, the exercise duration was 9 minutes, and the maximal heart rate was 140 beats/min (compared with inability to perform this exercise test before ablation). The Echocardiogram recorded 1 month after the ablation demonstrated normal left ventricular dimension (left ventricular end diastolic dimension = 48 mm) along with normal wall motion. The patient remained asymptomatic without any antiarrhythmic drug during the 3-month follow-up period.
In the present patient, an attempt has been made to modify the sinus node in order to relieve symptoms associated with inappropriate sinus tachycardia. Direct application of radiofrequency energy to the superior posterolateral wall of right atrium resulted in significant reduction in sinus rate. Control of sinus rate was accompanied by improvement in symptoms and preservation of normal chronotropic response.
The clinical and electrophysiological characteristics of patients with persistent inappropriate sinus tachycardia have been recently described in the literatures [4-8]. Bauernfeind et al. were the first to report that inappropriate sinus tachycardia was due to increased automaticity of the sinus node as a result of a defect in either sympathetic or vagal nerve control of resting heart rate [4]. However, Morillo et al. have recently suggested that the mechanism leading to inappropriate sinus tachycardia was related to a primary sinus node abnormality, which is characterized by a high intrinsic heart rate, beta-adrenergic hypersensitivity, and depressed efferent cardiovagal reflex [10]. A striking increase in intrinsic heart rate was observed in the present patient. This suggested that the mechanism leading to tachycardia in this patient was related to a primary sinus node abnormality resulting in a high intrinsic heart rate. However, cardiac vagal tone and beta adrenergic receptor response were not assessed for this patient.
The unique anatomic and functional characteristics of the sinus node have been well characterized [11-13]. The sinus P wave arises from a pacemaker complex distributed over an area extending from the junction of the superior vena cava and right atrial appendage in the inferior direction along the sulcus terminalis almost to the inferior vena cava. A close correspondence between the change in heart rate and change in the sites of impulse origin within this complex in response to certain autonomic manipulations has also been demonstrated [12,13]. Such site-specific differential sensitivity to autonomic inputs allows the possibility of targeted modification of sinus pacemaker function. Patients with inappropriate sinus tachycardia are usually controlled by medical therapy with beta-blockers. However, some patients may develop intolerable adverse effects or may be refractory to medical therapy. Nonpharmacological therapy includes subtotal right atrial surgical exclusion [9]. Recently, modification of sinus node function by graded epicardial laser radiation has been presented in a dog model, resembling inappropriate sinus tachycardia [14]. Even more recently, mechanical or chemical occlusion of the sinus node artery has been reported to modify sinus node function [15]. In these cases, the heart rate control might have been achieved by either the destruction of pacemaker tissue, interruption of autonomic neural inputs, or even by both. Kalman et al. have demonstrated an area of fibrosis with complete loss of both nodal cells and sympathetic innervation in the histological examination of canine sinus node after radiofrequency ablation. The demonstration of decrease in the intrinsic heart rate after radiofrequency ablation was consistent with destruction of sinus nodal cells and/or sympathetic innervation to the sinus node complex. Subsequent detailed activation mapping have localized the origin of the tachycardia to the region of sinus node. However, Boineau et al. have demonstrated that atrial pacemaker might be distributed over a fairly wide region of the right atrium; hence it was impossible to rule out the presence of an abnormal ectopic atrial focus in the vicinity of sinus node [13]. Similar to the present result, Packer et al. have reported that a reversal of dilated cardiomyopathy might develop in some patients suffering from chronic untreated atrial tachycardia [16].
In summary, sinus node modification could be considered as an suitable alternative to complete atrioventricular junctional ablation for patients with disabling inappropriate sinus tachycardia, refractory for appropriate medical management.
The authors gratefully acknowledge Jen-Chung Lee, Chou-Gui Lee and Chun-Hui Chiang for their excellent technical assistance in the electrophysiology laboratory.
Copyright: 1997, Chinese Medical Association (Taipei)