Indian Pacing Electrophysiol. J.

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Indian Pacing Electrophysiol. J. 2010;10(4):195-200                 Case Report

Development of Malignant Ventricular Arrhythmias in a Young Male with WPW Pattern

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Alim Erdem1, Nihat Madak2, Ahmet Yilmaz3, Osman Can Yontar3, Hasan Yucel3, Ibrahim Gul3, Izzet Tandogan3

1Cardiology Department, Sivas Public Hospital, Kars, Turkey
2Cardiology Department, Malatya Public Hospital, Malatya, Turkey
3Cardiology Department, School of Medicine, Cumhuriyet University, Sivas, Turkey

Address for correspondence:
Dr. Alim Erdem, Cardiology Department, Sivas Public Hospital, Kars, Turkey.  E-mail: dralimerdem/at/gmail.com.

Abstract

In Wolff-Parkinson-White Syndrome (WPW), presence of accessory pathways causes various tachyarrhythmias that lead to different symptoms and clinical conditions in patients. Atrial fibrillation is observed in about 20-30% of this group of patients. Life threatening malignant ventricular arrhythmias and sudden cardiac deaths are observed in patients having rapid conduction in accessory pathways and short antegrade refractory periods (<250 msn). We present a WPW syndrome case that presented to the emergency service with narrow QRS tachycardia and later developed malignant ventricular arrhythmia.

Keywords: WPW syndrome; life threatening arrhythmias

Case Report

A 32 years old male with no previous cardiac evaluation and clinical complaints presented to the emergency service with palpitation. Due to narrow QRS complex tachycardia, emergency service physicians (Figure 1) administered intravenous verapamil for rate control. Meanwhile, the patient developed atrial fibrillation with wide QRS and high ventricular response (Figure 2) and then ventricular fibrillation. Normal sinus rhythm was achieved after multiple defibrillations (220 joule, Biphasic). Hemodynamic parameters and respiration were stabilized. 12 lead ECG showed characterstic delta waves and short PR interval. (Figure 3). Given these findings, the case was diagnosed as Wolff-Parkinson-White (WPW) syndrome. His physical examination, biochemical parameters and echocardiography were normal. As the case was a WPW syndrome case and as malignant ventricular arrhythmia and cardiopulmonary arrest developed due to atrial fibrillation, he was assigned to electrophysiological (EPS) study. In our case, whose orthodromic tachycardia was induced again during EPS (Figure 4). An accessory pathway was found at left anterior localization based on intracardiac findings, and successful ablation was achieved in the same session (Figure 5). On the surface ECG, it was observed that PR interval was back to normal and delta wave was no more present. The case was asymptomatic and his ECG was normal during his controls at 1st and 6th months.



Figure 1: Narrow QRS complex tachycardia at presentation




Figure 2: Atrial fibrillation with wide QRS and high ventricular response




Figure 3: 12 lead ECG showing characterstic delta waves and short PR interval of WPW syndrome




Figure 4: Orthodromic tachycardia induced during EPS




Figure 5

Discussion

WPW syndrome is a clinical entity characterized by presence of an electrical signaling accessory pathway between atrium and ventricular that may cause tachyarrhythmia's sometimes and sudden cardiac death. Studies have shown that SCD occurs at the rate of 0.15% per year in patients with WPW. These deaths are caused by atrial fibrillation with rapid ventricular response that leads to ventricular fibrillation (VF) [1,2].

The most frequently encountered tachycardia in WPW syndrome is the reentrant tachycardia. The degeneration of reciprocating tachycardia to atrial fibrillation is not uncommon [3]. It has been estimated that atrial fibrillation (AF) is observed in approximately one third of WPW patients. AF may cause fatal arrhythmias in WPW syndrome [4]. Sudden death occurs due to transmission of AF into VF with a rapid ventricular response over one or more accessory pathways with a short antegrade refractory period [5]. The first presentation of some WPW patients with asymptomatic clinical course could be due to ventricular fibrillation [6].

