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Recognition of this type of tachycardia, has important practical value : we must know how to distinguish idiopathic ventricular tachycardia from supraventricular tachycardia with aberration since treatment will be very different. This review summarises the common forms of idiopathic ventricular tachycardias that the general cardiologist should know.
Idiopathic ventricular tachycardia in patients with an anatomically normal heart is a distinct entity whose management and prognosis differs from ventricular tachycardia associated with structural heart disease. The tachycardia's QRS morphology on surface electrocardiogram (ECG) predicts the site of origin and is commonly classified as right ventricular tachycardia or left ventricular tachycardia. Patients generally tolerate the tachycardia and sudden cardiac death is rare in this patient population. Treatment options include pharmacotherapy or catheter ablation. The prognosis of these patients remains excellent. Observed Ventricular tachycardias (VT) are usually related to structural heart disease. However in 10% of patients with VT, no structural heart disease, metabolic/electrolyte abnormalities or long QT syndrome can be found. These arrhythmias have been called idiopathic VT. They consist of various subtypes defined by their clinical presentation (repetitive monomorphic tachycardias, exercise-induced sustained ventricular arrhythmias) and/or their underlying mechanism (adenosine sensitive triggered arrhythmias, intrafascicular or interfascicular re-entrant arrhythmias). These arrhythmias have certain anatomic locations within the heart and manifest specific electrocardiographic (ECG) patterns which help to identify their site of origin. A characteristic common to most cases of idiopathic ventricular tachycardia is good prognosis, although patients should continue to have periodic cardiac follow-ups to rule out latent progressive heart disease such as arrhythmogenic right ventricular dysplasia or other forms of cardiomyopathies. This review summarises common forms of idiopathic ventricular tachycardias that the general cardiologist should know (Table 1).
Outflow tract ventricualr tachycardias (OT VT) comprise a subgroup of idiopathic VT that are predominantly localised in and around the right and left ventricular outflow tracts. OT VT are the most common form of idiopathic VTs and originate, in more than 80-90% of cases, from the right ventricular outflow tract. They manifest at a relatively early age (30-50 years, range, 6 to 80 years) with equal distribution between sexes in left ventricular outflow tract VT (LVOT VT) whereas right ventricular outflow tract VT (RVOT VT) is more common in females. The typical presentation of these arrhythmias consists of:
Clinical presentation, most patients present with palpitations, less frequently with dizziness and a minority of patients present syncope. Initial evaluation must include,
ECG recognition. RVOT VT is associated with a characteristic ECG morphology of LBBB with inferior axis (Figure 1a). Anterior sites in the RVOT shows a dominant Q-wave or a qR complex in lead I and a QS complex in aVL. Pacing at the posterior sites produce a dominant R-wave in lead I, QS or R-wave in aVL and an early precordial transition (R/S = 1 by V3)1. LVOT VT is suggested by LBBB morphology with inferior axis with small R-waves in V1 and early precordial transition (R/S = 1 by V2 or V3) or RBBB morphology with inferior axis2-3 and presence of S-wave in V64 (Figure 1b). Aortic sinus cusp origin is sometimes difficult to differentiate from RVOT VT because both are so close to each other. Coronary cusp origin has to be though when we fail an ablation in the RVOT , ECG shows a LBBB inferior axis morphology with taller monophasic R-waves in inferior leads and an early precordial R-wave transition by V2-V3. Ouyang et al5 evaluated the ECG differences between RVOT/aortic sinus cusp VT origin. They found that a broader R-wave duration and a taller R/S wave amplitude in V1-V2 favored VT arising from the aortic cusp.
The decision to treat patients with OT VT depends on frequency and severity of symptoms. Treatment options include medical therapy vs catheter ablation.
This form of idiopathic VT was first described by Zipes et al9 in 1979 with the following characteristics: induction with atrial pacing, RBBB morphology with left axis deviation and occurrence in patients without structural heart disease. In 1981, Belhassen et al10 showed that this form of VT could be terminated by verapamil, the fourth identifying featured. This tachycardia typically occurs in patients between the ages of 15 to 40 years 11-12. Most of the affected patients are males (60 to 70%). Clinical presentation. Symptoms include palpitations, fatigue, dyspnea, dizziness and presyncope. Syncope and sudden death are very rare. Most of the episodes occur at rest, although can be triggered by exercise and emotional stress. Tachycardia-induced cardiomyopathy due to incessant tachycardia has been described (11). The most likely mechanism of idiopathic left ventricular tachycardia is reentry with an excitable gap and a zone of slow conduction since can be initiated and terminated with programmed stimulation as well as the demonstration of entrainment of the tachycardia with rapid pacing (13-14). ECG recognition. The baseline 12-lead ECG is normal in most patients or it may show transient T-wave inversions related to T-wave memory shortly after a tachycardia episode terminates. The ECG during tachycardia is characterized by a right bundle branch block QRS configuration with a left superior axis, suggesting an exit site from the infero-posterior ventricular septum (Figure 2). The QRS duration in fascicular VT varies from 140 ms to 150 ms and the duration from the beginning of the QRS onset to the nadir of the S-wave in the precordial leads is 60 to 80 ms. This makes it difficult to differentiate this tachycardia from supraventricular tachycardia with aberrancy using the criteria based on QRS morphology and RS interval15. However a careful analysis of the surface ECG can demonstrate VA dissociation and rapid atrial pacing during tachycardia can demonstrate AV dissociation and favors the diagnosis of fascicular VT.
