Erdem DiRER,1 MD, Murat OZDEMIR, MD, U. Kemal TEZCAN, MD, Sinan AYDOGDU, MD, Sule KORKMAZ, MD, Yalcim SOZUTEK, MD, and Emine KUTUK, MD

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1 Can Isolated, Symptomatic, Frequent Ventricular Premature Depolarizations be a Predictor of an Inducible Ventricular Tachycardia? Treatment by Radiofrequency Catheter Ablation Erdem DiRER,1 MD, Murat OZDEMIR, MD, U. Kemal TEZCAN, MD, Sinan AYDOGDU, MD, Sule KORKMAZ, MD, Yalcim SOZUTEK, MD, and Emine KUTUK, MD SUMMARY In this report, we describe a case of sustained ventricular tachycardia of right ventricular outflow tract origin, induced by dobutamine infusion in a patient with symptomatic, frequent ventricular premature depolarizations but no documented clinical ventricular tachycardia. Radiofrequency catheter ablation abolished not only the ventricular tachycardia itself, but also the frequent ventricular premature depolarizations responsible for all the symptomatology. In conclusion, provocation by catecholamine infusion may have a place in the search for an alternative to antiarrhythmic therapy in patients with isolated, frequent and symptomatic ventricular premature depolarizations. (Jpn Heart J 1997; 38: ) Ventricular premature depolarizations, Radiofrequency abla- Key words: tion ENTRICULAR premature depolarizations occur in approximately 1% of clinically healthy subjects as recorded by routine electrocardiography.1) In the absence of cardiovascular abnormalities, ventricular premature depolarizations may be largely innocuous.2) In the light of this benign prognosis and the potentially unfavorable outcome of long-term antiarrhythmic therapy, suppression of ventricular premature depolarizations is not justified in asymptomatic subjects.3) Antiarrhythmic therapy may however, be warranted to provide symptomatic improvement in the presence of ventricular premature depolarizations From the 1Cardiology Department, Ankara University, School of Medicine, Ankara, and Cardiology Department, Turkiye Yuksek Ihtisas Hastanesi, Ankara, Turkey. Address for correspondence: Erdem Diker, MD, 1. Cadde (Taskent Cad), 69/10, 06500, Bahcelievler, Ankara, Turkey. Received for publication April 9, Accepted July 29,

2 128 DIKER ET AL Jpn Heart J January 1997 associated with palpitations and disturbed life quality. This creates a serious dilemma due to the inevitable risk of proarrhythmia. This report presents a case of symptomatic ventricular premature depolarizations in a structurally normal heart treated by a nonpharmacological modality. CASE REPORT A 24-year-old woman was admitted to our center with the complaint of palpitations for 3 years. The first electrocardiogram revealed frequent ventricular premature depolarizations of left bundle branch block morphology. The history and physical examination were normal except for the extrasystoles. The blood biochemistry and chest X-ray were likewise normal. The thyroid function tests revealed no abnormalities. Two-dimensional and Doppler echocardiographic examinations were within normal limits. The patient underwent right and left heart catheterization, including right and left ventriculography, and coronary arteriography, but no abnormalities were found. The 48-hour ambulatory Holter monitoring demonstrated frequent, isolated ventricular premature depolarizations (1180 ventricular premature depolarizations per hour) (Figure 1a). There were no ventricular runs or episodes of nonsustained or sustained ventricular tachycardia. Because the patient was too anxious about exercise, a treadmill exercise test could not be performed. Although the patient could not Figure 1. a: Holter monitoring recording before ablation procedure. Frequent ventricular premature depolarizations were recorded. b: Holter monitoring recording after ablation session. All ventricular premature depolarizations were eliminated.

