DEVICE ROUNDS Coexistent Brugada Syndrome and Wolff-Parkinson-White Syndrome: What Is the First Clinical Presentation? HAKAN HASDEMIR, M.D., AHMET T. ALPER, M.D., TOLGA S. G ¨ UVENC ¸, M.D., Y ¨ UCESIN ARSLAN, M.D., H ¨ USEYIN AKSU, M.D., ESRA POYRAZ, M.D., ZEKERIYA NURKALEM, M.D., AHMET L. ORHAN, M.D., and NAZMIYE C ¸AKMAK, M.D. From the Department of Cardiology, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Training and Research Hospital, Istanbul, Turkey The coexistence of Brugada syndrome and Wolff-Parkinson-White (WPW) syndrome is a very rare phenomenon. We describe a 31-year-old patient without any previous cardiac disorder admitted to our hospital due to palpitations and concomitantly diagnosed as WPW syndrome and treated with radiofrequency catheter ablation. He was later diagnosed with Brugada syndrome and followed-up 2 years without any symptoms. We discuss other previously reported cases in literature, in which these two conditions exist simultaneously. (PACE 2011; 34:760–763) Wolff-Parkinson-White syndrome, Brugada syndrome, sudden cardiac death Introduction Brugada syndrome is a primary electrical ab- normality that carries an increased sudden cardiac death (SCD) risk due to abnormal electrophysio- logic properties of right ventricular epicardium. Wolff-Parkinson-White (WPW) syndrome is the most common cause of preexcitation. It usually presents with supraventricular tachycardia, and in rare occasions, it may cause SCD. As both disor- ders may have similar symptoms, coexistence of these two disorders brings up problems regarding the exact pathophysical mechanisms underlying the patient’s complaints and a possible interaction between these two disorders. However, the most important question is “Could the combination of these two disorders cause an increased risk for SCD?” Case Report A 31-year-old male patient was admitted to our hospital due to palpitations that occurred five times in the past 1 year, and ended spontaneously. His electrocardiogram (ECG) revealed manifest preexcitated WPW syndrome with positive delta waves in leads V1–V6, I, II, aVL, and negative delta Conflicts of interest: The authors declare that they have no commercial associations or sources of support that might pose a conflict of interest. Address for reprints: Hakan Hasdemir, M.D., Siyami Ersek Hospital, Tıbbiye Str. No: 25, ¨ Usk ¨ udar/ ˙ Istanbul, Turkey. Fax: 90-216-337-97-19; e-mail: hakanhasdemir@yahoo.com Received May 31, 2010; revised July 22, 2010; accepted October 14, 2010. doi: 10.1111/j.1540-8159.2010.02997.x waves in leads III and aVF. In his initial ECG, one beat that was conducted on normal conduction pathway with a PR distance of 120 ms was compat- ible with Type 2 Brugada ECG (Fig. 1). He did not experience any episodes of syncope and had a neg- ative family history for SCD. His physical exami- nation, serum electrolyte levels, other biochemical analyses, and plain chest roentgenogram were all normal. Echocardiographic examination showed normally functioning left and right ventricles and chamber volumes were within physiologic limits. Valvular structures also appeared as normal. An electrophysiologic study (EPS) was scheduled for accessory way ablation on the next day. The earliest V wave was detected distal to coronary si- nus, and the shortest ventriculoatrial interval was recorded in coronary sinus anterolateral location during atrioventricular reciprocating tachycardia that was induced with rapid ventricular pacing and a cycle length of 294 ms. Accessory pathway was ablated using radiofrequency energy via using retrograde aortic approach. Both antegrade and retrograde conductions were disappeared, and tachycardia could not be induced again. As a type 2 Brugada pattern was also present in the first ECG, programmed electrical stimulation and rapid ventricular pacing was performed in right ventricular apex and right ventricular outflow tract with a cycle length of 500 ms and a coupling interval of 200/220/200 ms to induce ventricular tachyarrhythmia. As no ventricular arrhythmias could be induced, the study was terminated. To rule out arrhythmogenic right ventricular dysplasia, magnetic resonance imaging was per- formed but found as normal. Also, a coronary C 2010, The Authors. Journal compilation C 2010 Wiley Periodicals, Inc. 760 June 2011 PACE, Vol. 34