The long-term prognosis of patients with fascicular VT without structural heart disease is very good. Arrhythmias in patients with sporadic, well-tolerated episodes of idiopathic left ventricular tachycardia may not progress despite absence of pharmacologic therapy16. Patients with moderate symptoms can be treated with oral verapamil (120 to 480 mg/day). Radiofrequency catheter ablation is an appropriate management strategy for patients with severe symptoms or those intolerant or resistant to antiarrythmic therapy. It could been performed successfully by targeting the earliest high-frequency Purkinje potencial during VT17,18. Long-term success after catheter ablation is more than 92% with rare complications that include mitral regurgitation due to catheter entrapment in the chordae of the mitral valve leaflet and aortic regurgitation due to damage to the aortic valve using a retrograde aortic approach19.
Figure 1a/1b. RVOT non-sustained monomorphic ventricular tachycardia (on the left side) and LVOT ventricular bigeminy (on the right side). Figure 2. Fascicular VT with RBBB morphology and left anterior fascicular block pattern.
Ventricular arrhythmia in the absence of structural heart disease concerns a small subgroup of patients with VT. Recognition of this type of tachycardia has important practical value and we must distinguish it from supraventricular tachycardia with aberration since the treatment will be very different. Depending on tachycardia mechanism, idiopathic VT may respond to beta-blockers, Ca2+ channel blockers or to vagal manueuvers, although radiofrequency ablation is curative in most patients.
1.- Jadonath RL, Schwartman DS, Preminger MW, et al. Utility of the 12-lead electrocardiogram in localizing the origin of right ventricular outflow tract tachycardia. Am Heart J 1995;130:1107-13. 2.- Callans DJ, Menz V, Schwartzman D, et al. Repetitive monomorphic tachycardia from left ventricular outflow tract: electrocardiographic patterns consistent with a left ventricular site of origin. J Am Col Cardiol 1997;29:1023-7. 3.- Kamakura S, Shimizu W, Matsuo K, et al. Localization of optimal ablation site of idiopathic ventricular tachycardia from right and left ventricular outflow tract by body surface ECG. Circulation 1998;98:1525. 4.- Hachiya H, aonuma K, Yamauchi Y, et al. Electrocardiographic characteristic of left ventricular outflow tract tachycardia. Pacing Clin Electrophysiol 2000;23:1930-4. 5.- Ouyang F, Fotuchi P, Ho SY, et al. Repetitive monomorphic ventricular tachycardia originating from the aortic sinus cusp: electrocardiographic characterization for guiding catheter ablation. J Am Coll Cardiol 2002;39:500-8. 6.- Buxton AE, Waxman HL, Marchlinski FE, et al. Right ventricular tachycardia: clinical and electrophysiologic characteristics. Circulation 1983;68:917-27. 7.- Mont L, Seixas T, Brugada P, et al. Clinical and electrophysiologic characteristics of exercise-related idiopathic ventricular tachycardia. Am J Cardiol 1991;68:97-0. 8.- Joshi S, Wilber DJ. Ablation of idiopathic right ventricular outflow tract tachycardia: current perspectives. J Casrdiovasc Electrophysiol 2005,16(suppl 1):S52-8. 9.- Zipes DP, Foster PR, Troup PJ, et al. Atrial induction of ventricular tachycardia: reentry versus triggered automaticity. Am J Cardiol 1979;44:1-8. 10.- Belhassen B, Rotmensch HH, Laniado S. Response of recurrent sustained ventricular tachycardia to verapamil. Br Heart J 1981;46:679-82. 11.- Ward DE, Nathan AW, Camm AJ. Fascicular tachycardia sensitive to calcium antagonists. Eur Heart J 1984;5:8896-905. 12.- Ohe T, Aihara N, Kamakura S, et al. Long term outcome of verapamil-sensitive sustained left ventricular tachycardia in patients without structural heart disease. J Am Coll Cardiol 1995;25:54. 13.- Ohe T, Shimomura K, Aihara N, et al. Idiopathic sustained left ventricular tachycardia: clinical and electrophysiologic characteristics. Circulation 1988;77:560-8 14.- Okumura K, Olshansky B, Henthorn RW, et al. Demonstration of the presence of slow conduction during sustained ventricular tachycardia in man: use of transient entraintment of the tachycardia. Circulation 1987;75:369. 15.- Brugada P, Brugada J, Mont L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991;83:1649-59. 16.- Ohe T, Aihara N, Kamakura S, et al. Long-term outcome of verapamil-sensitive sustained left ventricular tachycardia in patients without structural heart disease. J Am Coll Cardiol 1995;25:54. 17.- Nakagawa H, Beckman KJ, McClelland JH, et al. Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by Purkinje potential. Circulation 1993;88:2607. 18.- Wen MS, Yeh SJ, Wang CC, et al. Successful radiofrequency ablation of idiopathic left ventricular tachycardia at a site away from the tachycardia exit. J Am Coll Cardiol 1997;30:1024. 19.- Page RL, Shenasa H, Evans JJ, et al. Radiofrequency catheter ablationof idiopathic recurrent ventricular tachycardia with right bundle branch block, left axis morphology. Pacing Clin Electrophysiol 1993;16:327-36.
Diego Pérez Díez, M.D., Josep Brugada, M.D., Ph.D. Arrhythmia Section, Thorax Institute, Hospital Clínic, University of Barcelona, Spain.