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J Thorac Cardiovasc Surg 1997;114:861-864
© 1997 Mosby, Inc.

BRIEF COMMUNICATIONS

SURGICAL EXCISION OF THE SINUS NODE IN A PATIENT WITH INAPPROPRIATE SINUS TACHYCARDIA

Bonn, Germany

Received for publication March 3, 1997 accepted for publication May 22, 1997. Address for reprints: Bahman Esmailzadeh, MD, Universitätsklinik und Poliklinik für Herz-und Gefäßchirurgie, Sigmund-Freud-Str. 25, 53105 Bonn—Venusberg, Germany.

Inappropriate sinus tachycardia is a rare arrhythmia occurring in otherwise healthy persons, possibly owing to increased automaticity of the sinus node or an automatic atrial focus located near the sinus node. The abnormality also may be related to a defect in autonomic control of sinoatrial automaticity. ¹ The current report supports the findings of previous studies concerning the role of surgical treatment of patients with this condition. ²

Clinical summary.

The patient, a 36-year-old woman, had had persistent tachycardia for 4 years. She had previously undergone two unsuccessful catheter ablation attempts for her tachycardia in a highly experienced ablation center. First radiofrequency energy and then direct current were used. The ablations were followed only by a transient and moderate deceleration of the heart rate. She continued to have an accelerated pulse rate at rest, rarely below 100 beats/min. Even with mild exertion (25 watts) the heart rate exceeded 150 beats/min and the associated symptoms of chest tightness and dyspnea resulted in a significant disability for the patient. Antiarrhythmic medication with verapamil, diltiazem, propranolol, atenolol, metoprolol, and bisoprolol failed to achieve permanent improvement of the symptoms, resulting only in a transient decrease of heart rate. Drug-induced hypotonia (<90/60 mm Hg) and dizziness precluded long-term administration. A preoperative twelve-lead electrocardiogram (ECG) at rest demonstrated sinus tachycardia at a rate of 120 beats/min, with normal P wave morphology and a PR interval of 0.14 seconds. Exercise stress testing showed the peak rate of 184 beats/min at 75 watts, with no ST segment abnormalities. A 24-hour Holter monitor recorded an average rate of 96 beats/min, the minimal rate of 60 beats/min occurring only during sleep.

Before the operation, the patient signed an informed consent form. The heart was exposed through a median sternotomy. After the aortic and venous cannulas had been placed, intraoperative electrophysiologic mapping was performed. The operator used a handheld probe with a quadripolar epicardial electrode, and the recorded potentials were compared with the surface ECG. The initial heart rate of 76 beats/min increased after administration of 1.5 mg atropine (to 120 beats/min) and 2.0 µg isoproterenol intravenously (to 150 beats/min). The earliest atrial activation site during tachycardia ocurred 80 msec before the onset of the P wave on the surface ECG and was recorded on the ventrolateral aspect of the junction between the superior vena cava and right atrium (Fig. 1, Fig. 2, A). Manual pressure at this location resulted in abrupt termination of the tachycardia. Fibrotic scars with some pericardial adhesions were noted approximately 1.5 cm from this point on the lateral wall of right atrium, presumably representing the sites of radiofrequency and direct-current catheter ablation attempts. The right atrium was then opened and an approximately 2 x 2 cm portion of right atrial wall surrounding the site of earliest atrial activation was excised. The tissue defect was closed with parts of the right atrial appendage by means of a continuous suture. No pericardial patch was needed.

View larger version (194K): [in this window] [in a new window]   Fig. 1. Intraoperative view of the heart before excision. The site of earliest atrial activation was found on the ventrolateral aspect of the junction between superior vena cava and right atrium (arrow). Note the fibrotic scars on the lateral aspect of right atrium, presumably representing the sites of ablation attempts.

View larger version (23K): [in this window] [in a new window]   Fig. 2. , A, Intraoperative epicardial mapping sequence showing the earliest atrial activation potential occurring 80 msec before the onset of the P wave on the surface ECG. B, Twelve-lead ECG tracing of a stable atrial escape rhythm after the operation. Note the significant change in the P wave morphology with negative tracing in inferior leads.

Histologic section of the excised material showed a marked fibrosis of the atrial tissue with hyalinization of fibrous fibers in the subendocardial and especially in the subepicardial zone. Muscle fibers of the sinoatrial node were adjacent to a small nodal artery. The fibers were smaller than those of the atrial muscle and loosely arranged with collagenous fibers. A marked fibrosis was noted within the node.

