Color Atlas and Synopsis of Electrophysiology, 1st Ed.


Sean D. Pokorney, MD, MBA and Sana M. Al-Khatib, MD, MHS


The patient is a 61-year-old man with a history of ischemic cardiomyopathy, a left ventricular ejection fraction (LVEF) of <15%, and a history of percutaneous coronary interventions on the mid-left anterior descending artery and the right coronary artery. He had a primary prevention implantable cardioverter-defibrillator (ICD) placed 3 years ago. He received an ICD shock for monomorphic ventricular tachycardia (VT) approximately 6 months after his ICD was implanted. He was started on sotalol at that time. The patient did not tolerate sotalol due to gastrointestinal symptoms, and he stopped taking the medication after a few doses. Approximately 2 years after his first ICD shock, the patient presented with electrical storm, having received 3 ICD shocks for monomorphic VT in the 24 hours prior to presentation. He had a cardiac catheterization that showed nonobstructive coronary artery disease with the most severe lesion being a 40% stenosis in the second diagonal artery. The patient was taken to the electrophysiology lab for an electrophysiology study and possible VT ablation.

The patient had two morphologies of easily inducible VT. The first VT had a tachycardia cycle length of 410 ms and right bundle branch block (RBBB) morphology with a superior axis and a transition at V3. This VT was found to arise from the inferior apex (Figure 66-1). The second VT had a tachycardia cycle length of 410 ms and left bundle branch block (LBBB) morphology with an inferior axis and a transition at V3. This VT was mapped to the anterior septum (Figure 66-2). Identical morphologies to the VTs were achieved by pacing in the respective scar border zones (Figure 66-3). Extensive ablation was performed at the scar border zones for each region, targeting areas of electrical excitability and diastolic potentials (Figure 66-4). The clinical VTs were noninducible at the completion of the procedure.


FIGURE 66-1 A 12-lead ECG of the patient’s first VT (VT1).


FIGURE 66-2 A 12-lead ECG of the patient’s second VT (VT2).


FIGURE 66-3A Pace map match for VT1 from the inferior apex.


FIGURE 66-3B Pace map match for VT2 from the anterior septum.


FIGURE 66-4 Activation/ablation map with straight anteroposterior view on the left and left anterior oblique view on the right. The grey dot is the dense scar. The aqua dot is the site of the pace map. The red dots are the ablation sites for the VT from the inferior apex (VT1) and from the anterior septum (VT2).


• ICDs have been clearly demonstrated to improve the survival of patients at an increased risk of sudden cardiac death either due to prior cardiac arrest, VT, or significant left ventricular dysfunction.1-5

• A survey of ICD use in 61 countries in 2009 showed 222 407 new implants and 105 620 replacements worldwide, and the survey demonstrated a nearly 12% increase in ICD implantation in the United States between 2005 and 2009.6

• Primary prevention ICD trials demonstrated appropriate ICD shocks for VT/ventricular fibrillation (VF) in 18% of patients in Multicenter Automatic Defibrillator Implantation Trial II (MADIT-II) at 21 months7 and 22% of patients in Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) at 45 months.8

• Secondary prevention trials found appropriate ICD shocks for VT/VF in 47% of patients in the Ventricular Tachycardia Ablation in Coronary Heart Disease (VTACH) study at 23 months9 and 31% of patients in the Substrate Mapping and Ablation in Sinus Rhythm to Halt Ventricular Tachycardia (SMASH-VT) trial at 23 months.10

• Appropriate ICD shocks have serious consequences, despite their proven, life-saving efficacy.

Images Long-term follow-up data from MADIT-II11 and SCD-HeFT8 found that patients have a significantly higher risk of death after appropriate ICD termination of VT or VF. Specifically, compared with patients who did not receive an appropriate ICD shock, those who did had a 3.5 times and 5.7 times higher risk of mortality in MADIT-II and SCD-HeFT, respectively.

Images Patients have a decline in physical functioning and mental well-being after one or more ICD shock.12


• If the VT rate is at or above the programmed detection rate of the ICD, the VT episode is captured by the device, which makes management easier as it is often difficult to capture the VT by any other modality. Multiple VT morphologies are commonly inducible during an electrophysiology (EP) study, and the stored electrograms (EGMs) may help one identify a patient’s clinical VT.13

Images Stored EGM data provide the cycle length of the clinical VT.

Images In 13 postinfarct patients with an ICD and with 12-lead ECGs of the clinical VT, visual inspection and computer analysis of the ICD EGMs correctly differentiated the clinical VT in 96% and 98% of the cases, respectively. This was achieved despite the fact that 67% of patients had an inducible, previously undocumented VT with a cycle length within 10% of the cycle length of the clinical VT.

• The stored EGMs of VT episodes may also be useful in patients who are noninducible in the EP lab, which could be due to recent administration of an antiarrhythmic medication, and with normal voltage maps that preclude substrate modification.14

Images A target ablation area can be identified by pacing at the tachycardia cycle length and matching the morphology of the recorded paced tachycardia to the EGM morphology.