3 Vol 38 No 1 ISOLATED VENTRICULAR PREMATURE DEPOLARIZATIONS 129 perform a maximal exercise test, Holter monitoring revealed a maximum heart rate of 139 beats per minute and multiple episodes of heart rates above 120 beats per minute, but no ventricular tachycardia runs during either of these periods. To further evaluate the ventricular premature depolarizations, we performed programmed electrical stimulation. No tachycardia was induced by two extrastimuli applied to the right ventricular apex at 3 drive cycle lengths (600, 500 and 400ms). Various antiarrhythmic agents were administered in an attempt to suppress the ventricular premature depolarizations as the patient had severe discomfort due to palpitations. No suppression was achieved with either mexiletine, procainamide, quinidine, propafenone or metoprolol. The patient was then put on amiodarone (400mg per day, PO). At the end of three weeks of therapy, there was no suppression of ventricular premature depolarizations on Holter monitoring and the complaint of palpitation persisted. Therefore, the drug was discontinued. A reevaluation by a second electrophysiologic study was planned. All Figure 2. Intracardiac recording during ventricular tachycardia arising from the right ventricular outflow tract. Note that the endocardial electrogram recorded from the distal electrode of the right ventricular outflow tract catheter precedes the onset of the QRS complex (vertical line) during ventricular tachycardia by 40ms. This was the site at which radiofrequency current was delivered. The second activity recorded from the ablation catheter represents atrial activity resulting from 1:1 ventriculoatrial conduction during the tachycardia. HRA=high right atrium; RV=right ventricle; LV=left ventricle. Paper speed: 100 mm/sec.

4 130 DIKER ET AL Jpn Heart J January 1997 tachycardia runs with a morphology similar to the ventricular premature depolarizations were seen. Thereafter sustained ventricular tachycardia with a rate of 142 beats per minute and left bundle branch block right axis morphology appeared. Because of the lack of His deflection recording, we performed rapid atrial pacing, which produced supraventricular capture during ventricular tachycardia and clarified that the tachycardia was ventricular in origin. To determine the origin of the tachycardia, activation mapping was performed during ventricular tachycardia. The right ventricular outflow tract was found to be the origin of the tachycardia and it was decided to proceed with radiofrequency catheter ablation at the same session. The first activation focus was found to be the anteroseptal aspect of the right ventricular outflow tract and a radiofrequency current of 30 Watts was applied to this localization in three pulses, each lasting for 45 seconds (Figure 2). The tachycardia disappeared at the 15th second of the second radiofrequency energy application. Despite programmed stimulation and increasing doses of dobutamine, the tachycardia failed to reappear. No more ventricular premature depolarizations were visible in the catheterization laboratory. The subsequent 48-hour Holter monitoring revealed no ventricular premature depolarizations (Figure 1b). The patient performed a treadmill exercise test during the postablation period when her anxiety about exercise had disappeared and she achieved a heart rate of 165 beats per minute at the 3rd stage of the Bruce Protocol, but neither ventricular premature depolarizations nor ventricular tachycardia runs appeared. She was discharged on aspirin, 300mg per day. At 3 and 6 month followups, she had no complaint of palpitations and Holter recordings revealed no ventricular premature depolarizations. DISCUSSION It has been suggested that the site of origin of ventricular premature depolarizations can be identified by QRS morphology in healthy subjects. Specifically, right ventricular, premature depolarizations are characterized by QRS complexes with a left bundle branch block pattern and, premature beats arising from the left

5 Vol 38 ISOLATED VENTRICULAR PREMATURE DEPOLARIZATIONS 131 No 1 ventricle are characterized by a right bundle branch block pattern.8,9) Studies based on electrocardiographic morphology proposed a right ventricular origin in 75% of ventricular premature depolarizations seen in subjects without organic heart disease.8,9) A similar situation holds for idiopathic ventricular tachycardia. In those with structurally normal hearts, ventricular tachycardias with right bundle branch block morphology have been shown to originate from the left ventricle, whereas those with left bundle branch block morphology have been shown to originate from the right ventricle.5) It may be suggested in our case that the ventricular premature depolarizations with left bundle branch block morphology originate from the right ventricle because there are no clues as to the presence of any underlying organic heart disease. Moreover, we consequently demonstrated that the ventricular tachycardia which was induced by dobutamine infusion and which had morphological properties similar to the ventricular premature depolarizations, originated from the right ventricle. Catecholamine dependent ventricular tachycardias with right ventricular outflow tract origin, that usually present in women as episodes of nonsustained ventricular tachycardia, are termed repetitive monomorphic ventricular tachycardia.10) Our case is consistent with the diagnosis of repetitive monomorphic ventricular tachycardia except for the absence of nonsustained ventricular tachycardia attacks despite prolonged periods of Holter monitoring. This absence remains an obstacle to this diagnosis. On the other hand, the inducibility of the tachycardia by dobutamine infusion suggests a possible relation between the tachycardia mechanism and the ventricular premature depolarizations. In fact, there are three proposed mechanisms of ventricular premature depolarization formation. These are automaticity, triggered activity and reentry.4) In most instances it will be impossible to indicate with certainty the mechanism involved. The same mechanisms apply to the formation of ventricular tachycardia, but it is relatively easier to detect the mechanism responsible for its formation.5) The inability to induce the tachycardia by programmed stimulation suggests that reentry is an unlikely underlying mechanism in our case. The inducibility of the tachycardia under catecholamine infusion provides strong support for either triggered activity or automaticity as the underlying mechanism.6,7) Since we did not investigate the response of the tachycardia to either adenosine or a calcium channel blocker, we do not have a clear idea as to the underlying mechanism in our case. Radiofrequency catheter ablation has a high success rate in tachycardias originating from the right ventricular outflow tract.11) We demonstrated that the induced tachycardia disappeared after radiofrequency catheter ablation. Interestingly, the ventricular premature depolarizations also disappeared. In a case report by Gumbrielle et al., VPDs originating from the right ventricular outflow

