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ARRHYTHMIA ROUNDS Section Editor: George J. Klein, M.D.

A Case of Narrow Complex Tachycardia AMIR ABDELWAHAB, M.B. B.CH., M.SC., JOHN L. SAPP, M.D., F.R.C.P.C., MARTIN GARDNER, M.D., F.R.C.P.C., F.A.C.C., and MAGDY N. BASTA, M.B. B.CH., F.R.A.C.P. From the Cardiac Electrophysiology Service, Cardiology Division, Queen Elizabeth II Health Sciences Center, Dalhousie University, Halifax, Nova Scotia, Canada

A 49-year-old man with no previous cardiac history presented to hospital with 2-week history of progressive dyspnea and orthopnea. He was diagnosed with severe heart failure and pulmonary edema, and responded to intravenous (IV) diuretics and morphine. His electrocardiogram revealed narrow complex tachycardia at 140 beats per minute (Fig. 1). Initially, carotid sinus massage, intravenous adenosine 6 and 12 mg, and diltiazem 25 mg were tried, but did not influence his tachycardia. Echocardiography study showed mild left ventricular (LV) dilation with severe systolic dysfunction with an ejection fraction 20%. Intravenous amiodarone was initiated with a 300 mg bolus, followed by 1 mg/minute infusion with slight slowing of tachycardia to 130 beats Dr. Gardner served as principal investigator in a research study funded by the Heart and Stroke foundation of Nova Scotia and received significant funding for their work on Electrocardiographic Characteristics of Arrhythmogenic Right Ventricular Dysplasia. J Cardiovasc Electrophysiol, Vol. 19, pp. 330-331, March 2008. Address for correspondence: Dr. Magdy N. Basta, Associate Professor of Medicine, Dalhousie University, Rm. 2501E Halifax Infirmary, 1796 Summer Street, Halifax, NS B3H 3A7. Fax: 902-473-3158; E-mail: mbasta@ dal.ca doi: 10.1111/j.1540-8167.2007.00986.x

per minute, but his tachycardia never terminated with drug therapy. Thus, he underwent an electrophysiology study. His tachycardia was terminated with burst ventricular pacing and ventricular extrastimuli, but restarted promptly. The onset of the tachycardia is shown below (Fig. 2). Burst atrial pacing was attempted during the tachycardia (Fig. 3). What is the mechanism of this tachycardia? Discussion The tachycardia electrocardiogram (Fig. 1) demonstrates a relatively narrow complex tachycardia with cycle length of 430 ms, right axis deviation, and no visible P waves. The QRS duration is 108 ms with rSr’ pattern in V1. Based on this ECG, supraventricular tachycardia (SVT), particularly atrioventricular nodal reentrant tachycardia (AVNRT), was suspected; however, it was unusual that SVT was not affected by adenosine or diltiazem. The HV interval measured 53 ms during sinus rhythm; however, during tachycardia, it was only 30 ms (Fig. 2). There was a 1:1 VA relationship during tachycardia with the earliest atrial activation recorded near the His bundle region, suggesting a normal concentric retrograde atrial activation. Entrainment of the tachycardia from the right ventricular apex resulted in VAHV response (not shown here). The atrium could not be preexcited when the His bundle was refractory.

Figure 1. Presenting ECG showing narrow complex tachycardia with HR 140 beats.

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A Case of Narrow Complex Tachycardia

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Figure 3. Atrial pacing at a cycle length of 420 ms did not influence this tachycardia, which continues at cycle length 440 ms. Figure 2. A: Spontaneous initiation of the tachycardia. Surface ECG, His and right ventricular apex (RVA) recordings are shown. The first beat is a sinus beat followed by 2 beats of the tachycardia. B: RVA catheter was moved to high right atrium (HRA). Atrial recordings during two beats of tachycardia are shown.

AVNRT, junctional tachycardia, and orthodromic atrioventricular reentrant tachycardia (AVRT) can be ruled out by the shortening of the HV interval during tachycardia (Fig. 2). HV shortening during tachycardia can be explained by either preexcited SVT or ventricular tachycardia (VT). The former can be ruled out as atrial pacing during tachycardia clearly dissociated the atrium from the ventricle, indicating that the atrium is not part of the tachycardia circuit (Fig. 3). The correct diagnosis of this case is VT. The close similarity in QRS morphology between VT and sinus rhythm suggests that it arises from the proximal His-Purkinje network. The likely mechanism of this VT is idiopathic fascicular tachycardia originating close to the LV His bundle. Administration of procainamide resulted in slowing of the tachycardia cycle length to 530 ms, with subsequent high-grade VA block, which further supported the diagnosis of VT. The tachycardia was not terminated and retrograde 1:1 VA conduction was resumed later on. The left ventricle was mapped during VT. The tachycardia terminated during catheter manipulation at the basal septum and could not be reinduced, despite ventricular pacing and programmed stimulation. Mapping of the His Purkinje sys-

tem during sinus rhythm revealed Purkinje potentials along the LV interventricular septum. Pacing with Purkinje capture demonstrated a near-match to tachycardia high on the interventricular septum. No His-Purkinje late potentials or diastolic potentials were observed. As the VT became noninducible and the best pace map was close to the LV His bundle, no radiofrequency ablation was performed. Follow-Up After the procedure, no arrhythmias were recorded and he had remarkable improvement of his heart failure symptoms during the subsequent 3 days of hospital stay. Over 3 years of follow-up, the patient remains asymptomatic without antiarrhythmic medications. Repeated 24-hour Holter monitoring has not shown any recurrent arrhythmias. His LV ejection fraction went up to 55% 1 month after the procedure and remains normal at last follow-up. Conclusion This is a case of incessant narrow complex VT, possibly fascicular, presenting with tachycardia-induced cardiomyopathy. Mechanical interruption of the tachycardia related to catheter manipulation during the electrophysiologic study resulted in long-term cure with subsequent improvement of LV function and no recurrence over 3 years of follow-up.