Discussion.

The clinical and electrophysiologic findings in our patient were consistent with the diagnosis of inappropriate nonparoxysmal sinus tachycardia. ¹ Thorough clinical investigation has excluded various identifiable causes of the sinus tachycardia. The tachyarrhythmia was neither provoked nor terminated by pacing, implicating an automatic origin and excluding a reentrant mechanism. The cause for the arrhythmia may be sought in autonomic imbalance of the sinus node, either because of increased sympathetic or decreased parasympathetic nerve influence. The importance of autonomic pathways in the genesis of this tachycardia is further underscored by reports of occurrence of inappropriate sinus tachycardia after catheter ablation of supraventricular arrhythmias with subsequent damage to the autonomic fibers. However, an excessive intrinsic heart rate (as achieved after pharmacologic denervation of the sinus node) may also be responsible for the arrhythmia. The significance of this mechanism in our patient was emphasized by the intraoperative pharmacologic induction of tachycardia.

The key role of precise intraoperative mapping is highlighted by the fact that the region of origin of the tachycardia in this patient was on the anterior aspect of the superior vena caval–right atrial junction, whereas previous experimental studies suggested a slightly more lateral location of the sinus node. Although various types of atrial rhythm may occur after the exclusion of the sinus node, most frequently the pacemaker site that achieves predominance is located in the distal coronary sinus area. This appeared to be the case in our patient.

This case raises the question of failure of two previous catheter ablation attempts to inactivate the sinus node. Boineau and coworkers ³ showed that the atrial pacemaker cells may be distributed over a large area of right atrial tissue and that in addition to unifocal nodal or extranodal impulse origin, there may be multifocal impulse origin from two or more extranodal pacemaking sites. Furthermore, experimental studies have shown that extrinsic nerve activity might alter the level of the resting potential in the pacemaker cells, thus causing latent pacemaker cells to develop leading automaticity. ⁴ Such observations in patients with inappropriate sinus tachycardia would make the catheter ablation approach extremely difficult. Indeed, it became evident during the operation in our patient that the ablation scars were 1.5 to 2 cm away from the site of earliest atrial activation demonstrated by intraoperative epicardial mapping. We believe that a more epicardial location of the impulse origin also could have been the reason for the failure of catheter ablation in our patient.

The role of surgery in the treatment of this disorder so far is unclear. Hendry and associates ² found the surgical treatment of inappropriate sinus tachycardia to be less effective than for other forms of atrial arrhythmias. Only one of three patients remained free of symptoms during the follow-up period. Recent reports have advocated the feasibility of radiofrequency catheter ablation in curing this arrhythmia. ⁵ In their recent review on inappropriate sinus tachycardia, Krahn and coworkers ⁶ stated that the therapy of this arrhythmia is empiric. Therefore we believe that considering the severity of symptoms and the failure of catheter ablation attempts, a decisive therapeutic approach in these patients, including cardiac surgery, is justified.

Footnotes

From the Departments of Cardiac and Vascular Surgery,^a Cardiology,^b and Pathology,^c University of Bonn Medical School, Bonn, Germany.

References

1. Bauernfeind RA, Amat-Y-Leon F, Dhingra RC, Kehoe R, Wyndham C, Rosen KM. Chronic nonparoxysmal sinus tachycardia in otherwise healthy persons. Ann Intern Med 1979;91:702-10.
   
2. Hendry PJ, Packer DL, Anstadt MP, Plinkett MD, Lowe JE. Surgical treatment of automatic atrial tachycardias. Ann Thorac Surg 1990;49:253-60. [Abstract]
   
3. Boineau JP, Canavan TE, Schuessler RB, Cain ME, Corr PB, Cox JL. Demonstration of a widely distributed atrial pacemaker complex in the human heart. Circulation 1988;77:1221-37. [Abstract/Free Full Text]
   
4. Goldberg JM, Geesbreght JM, Randall WC, Brynjoefsson G. Sympathetically induced pacemaker shifts following sinus node excision. Am J Physiol 1973;224:1468-74. [Free Full Text]
   
5. Lee RJ, Kalman JM, Fitzpatrick AP, et al. Radiofrequency catheter modification of the sinus node for "inappropriate" sinus tachycardia. Circulation 1995;92:2919-28. [Abstract/Free Full Text]
   
6. Krahn AD, Yee R, Klein GJ, Morillo C. Inappropriate sinus tachycardia: evaluation and therapy. J Cardiovasc Electrophysiol 1995;6:1124-8.[Medline]
   

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