Risks factors for sudden death in WPW are presence of more than one AP, development of AVRT along with AF and the shortest preexcitation RR interval less than 260 msn [1,2,7]. Development of atrial fibrillation as a result of  IV verapamil administration for rate control in reciprocal tachycardia is not rare [8]. Straberg et al reported 3 cases presented with  atrial fibrillation and rapid ventricular response with wide preexcitation QRS, all of whom received intravenous verapamil (5-10 mg); and they stated that one of the patients developed ventricular fibrillation requiring several defibrillations, the other had hemodynamic deterioration and the last one had a  marked increment in the ventricular response. When verapamil is used to treat reentrant supraventricular tachycardia complicating the WPW syndrome, the electrophysiologic effects of verapamil on accessory pathway conduction during atrial fibrillation become critical. Patients with WPW syndrome have a higher incidence of atrial fibrillation than the general population [10,11]. We think that verapamil administered for rhythm and rate control at emergency service induced AF with wide QRS and consequent VF development in our case too. Antz et al. stated that patients with WPW syndrome who had undergone CPR for malignant ventricular function had normal left ventricular function at echocardiography and no ECG abnormalities and ablation of their accessory pathways prevented cardiac arrest recurrences [12]. Catheter ablation is suggested for patients resuscitated from VF or for patients at high risk for clinical atrial fibrillation with a rapid ventricular response [13].

As a result, Using AV node suppressive medicines in patients with WPW syndrome may cause atrial fibrillation followed by development of fatal cardiac arrhythmias. We believe that it is important to acquaint all the clinicians, especially the emergency service and ambulance physicians who are the first to face SVT patients in daily practice, with this issue.

References

1. Klein GJ, Bashore TM, Sellers TD, et al. Ventricular fibrillation in Wolf-Parkinson-White syndrome.  N Engl J Med 1979;301:1080-1085.

2. Torner-Montoya P, Brugada P, Smeets J et al. On behalf of the European Registry on sudden death  in the  Wolff-Parkinson- White. Ventricular fibrillation in the Wolff-Parkinson-White sydrome. Eur Heart J 1991;12:144-150.

3. Sung RJ, Castellanos D, Mallon SM, Bloom MG,  Gelband H, Myerburg RJ; Mechanisms of spontaneous alteration between reciprocating tachycardia and atrial flutter fibrilation  in the Wolff-parkinson-White syndrome. Circulation 1977;56:409.

4. Sethi KK, Dhall  A, Chadha DS, Garg S, Malani SK, Mathew OP.  J Assoc Physicians India. 2007;55:10-5.

5. Fare J, Anderson RH, Cabrera JA et al. Fluoroscopic cardiac anatomy for catheter ablation of tachycardia. Pacing Clin Electrophysiol 2002; 25:76-94.

6. Pappone C, Santinelli V, Rossanio S,  Vicedomini G, Nardi S, et al. Usefulness of invasive electrophysiologic testing to stratify the risk of arrthythmic events in asymptomatic patients with Wolff-Parkinson-White pattern: results prospective long-term follow-up study. J Am Coll Cardiol 2003;41:239-44.

7. Wellens HJJ, Bar FW, Fare J et al. Sudden death in the Wolff-Parkinson-White syndrome. In: Kulbertus HE, Wellens HJJ (eds). Sudden death, 1980. The Hague: Martinus Nijhoff, pp.392-399.

8. Wyndham CRC,  Amat-y-Leon F, Wu D, Denes P, Dhingra R, Simpson R, Rosen KM: Effects of cycle length on atrial vulnerability. Circulation 1977;55: 260.

9. Strasberg B, Sagie A, Rechavia E, Katz A, Ovsyscher IA, Sclarovsky S, Agmon J: Deleterious effects of intravenous verapamil in Wolff-Parkinson-White patients and atrial fibrillation. Cardiovasc Drugs Ther. 1989;2:801-6.

10. Zipes DP, Foster PR, Troup PJ, Pederson DH: Atrial induction of ventricular tachycardia: reentry versus triggered automaticity Am J Cardiol. 1979; 44: 1.

11. Wellens HJ, Durrer D: Wolff-Parkinson-White Syndrome and atrial fibrillation: relation between refractory period of accessory pathway and ventricular rate during atrial fibrillation. Am J cardiol 1974; 34;777.

12. Antz M, Weiss C, Volkmer M, Hebe J, Ernst S, Ouyang F, et al. Risk of sudden death after successful accessory atrioventricular pathway ablation in resuscitated patients with Wolff-Parkinson-White syndrome. J Cardiovasc Electrophysiol 2002; 13: 231-6.

13. Zipes DP, DiMarco JP, Gillett PC, et al. Guidelines for clinical intracardiac electrophysiological and catheter ablation procedures. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Clinical Intracardiac Electrophysiologic and Catheter Ablation Procedures), developed in collaboration with the North American Society of Pacing and Electrophysiology.  J Am Coll Cardiol 1995; 26: 555-73.

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