Title: Inappropriate sinus node tachycardia successfully treated with radiofrequency ablation at the arcuate ridge Authors: F. Syed 1, A. Killu 1, J. Gard 2, W. Shen 3, D. Packer 2, S. Asirvatham 2 (1) Mayo Clinic, Department of Internal Medicine, Rochester, United States of America (2) Mayo Clinic, Division of Cardiovascular Diseases and Internal Medicine, Rochester, United States of America (3) Mayo Clinic, Division of Cardiovascular Diseases, Scottsdale, United States of America Topic: 01.12 - Catheter ablation Inappropriate sinus node tachycardia successfully treated with radiofrequency ablation at the arcuate ridge Introduction Inappropriate sinus tachycardia (IST) manifests with persistently elevated heart rate and an exaggerated heart rate response for the level of physiological, pathological or pharmacological stress. Usually there is evidence of autonomic dysfunction and modification of the sinus node with radiofrequency ablation is ineffective in alleviating symptoms [1]. In contrast, focal atrial tachycardia (AT) arising from structures in close proximity to the sinoatrial node (SAN), such as the crista terminalis, is amenable to ablation therapy [2]. We describe a case with clinical features of IST and evidence of autonomic dysfunction which was successfully treated by radiofrequency ablation at the arcuate ridge. Case A 48 year old previously well woman was evaluated for a four-year history of rapid palpitations at rest, exertional dyspnea, episodes of presyncope and syncope and persistent tachycardia previously diagnosed as IST. Ambulatory electrocardiographic monitoring had correlated symptoms with episodes of sinus tachycardia with rates ranging from 100 to 170 per minute. She denied excessive caffeine or alcohol intake and there was no significant family history. Transthoracic and transesophageal echocardiography, cardiac magnetic resonance imaging, cardiac catheterization with intracardiac pressure and oxygen saturation measurements and coronary angiography were normal. Previously she had tried flecainide, propafenone and sotalol without benefit. She had undergone four previous radiofrequency ablations between two to three years prior to her current presentation, when a tachycardia of 300 to 410 millisecond cycle length with characteristics of a triggered mechanism was repeatedly mapped to the vicinity of the sinus node and ablated. Symptoms improved initially but returned within a few days to weeks after each ablation, and were partially controlled with metoprolol succinate at the time of her current presentation. She presented for consideration of a fifth ablation attempt on account of ongoing debilitating symptoms with significant impact on quality of life. Cardiac and general clinical examinations were normal except for resting tachycardia. Pulse rate was noted to be higher when standing (125 per minute) than when sitting or lying (100 per minute), without a corresponding change in blood pressure and with a reduction in rate when standing with thighs crossed (104 per minute). Full blood count, fasting blood glucose, renal and liver function, thyroid function, serum catecholamine levels when supine and upright, and plain chest radiography were normal. On 12-lead electrocardiography, sinus rhythm at a rate of 111 per minute, right bundle branch block, p-pulmonale and right axis deviation were present. On ambulatory monitoring, average heart rate was 117 per minute when awake and 94 per minute when asleep. Symptom-limited cardiopulmonary exercise testing demonstrated resting heart rate 129 per minute, increasing to 193 per minute at peak exertion, 146 per minute three minutes post exercise and 125 per minute after recovery; oxygen uptake, blood pressure response, and ventilation during exercise was normal. During prolonged (45 minutes) tilt to 70 degrees with and without isoproterenol, an abrupt change in heart rate and p-wave morphology was seen (Figure 1) but there were no features of vasodepression. A quantitative sudomotor axon reflex test demonstrated normal adrenergic and cardiovagal function. Thermoregulatory sweat testing and response to carotid sinus massage were normal. Procedure With written informed consent, the patient was studied in the electrophysiology laboratory in a fasted state and was lightly sedated with 2 mg midazolam and 100 mcg fentanyl. Blood pressure was monitored with a right femoral arterial line. Peripheral venous access was obtained for intravenous fluids. Therapeutic anticoagulation during the procedure was achieved with intravenous heparin. Using strict aseptic technique, 1% lidocaine local anesthesia and a standard percutaneous approach, 6 multipolar electrode catheters were placed as follows: Orbiter (size 7F) in the coronary sinus through the right internal jugular vein; intracardiac echo catheter (size 10F) and ablation catheter (size 8F) in the right atrium through the right femoral vein; steerable quadripolar (size 7F) in high right atrium, Octapolar (size 6F) in bundle of His region and Quadripolar (size 5F) in the right ventricle all through the left femoral vein. Abrupt changes in heart rate were noted spontaneously and also secondary to catheter manipulation. Without isoproterenol, the changes in heart rate were from 80 beats per minute to 120 beats per minute. With 2 mcg/ min of isoproterenol, they occurred from 130 beats per minute to 160 beats per minute. A linear multi-electrode catheter was placed along the crista terminalis. A Lasso mapping catheter was placed in the superior vena cava. In the presence of isoproterenol, a tachycardia of 400 millisecond cycle length was reliably inducible with burst atrial pacing. However, it was not entrainable and had characteristics of triggered automaticity. Distinguishing whether this was a discrete atrial tachycardia or a portion of the sinus node complex that gave rise to faster rates than other sites was not possible. However, based on 3-dimensional electroanatomic, the early activation site of the sinus node during slow rates was distinct from those during faster rates. Using intracardiac echocardiography, a prominent arcuate ridge going from the crista terminalis to the limbus region was noted and the earliest site of activation correlated with an area just below the junction of the superior vena cava and right atrium on the ridge (Figure 2). After delivering radiofrequency energy for the first time to this location, the tachycardia ceased. A further eleven ablation pulses were performed around this site. After ablation, no tachycardia was seen. Phrenic nerve pacing during, and at the end of, the procedure was used to ensure that its function was not affected by the ablation. There were no procedural complications. Outcome The patient was started on midodrine and recommended to ensure adequate solute intake and use a compression stocking hose. Metoprolol was tapered down and stopped. On follow-up at 8 months, the patient remained asymptomatic, with resolution of exertional dyspnea and debilitating palpitations. Repeat ambulatory electrocardiographic monitoring demonstrating persistent sinus rhythm with an average rate of 71 per minute, ranging from 61 to 111 per minute. Conclusion The mechanisms underlying IST are not completely understood and management is challenging. This case of atrial tachycardia arising from a focus very close to the sinoatrial node had evidence of autonomic dysfunction and clinical features consistent with IST, but was successfully treated with radiofrequency ablation at the arcuate ridge. We discuss the implications for understanding novel mechanisms underlying IST and when it may be appropriate to consider ablating such inappropriate tachycardia. References 1. Shen WK. How to manage patients with inappropriate sinus tachycardia. Heart Rhythm. 2005; 2(9):1015-9 2. Kalman JM, Olgin JE, Karch MR, Hamdan M, Lee RJ, Lesh MD. "Cristal tachycardias": origin of right atrial tachycardias from the crista terminalis identified by intracardiac echocardiography. J Am Coll Cardiol. 1998; 31(2):451-9. Figures Figure 1 - Prolonged tilt testing with and without isoproterenol, reveals an abrupt change in heart rate and p-wave morphology. Figure 2: Intracardiac echocardiography shows a prominent arcuate ridge extending from the crista terminalis to the limbus region. The earliest site of activation correlated with an area just below the junction of the superior vena cava and right atrium on the ridge.