evidence suggesting cyclic AMP-mediated triggered activity. Circulation 1986; 74:270. 57. Sung RJ, Shapiro WA, Shen EN, et al. Effects of verapamil on ventricular tachycardias possibly caused by reentry, automaticity, and triggered activity. J Clin Invest 1983; 72:350. 58. Sung RJ, Keung EC, Nguyen NX, Huycke EC. Effects of beta-adrenergic blockade on verapamil-responsive and verapamil-irresponsive sustained ventricular tachycardias. J Clin Invest 1988; 81:688. 59. Farzaneh-Far A, Lerman BB. Idiopathic ventricular outflow tract tachycardia. Heart 2005; 91:136. 60. Lerman BB, Dong B, Stein KM, et al. Right ventricular outflow tract tachycardia due to a somatic cell mutation in G protein subunitalphai2. J Clin Invest 1998; 101:2862. 61. Viskin S, Rosso R, Rogowski O, Belhassen B. The "short-coupled" variant of right ventricular outflow ventricular tachycardia: a not-so-benign form of benign ventricular tachycardia? J Cardiovasc Electrophysiol 2005; 16:912. 62. Noda T, Shimizu W, Taguchi A, et al. Malignant entity of idiopathic ventricular fibrillation and polymorphic ventricular tachycardia initiated by premature extrasystoles originating from the right ventricular outflow tract. J Am Coll Cardiol 2005; 46:1288. https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 24/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate 63. Viskin S, Antzelevitch C. The cardiologists' worst nightmare sudden death from "benign" ventricular arrhythmias. J Am Coll Cardiol 2005; 46:1295. 64. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2018; 72:e91. 65. Gill JS, Blaszyk K, Ward DE, Camm AJ. Verapamil for the suppression of idiopathic ventricular tachycardia of left bundle branch block-like morphology. Am Heart J 1993; 126:1126. 66. Aliot EM, Stevenson WG, Almendral-Garrote JM, et al. EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias: developed in a partnership with the European Heart Rhythm Association (EHRA), a Registered Branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA). Europace 2009; 11:771. 67. Cronin EM, Bogun FM, Maury P, et al. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias. Heart Rhythm 2020; 17:e2. 68. Rodriguez LM, Smeets JL, Timmermans C, Wellens HJ. Predictors for successful ablation of right- and left-sided idiopathic ventricular tachycardia. Am J Cardiol 1997; 79:309. 69. Gerstenfeld EP, Dixit S, Callans DJ, et al. Quantitative comparison of spontaneous and paced 12-lead electrocardiogram during right ventricular outflow tract ventricular tachycardia. J Am Coll Cardiol 2003; 41:2046. 70. Schweikert RA, Saliba WI, Tomassoni G, et al. Percutaneous pericardial instrumentation for endo-epicardial mapping of previously failed ablations. Circulation 2003; 108:1329. 71. Chinushi M, Aizawa Y, Takahashi K, et al. Radiofrequency catheter ablation for idiopathic right ventricular tachycardia with special reference to morphological variation and long- term outcome. Heart 1997; 78:255. 72. Flemming MA, Oral H, Kim MH, et al. Electrocardiographic predictors of successful ablation of tachycardia or bigeminy arising in the right ventricular outflow tract. Am J Cardiol 1999; 84:1266. 73. Lerman BB, Stein KM, Markowitz SM. Idiopathic right ventricular outflow tract tachycardia: a clinical approach. Pacing Clin Electrophysiol 1996; 19:2120. 74. Zipes DP, Foster PR, Troup PJ, Pedersen DH. Atrial induction of ventricular tachycardia: reentry versus triggered automaticity. Am J Cardiol 1979; 44:1. https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 25/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate 75. Belhassen B, Rotmensch HH, Laniado S. Response of recurrent sustained ventricular tachycardia to verapamil. Br Heart J 1981; 46:679. 76. Nakagawa H, Beckman KJ, McClelland JH, et al. Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a Purkinje potential. Circulation 1993; 88:2607. 77. Wen MS, Yeh SJ, Wang CC, et al. Radiofrequency ablation therapy in idiopathic left ventricular tachycardia with no obvious structural heart disease. Circulation 1994; 89:1690. 78. German LD, Packer DL, Bardy GH, Gallagher JJ. Ventricular tachycardia induced by atrial stimulation in patients without symptomatic cardiac disease. Am J Cardiol 1983; 52:1202. 79. Klein GJ, Millman PJ, Yee R. Recurrent ventricular tachycardia responsive to verapamil. Pacing Clin Electrophysiol 1984; 7:938. 80. Ward DE, Nathan AW, Camm AJ. Fascicular tachycardia sensitive to calcium antagonists. Eur Heart J 1984; 5:896. 81. Ouyang F, Cappato R, Ernst S, et al. Electroanatomic substrate of idiopathic left ventricular tachycardia: unidirectional block and macroreentry within the purkinje network. Circulation 2002; 105:462. 82. Okumura K, Matsuyama K, Miyagi H, et al. Entrainment of idiopathic ventricular tachycardia of left ventricular origin with evidence for reentry with an area of slow conduction and effect of verapamil. Am J Cardiol 1988; 62:727. 83. Kinoshita O, Kamakura S, Ohe T, et al. Spectral analysis of signal-averaged electrocardiograms in patients with idiopathic ventricular tachycardia of left ventricular origin. Circulation 1992; 85:2054. 84. Nogami A, Naito S, Tada H, et al. Demonstration of diastolic and presystolic Purkinje potentials as critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia. J Am Coll Cardiol 2000; 36:811. 85. Nogami A, Naito S, Tada H, et al. Verapamil-sensitive left anterior fascicular ventricular tachycardia: results of radiofrequency ablation in six patients. J Cardiovasc Electrophysiol 1998; 9:1269. 86. Francis J, Venugopal K, Khadar SA, et al. Idiopathic fascicular ventricular tachycardia. Indian Pacing Electrophysiol J 2004; 4:98. 87. Gupta AK, Kumar AV, Lokhandwala YY, et al. Primary radiofrequency ablation for incessant idiopathic ventricular tachycardia. Pacing Clin Electrophysiol 2002; 25:1555. 88. Eisenberg SJ, Scheinman MM, Dullet NK, et al. Sudden cardiac death and polymorphous ventricular tachycardia in patients with normal QT intervals and normal systolic cardiac https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 26/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate function. Am J Cardiol 1995; 75:687. 89. Priori SG, Napolitano C, Memmi M, et al. Clinical and molecular characterization of patients with catecholaminergic polymorphic ventricular tachycardia. Circulation 2002; 106:69. 90. Wilde AA, Bhuiyan ZA, Crotti L, et al. Left cardiac sympathetic denervation for catecholaminergic polymorphic ventricular tachycardia. N Engl J Med 2008; 358:2024. 91. Tan JH, Scheinman MM. Exercise-induced polymorphic ventricular tachycardia in adults without structural heart disease. Am J Cardiol 2008; 101:1142. 92. Meissner MD, Lehmann MH, Steinman RT, et al. Ventricular fibrillation in patients without significant structural heart disease: a multicenter experience with implantable cardioverter- defibrillator therapy. J Am Coll Cardiol 1993; 21:1406. Topic 965 Version 31.0 https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 27/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate GRAPHICS Criteria for the diagnosis of arrhythmogenic right ventricular dysplasia Family history Major Familial disease confirmed at necropsy or surgery Minor Family history of premature sudden death (<35 years) caused by suspected ARVD Family history (clinical diagnosis based on present criteria) ECG depolarization/conduction abnormalities Major Epsilon waves or localized prolongation (>110 ms) of the QRS complex in the right precordial leads (V1 to V3) Minor Late potentials seen on signal averaged ECG Repolarization abnormalities Minor Inverted T waves in right precordial leads (V2 and V3) in people >12 years and in the absence of right bundle branch block Tissue characterisation of walls Major Fibrofatty replacement of myocardium on endomyocardial biopsy Global and/or regional dysfunction and structural alterations (detected by echocardiography, angiography, magnetic resonance imaging, or radionuclide scintigraphy) Major Severe dilatation and reduction of right ventricular ejection fraction with no (or only mild) left ventricular impairment Localized right ventricular aneurysms (akinetic or dyskinetic areas with diastolic bulging) Severe segmental dilatation of the right ventricle Minor https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 28/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate Mild global right ventricular dilatation and/or ejection fraction reduction with normal left ventricle Mild segmental dilatation of the right ventricle Regional right ventricular hypokinesia Arrhythmias Minor Left bundle branch block type ventricular tachycardia (sustained or nonsustained) documented on ECG, Holter monitoring, or during exercise testing Frequent ventricular extrasystoles (more than 1000/24 h) on Holter monitoring ARVD: arrhythmogenic right ventricular dysplasia; ECG: electrocardiogram. Data from: McKenna WJ, Thiene G, Nava A, et al. Br Heart J 1994; 71:215. Graphic 54842 Version 3.0 https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 29/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate Telemetry recording (lead II) from a patient with RMVT Repetitive monomorphic ventricular tachycardia (RMVT) is characterized by frequent short "salvos" or bursts of monomorphic nonsustained VT. The bursts may vary in duration, but all demonstrate the same QRS morphology. Graphic 66679 Version 2.0 https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 30/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate Nine site mapping schema for RVOT tachycardia The septal aspect of the right ventricular outflow tract (RVOT) is depicted as seen in the 30 RAO view, divided into posterior (1, 4, and 7), intermediate (2, 5, and 8), and anterior (3, 6, and 9) sites. Pacing from posterior sites (1 and 7) results in a dominant R wave in lead I, and frequently in a small R wave before a dominant S wave in lead aVL. Pacing from anterior sites (3 and 9) always produces an initial Q wave (QS, Qr, or qR) in lead I, and a QS complex in a VL. Early precordial R wave transition (R/S >1 in V1, V2, or V3) is observed during pacing from posterior and superior sites. Moving diagonally from superior-posterior to inferior-anterior results in progressive delay in the precordial R wave transition. Redrawn with permission from: Callans DJ. J Cardiovasc Electrophysiol 1994; 5:880. Futura Publishing Company. Graphic 72301 Version 3.0 https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 31/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate 12-lead electrocardiogram (ECG) recorded in a patient with repetitive monomorphic ventricular tachycardia (RMVT) arising from the left ventricular outflow tract (LVOT) This electrocardiogram (ECG) illustrates repetitive monomorphic ventricular tachycardia (RMVT) with a right bundle, inferior axis morphology signifying its left ventricular site of origin. This VT was localized to the area of the aorto-mitral continuity in the left ventricular outflow tract (LVOT). Graphic 81690 Version 3.0 https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 32/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate Revised (2018) Vaughan Williams classification of antiarrhythmic drugs abridged table Class 0 (HCN channel blockers) Ivabradine Class I (voltage-gated Na+ channel blockers) Class Ia (intermediate dissociation): Quinidine, ajmaline, disopyramide, procainamide Class Ib (rapid dissociation): Lidocaine, mexilitine Class Ic (slow dissociation): Propafenone, flecainide Class Id (late current): Ranolazine Class II (autonomic inhibitors and activators) Class IIa (beta blockers): Nonselective: carvedilol, propranolol, nadolol Selective: atenolol, bisoprolol, betaxolol, celiprolol, esmolol, metoprolol Class IIb (nonselective beta agonists): Isoproterenol Class IIc (muscarinic M2 receptor inhibitors): Atropine, anisodamine, hyoscine, scopolamine Class IId (muscarinic M2 receptor activators): Carbachol, pilocarpine, methacholine, digoxin Class IIe (adenosine A1 receptor activators): Adenosine Class III (K+ channel blockers and openers) Class IIIa (voltage dependent K+ channel blockers): Ambasilide, amiodarone, dronedarone, dofetilide, ibutilide, sotalol, vernakalant Class IIIb (metabolically dependent K+ channel openers): https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 33/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate Nicorandil, pinacidil Class IV (Ca++ handling modulators) Class IVa (surface membrane Ca++ channel blockers): Bepridil, diltiazem, verapamil Class IVb (intracellular Ca++ channel blockers): Flecainide, propafenone Class V (mechanosensitive channel blockers): No approved medications Class VI (gap junction channel blockers) No approved medications Class VII (upstream target modulators) Angiotensin converting enzyme inhibitors Angiotensin receptor blockers Omega-3 fatty acids Statins HCN: hyperpolarization-activated cyclic nucleotide-gated; Na: sodium; K: potassium; Ca: calcium. Graphic 120433 Version 3.0 https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 34/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate 12-lead electrocardiogram (ECG) showing idiopathic left ventricular tachycardia The typical ECG features of an idiopathic left ventricular tachycardia are QRS complexes that are relatively narrow (0.12 sec) and have a right bundle branch morphology (tall R waves in V1 and V2 and a terminal S wave in V5 and V6); the frontal plane axis is extremely leftward (negative QRS complexes in leads II, III, and aVF), suggesting a left anterior fascicular block. The tachycardia was localized to the inferior apical left ventricular septum, accounting for the extreme leftward axis. Graphic 64279 Version 4.0 https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 35/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate Electrophysiology study (EPS) tracing of idiopathic left ventricular tachycardia Idiopathic LV tachycardia originates from the inferior portion of the ventricular septum. Surface leads (I, II, III, V1, and V6), and intracardiac recordings from the high right atrium (HRA), His bundle region (HBE), right ventricular apex (RVA), right ventricular outflow tract (RVOT), and several recordings from the left ventricle at the site of successful ablation (LV fixed, LV var, LV bipol, LV uni) are shown. The presence of a sharp potential in the LV recordings (arrow) is consistent with local activation of the Purkinje system. This potential precedes the onset of the QRS during ventricular tachycardia (VT) by 40 msec. Reprinted with permission of Futura Publishing Company. Graphic 51420 Version 4.0 https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 36/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate Noncontact endocardial map during sinus rhythm The sequence of isopotential maps of the left ventricular endocardium (purple) is modeled to the ventricular chamber dimensions. The location of the multielectrode array is represented by the orange ellipsoid. Surface ECG lead I and selected virtual electrograms from a line following fascicular activation are shown beneath each map. Initial activation (arrow, panel A) occurs in the upper part of the fascicles and then progresses toward the apex (arrow, panel B). At the apex, fascicular activation initiates ventricular activation (white area, panel C). Data from: Peters NS, Jackman WM, Schilling RJ, et al. Circulation 1997; 95:1658. Graphic 68778 Version 3.0 https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 37/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate Noncontact endocardial map of fascicular tachycardia During tachycardia, the fascicular activation sequence is altered; panel A shows that activation begins near the left ventricular apex (red arrow) and panel B shows that activation (red arrow) propagates toward His bundle (white arrow). This rapid retrograde fascicular activation is closely followed by ventricular activation, seen as a white area in panel C. The relative delay in right ventricular activation produces a QRS complex with right bundle branch block pattern in ECG lead I. With permission from: Peters NS, Jackman WM, Schilling RJ, et al. Circulation 1997; 95:1658. Graphic 76252 Version 3.0 https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 38/39 7/6/23, 3:40 PM Ventricular tachycardia in the absence of apparent structural heart disease - UpToDate Contributor Disclosures David J Callans, MD Consultant/Advisory Boards: Abbott [Catheter ablation, leadless pacing, clinical events committee member for Nanosense trial]; Biosense Webster [Catheter ablation]; Boston Scientific [Catheter ablation, directing fellows programs]; Medtronic [Catheter ablation]. All of the relevant financial relationships listed have been mitigated. N A Mark Estes, III, MD Consultant/Advisory Boards: Boston Scientific [Arrhythmias]; Medtronic [Arrhythmias]. All of the relevant financial relationships listed have been mitigated. Nisha Parikh, MD, MPH No relevant financial relationship(s) with ineligible companies to disclose. Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence. Conflict of interest policy https://www.uptodate.com/contents/ventricular-tachycardia-in-the-absence-of-apparent-structural-heart-disease/print 39/39