6 132 DIKER ET AL Jpn Heart J January 1997 tract were successfully ablated by radiofrequency current.12) In this report, no sustained tachycardia was induced despite isoproterenol infusion and ventricular ectopy mapping was performed. In our case, it is not clear whether the high dose dobutamine infusion had any particular role in the induction of tachycardia. In conclusion, ventricular premature depolarizations without organic heart disease are still enigmatic. When severely symptomatic, they may warrant antiarrhythmic therapy which obviously almost always carries its own risks. With this case, we demonstrated that isolated ventricular premature depolarizations proposed to originate from the right ventricle may be related to repetitive monomorphic ventricular tachycardia. Thus, we speculate that provocation by catecholamine infusion be part of the evaluation of isolated ventricular premature depolarizations. A substrate of isolated ventricular premature depolarizations suitable for ablation therapy may be detected in this way. REFERENCES 1. Barrett PA, Peter CT, Swan HJC, Singh BN, Mandel WJ. The frequency and prognostic significance of electrocardiographic abnormalities in clinically normal individuals. Prog Cardiovasc Dis 1981; 23: Kennedy HL, Whitlock JA, Sprague MK, Kennedy LJ, Buckingham TA, Goldberg RJ. Long-term follow-up of asymptomatic healthy subjects with frequent and complex ventricular ectopy. N Engl J Med 1985; 312: The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. N Engl J Med 1989; 321: Nabil E1-Sherif. The Premature Complex: Mechanisms and Significance-An update. In: Mandel WJ, editor. Cardiac Arrhythmias. Their mechanisms, diagnosis, and management. Philadelphia: J.B. Lippincott Company, 1987; Akhtar M. Clinical spectrum of ventricular tachycardia. Circulation 1990; 82: Buxton AE, Marchlinski FE, Doherty JU, et al. Repetitive monomorphic ventricular tachycardia: clinical and electrophysiologicharacteristics in patients with and patients without organic heart disease. Am J Cardiol 1984; 54: Palileo E, Ashley W, Swiryn S, et al. Exercise provokable right ventricular outflow tract tachycardia. Am Heart J 1982; 104: Kennedy HL, Undenhill SJ. Frequent or complex ventricular ectopy in apparently healthy subjects. A clinical study of 25 cases. Am J Cardiol 1976; 38: Lewis S, Kanakis C, Rosen KM, Denes P. Significance of site of origin of premature ventricular contractions. Am Heart J 1979; 97: Hurwitz JL, Josephson ME. Ventricular tachycardia in noncoronary disease. In: Josephson ME, Wellens HJJ, editors. Tachycardias: Mechanisms and Management. New York: Futura Publishing Company, Inc. 1993; Calkins H, Kalbfleisch SJ, E1-Atassi R, Langberg JJ. Morady F. Relation between efficacy of radiofrequency catheter ablation and site of origin of idiopathic ventricular tachycardia. Am J Cardiol 1993; 71: Gumbrielle T, Bourke JP, Furniss SS. Is ventricular ectopy a legitimate target for ablation? Br Heart J 1994; 72: