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Europace (2008) 10, 1343–1345 doi:10.1093/europace/eun239 SHORT COMMUNICATION Idiopathic ventricular tachycardia arising from the right ventricular apex Antonio Navarrete* Department of Clinical Cardiac Electrophysiology, Medical Consultants, Muncie, IN 47304, USA Received 19 May 2008; accepted after revision 4 August 2008; online publish-ahead-of-print 28 August 2008 KEYWORDS Idiopathic ventricular tachycardia; Ablation; Non-contact mapping Idiopathic, focal ventricular tachycardia that originates from the right ventricular apex is presented. Arrhythmogenic ventricular dysplasia needs to be ruling out prior to making this diagnosis. This is a rare entity that can be cured with an ablation and therefore it needs to be considered in the differential diagnosis of idiopathic VTs before implanting a defibrillator. Case A 53-year-old Caucasian male presented to the ER complaining of palpitations and mild chest pain lasting for 40 min that started while he was working at his desktop. Twelvelead ECG showed wide QRS complex tachycardia, left bundle with left superior axis morphology, late transition at a cycle length of 230 ms (Figure 1B). The tachycardia was haemodynamically well tolerated. Following failure to convert the patient with amiodarone 300 mg intravenously, a 200 J biphasic synchronized shock restored sinus rhythm. He had neither past cardiac history nor family history of sudden death. Twelve-lead ECG in sinus rhythm revealed no acute coronary ischaemia (Figure 1A) with no evidence of pre-excitation. He underwent an echocardiogram, a right and left heart catheterization, a cardiac CT, and a magnetic resonance image (MRI) that show no anomalies. Sarcoidosis was ruled out and he did not have clinical symptoms suggestive of Myocarditis. The patient was taken to the electrophysiology laboratory. Typical AVNRT was induced several times, so the slow pathway was ablated despite no clinical documentation. After that, Isoproterenol was administered up to 3 mcg/m, and ventricular tachycardia was induced by ventricular pacing at 400 ms from the right ventricular apex and introducing ventricular extra stimuli at 230 ms. This tachycardia was difficult to sustain. High-density mapping showed normal right ventricular electrograms (Figure 3A). There was not an epsilon wave or T-wave inversion in the precordial leads (Figure 1A). Right ventriculography was normal (not shown). This suggests that the ventricular tachycardia Commentary The width of the QRS (.160 ms) left superior axis, rS . 100 ms, deep S-wave in V6 (Figure 1B), and fusion beats (Figure 1A) are all very suggestive of ventricular tachycardia. Atrio-ventricular dissociation (Figure 1C) is diagnostic of it.1 Arrhythmogenic ventricular dysplasia (ARVD) was suspected but two cardiac MRI performed 6 months apart did not show the presence of right ventricular fatty infiltration (Figure 2A). * Corresponding author. Tel: þ1 7652812000; fax: þ1 3178413185. E-mail address: [email protected] Figure 1 (A) Baseline 12-lead electrocardiogram. (B) Wide-QRS tachycardia. (C ) ECG leads III and AVF are shown. The sinus P-waves are marked with black arrows follow by fusion beats. Atrioventricular dissociation is presented. Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2008. For permissions please email: [email protected]. 1344 A. Navarrete Figure 2 (A) Magnetic resonance imaging of the heart. (B) Thirty degrees right anterior oblique fluoroscopic image showing the balloonmounted multielectrode array, the ablation catheter, three quadripolar catheters in the right atrium, right ventricle, and inferior vena cava. Figure 3 (A) Intracardiac ventricular electrograms from three different locations within the right ventricle. (B) Surface leads I, AVF, V1, intracardiac electrograms from the ablation catheter at the successful site and virtual unipolar electrograms computed by the ESI system are shown. (C) Isopotential map showed the earliest activation site located near the antero-lateral right ventricular apex. Colour scale has been set to that white indicates most negative potential and blue indicates least negative potential. is idiopathic. However, a concealed form of ARVD2 cannot be completely rule out and additional follow-up is needed. The Ensite array 64-electrode catheter (St Jude Medical, St Paul, MN, USA) was placed in the right ventricle. An isopotential map depicted an earliest ventricular impulse site propagating in a centripetal pattern. This map is compatible with a focal mechanism (abnormal automatism vs. triggered) though micro-re-entry cannot be ruled out. Induction with programmed stimulation and the absence of over-drive suppression is indicative of triggered mechanism. The earliest tachycardia break-through was found at the right anterolateral ventricular apex (Figure 3C). Pace mapping at that site showed 11 out of 12-pace match. The ventricular electrogram preceded the QRS by 42 ms (Figure 3B). A 4 mm tip electrode deflectable catheter (Sapphire, St Jude Medical) was utilized in a temperature control mode. One RF application at this site with a maximum temperature of 55º and maximum power of 50 W terminated the tachycardia within 5 s preceded by acceleration. During 1 year follow-up, the patient is asymptomatic on no medications. Tada et al. 3 reported premature ventricular contractions rising from the mid septum and postero-lateral along the tricuspid valve with similar electrocardiographic appearance to this case. They both have a predominant R-wave in augmented lead in contrast with the right outflow ventricular tachycardias because their axis is directed superiorly and leftwards. Although, this one is unique in that there is a later transition zone (V5–V6), probably due to a more sequential activation of both ventricles and the absence of an atrial electrogram at the ablation site. Idiopathic monomorphic ventricular tachycardia4 includes the outflow tract (right and left, aortic cusp VT), fascicular VT (anterior–posterior fascicular VT), septal VT (right and left), the pulmonary artery, adrenergic monomorphic VT, and annular VT-(mitral and tricuspid). To my knowledge, there are no reports in the medical literature of idiopathic ventricular tachycardia rising from the apex. Idiopathic ventricular tachycardia arising from the right ventricular apex Conflict of interest: A.N. is currently conducting research sponsored by, and is also a consultant for, St Jude Medical. References 1. Miller JM, Das M et al. Differential diagnosis of wide QRS complex tachycardia. In Zipes DP, Jalife J. (eds.), Cardiac Electrophysiology: From Cell to Bedside. 4th ed. Philadelphia: WB Saunders; 2004. p747–57. 2. Nava A, Thiene G, Canciani B, Martini B, Daliento L, Buja G et al. Clinical profile of concealed form of arrhythmogenic right ventricular 1345 cardiomyopathy presenting with apparently idiopathic ventricular arrhythmias. Int J Cardiol 1992;35:195–206. 3. Tada H, Tadokoro K, Ito S, Naito S, Hashimoto T, Kaseno K et al. Idiopathic ventricular arrhythmias originating from the tricuspid annulus: prevalence, electrocardiographic characteristics, and results of radiofrequency catheter ablation. Heart Rhythm 2007;4: 7–16. 4. Badhwar N, Sheinman M. Idiopathic ventricular tachycardia: diagnosis and management. Curr Probl Cardiol 2007;32:17–43.