Understanding VT

The Role of Catheter Ablation in Controlling Ventricular Arrhythmia

Georgy Kaspar, MD and Christian Machado, MD, FACC, FHRS 
Providence Ascension Hospital and Medical Centers  
Southfield, Michigan

Georgy Kaspar, MD and Christian Machado, MD, FACC, FHRS 
Providence Ascension Hospital and Medical Centers  
Southfield, Michigan


With rapid evolvement of new technologies, catheter ablation of ventricular tachycardia (VT) is not only a proven effective therapy, but also a major addition to other medical options, especially in patients with recurrent defibrillator shocks. In the last decade, ablation was usually retained as a last option when all pharmacological options were depleted. Antiarrhythmic drug (AAD) therapy can lower the frequency of ICD therapies, but have discouraging side effects.1 Nevertheless, both expert opinion2 and new emerged data3 support the proposition of catheter ablation for VT as early treatment. 

Understanding the Etiology of VT and Indications of Catheter Ablation

There are two main mechanisms of VT etiology defined in the EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias2:

  • Scar-related reentry describes arrhythmias that have characteristics of reentry and originates from an area of myocardial scar identified from electrogram characteristics or myocardial imaging. Large reentry circuits that can be defined over several centimeters are commonly referred to as ‘macroreentry’.2
  • Focal VT has a point source of earliest ventricular activation with a spread of activation away in all directions from that site. The mechanism can be automaticity, triggered activity, or microreentry.2

Scar-related VT arises from multiple cardiac pathologies, including post myocardial infarction (MI), arrhythmogenic right ventricular cardiomyopathy (ARVC), sarcoidosis, Chagas’ disease, dilated cardiomyopathy, and after cardiac surgery for congenital heart disease or valve replacement.2,4-6

The majority of reentry circuit isthmuses are endocardial, mainly seen in post-MI VT, whereas critical reentry circuit sites may exist in intramural, subepicardial, and perivalvular areas, particularly in patients with non-ischemic cardiomyopathies.2,5

Despite the availability of different approaches to VT ablation for hemodynamically stable VTs, noninducibility is the most common endpoint used for success of VT ablation and substrate mapping for unmappable or hemodynamically intolerable VT.7 Ablation guided by activation is an approach in which inducible zones can be recognized and ablated. Moreover, substrate mapping is an emerging modern technology to detect low voltage and slow conduction areas. Local abnormal ventricular activity (LAVA) is in reference to local electric activity that commences from pathological tissue. Those signals appear on ventricular electrogram as sharp, high-frequency ventricular potentials, possibly of low amplitude, distinct from other ventricular electrogram signals.8 They are present in about 90% of patients with recurrent VT. A strategy aimed at careful LAVA mapping, ablation, and elimination is feasible and can be achieved in about 70% of patients.9 The principle for substrate mapping is based on identifying these zones and harboring possible reentry circuits around them. A recent meta-analysis demonstrated similar outcomes when comparing both approaches (acute procedural efficacy, complications, VT recurrence, and mortality rates).10

Table 1 provides a summary of catheter ablation indications as listed in the EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias.2

Major Trials 

The three major trials of catheter ablation in patients with ischemic cardiomyopathy and ventricular tachycardia are:

Ventricular Tachycardia Ablation versus Escalation of Antiarrhythmic Drugs (VANISH) trial3

A total of 259 patients with ischemic cardiomyopathy and an ICD who had ventricular tachycardia despite antiarrhythmic drug therapy were randomly assigned to a group undergoing catheter ablation and a control group where escalation of medical treatment provided with no additional intervention. There was a significantly lower rate of the composite primary outcome of death, ventricular tachycardia storm, or appropriate ICD shock among patients undergoing catheter ablation than among those receiving an escalation in antiarrhythmic drug therapy. 

Ventricular Tachycardia Ablation in Coronary Heart Disease (VTACH) trial11

This trial included 110 patients with ischemic cardiomyopathy and reduced left ventricular ejection fraction (LVEF) <50% who were scheduled to receive an ICD for hemodynamically stable monomorphic ventricular tachycardia (secondary prevention). Those patients were randomly assigned to a group undergoing catheter ablation before ICD implantation or to a control group receiving no additional intervention. Catheter ablation was shown to prolong time to recurrence of VT in the studied population. The rate of ventricular tachycardia was 29% among patients in the ablation group compared with 47% in the control group. 

Substrate Mapping and Ablation in Sinus Rhythm to Halt Ventricular Tachycardia (SMASH-VT) trial12

This trial targeted 128 patients with ischemic cardiomyopathy who had hemodynamically unstable ventricular tachycardia. Those patients, in contrast to VTACH trial patients, received an ICD for secondary prevention within 6 months. They were randomly assigned to undergo substrate-guided ablation or no ablation. Prophylactic substrate-based catheter ablation reduced the incidence of ICD therapy. At 2 years, the rate of ventricular tachycardia was 12% among patients in the ablation group compared with 33% in the control group. 

Comparing all three trials, we noticed the following:

  • All three studies targeted patients with a history of myocardial infarction who received ICDs for the secondary prevention of sudden death.
  • All three studies enrolled patients with advanced cardiac disease. 
  • All three studies used open-label design that allows for the introduction of bias and placebo effects; however, the outcome adjudication was blinded. 
  • None of the three studies targeted specialized referral centers for ablation of ventricular tachycardia, which could have achieved better procedural outcomes.
  • The VTACH and SMASH-VT trials did not use systematic treatment with escalated AAD therapy in the control group.
  • Superior outcome was observed in the VANISH trial among subgroup patients in whom the index arrhythmia had occurred despite amiodarone therapy at baseline. 
  • The VANISH trial was not powered to assess the effect of the two treatments on mortality. Indeed, it was powered to show the composite outcome of VT ablation in reducing death, ventricular tachycardia storm, or appropriate ICD shock. 

Table 2 compares patients, inclusion criteria, exclusion criteria, follow-up periods, and endpoints among all three trials. 


Isolation of scar tissue comes across as a rational approach in controlling VTs, but the challenge remains to prove its efficiency and safety by randomized controlled trials. Hence, consensus statements and guidelines recommend the use of catheter ablation post antiarrhythmic therapy.2 The VANISH trial3 provided new evidence to promote the role of catheter ablation over escalation of AAD therapy for the reduction of recurrent ventricular tachycardia in patients with ischemic cardiomyopathy. Until more evidence emerges, a comprehensive shared decision making between patients and their electrophysiologist is still ideal and essential before ablation.

Disclosures: The authors have no conflicts of interest to report regarding the content herein.


  1. Bollmann A, Husser D, Cannom DS. Antiarrhythmic drugs in patients with implantable cardioverter-defibrillators. Am J Cardiovasc Drugs. 2005;5:371-378.
  2. 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;11:771-817.
  3. Sapp JL, Wells GA, Parkash R, et al. Ventricular tachycardia ablation versus escalation of antiarrhythmic drugs. N Engl J Med. 2016;375(2):111-121.
  4. Belhassen B, Caspi A, Miller H, Shapira I, Laniado S. Extensive endocardial mapping during sinus rhythm and ventricular tachycardia in a patient with arrhythmogenic right ventricular dysplasia. J Am Coll Cardiol. 1984;4:1302-1306.
  5. Delacretaz E, Stevenson WG, Ellison KE, Maisel WH, Friedman PL. Mapping and radiofrequency catheter ablation of the three types of sustained monomorphic ventricular tachycardia in nonischemic heart disease. J Cardiovasc Electrophysiol. 2000;11:11-17.
  6. Eckart RE, Hruczkowski TW, Tedrow UB, Koplan BA, Epstein LM, Stevenson WG. Sustained ventricular tachycardia associated with corrective valve surgery. Circulation. 2007;116(18):2005-2011.
  7. Ghanbari H, Baser K, Yokokawa M, et al. Noninducibility in postinfarction ventricular tachycardia as an end point for ventricular tachycardia ablation and its effects on outcomes: a meta-analysis. Circ Arrhythm Electrophysiol. 2014;7:677-683. 
  8. Jaïs P, Maury P, Khairy P, et al. Elimination of local abnormal ventricular activities: a new end point for substrate modification in patients with scar-related ventricular tachycardia. Circulation. 2012;125(18):2184-2196. 
  9. Sacher F, Lim HS, Derval N, et al. Substrate mapping and ablation for ventricular tachycardia: the LAVA approach. J Cardiovasc Electrophysiol. 2015;26(4):464-471. 
  10. Kumar S, Baldinger SH, Romero J, et al. Substrate-Based Ablation Versus Ablation Guided by Activation and Entrainment Mapping for Ventricular Tachycardia: A Systematic Review and Meta-Analysis. J Cardiovasc Electrophysiol. 2016 Oct 6. 
  11. Kuck KH, Schaumann A, Eckardt L, et al. Catheter ablation of stable ventricular tachycardia before defibrillator implantation in patients with coronary heart disease (VTACH): a multicentre randomised controlled trial. Lancet. 2010;375:31-40. 
  12. Reddy VY, Reynolds MR, Neuzil P, et al. Prophylactic catheter ablation for the prevention of defibrillator therapy. N Engl J Med. 2007;357:2657-2665.