Pharmacologic Treatment of VT in ICD Patients

• Medications can reduce ICD shocks, as seen in the Optimal Pharmacological Therapy in Cardioverter Defibrillator Patients (OPTIC) trial. OPTIC was a randomized controlled trial, in which 412 patients received β-blockers alone, sotalol, or a combination of amiodarone and β-blockers.15

Images Cumulative rates of shock over 1 year were 39% with β-blocker alone, 24% with sotalol, and 10% with amiodarone and a β-blocker.

Images Amiodarone reduced shocks by a statistically significant amount compared with a β-blocker alone or sotalol, while sotalol had a nonstatistically significant trend toward reduction in ICD shocks compared with a β-blocker.

• Antiarrhythmic medications have adverse events, despite their utility in preventing tachyarrhythmias.

Images In OPTIC, the discontinuation rates of amiodarone and sotalol were high even during the first year: 18% and 24%, respectively.15

Images Amiodarone increases defibrillation threshold by a statistically significant amount.16

Catheter Ablation in Electrical Storm

• Four analyses of VT ablation that included ≥10 patients with electrical storm have been published, and the details of these can be found in Table 66-1.17-20

TABLE 66-1 VT Ablation in Patients with Electrical Storm*


• The largest evaluation of the efficacy of VT ablation in electrical storm was a prospective study with 95 patients.18

Images The patients were mostly men with ischemic cardiomyopathy.

Images The clinical VT was ablated in 89% of patients, and 72% of patients had no inducible VT postablation.

Images Patients were followed for a mean of 22 ± 13 months, and 66% of patients had no VT recurrence during follow-up, while only 8% of patients had recurrence of electrical storm.

Images There were no periprocedural deaths, but there were two transient ischemic attacks and two vascular complications.

• Similar rates of recurrence of VT at 62% to 69% and electrical storm at 6% to 13% were seen in the other smaller, retrospective studies.17,19,20

• The longest mean follow-up in the published studies was 28 months, and there were no long-term outcomes available on this patient population, so the durability of the effect of VT ablation remains unknown.

Catheter Ablation in Incessant Ventricular Tachycardia

• Endocardial and epicardial approaches to VT ablation have been effective in treating incessant VT with success rates of ablating the clinical VT of 90% to 94%, as shown in Table 66-2.21,22

TABLE 66-2 VT Ablation in Patients with Incessant VT*


• The two studies that examined catheter ablation in incessant VT had a minority (35%-40%) of patients with an ICD.

• In these two studies, there was only one procedure-related death, resulting in a 6% periprocedural death rate in that study with 17 patients.22

• There was a significant difference in VT recurrence rates between the two studies with 90% of patients having no recurrent VT after epicardial ablation and 65% having no recurrent VT after endocardial ablation. This may be due to the better durability of the epicardial approach compared with the endocardial one; however, unmatched patient populations, the relatively small number of patients in these studies, and the disparity in mean follow-up of 18 versus 30 months may also account for this difference.

Catheter Ablation After Appropriate ICD Therapy

• The available data on catheter ablation in ICD recipients have been summarized for retrospective studies in Table 66-323-28 and prospective studies in Table 66-4.29-33

TABLE 66-3 Retrospective Studies of VT Ablation in Patients after Appropriate ICD Therapy*


TABLE 66-4 Prospective Studies of VT Ablation in Patients after Appropriate ICD Therapy*


• The majority of the studies have been conducted in patients with ischemic cardiomyopathy.

• Postablation, the percentage of patients who were noninducible for any VT ranged from 22% to 78%.

• The rates of noninducible patients postablation and successfully ablated clinical VT in the two largest, prospective studies were 40% to 49% and 72% to 92%, respectively.30-31 Despite the variation in success of ablation, both studies had similar rates of recurrence of VT at 46% to 47% with 6 to 8 months of follow-up.

• The Cooled RF Ablation trial found that 81% of patients had ≥75% reduction in VT events, when comparing the 2-month periods before and after VT catheter ablation, and the 1-year recurrence rate after ablation was 56%.30

• The Thremocool VT Ablation Study also showed a significant impact on VT events postablation with 67% of patients having ≥75% reduction in VT events, when comparing the 6-month periods before and after ablation. This 231 patient experience found that patients had a median of 11.5 episodes of VT in the 6 months prior to ablation, which was reduced to a median of 0 (interquartile range of 0-7) episodes of VT in the 6 months after ablation.31

• There are no randomized controlled trials of VT catheter ablation powered to assess mortality.

• There are no data available on the impact of reduction of VT events and ICD shocks with VT catheter ablation on quality of life.

• Periprocedure mortality rates range from 0% to 5%, and the most frequently experienced complications included heart failure, stroke, cardiac tamponade, and vascular injury.

Catheter Ablation as Prophylaxis for Appropriate ICD Therapy

• The only two randomized controlled trials of VT catheter ablation in ICD recipients are the VTACH and SMASH-VT trials. Both of these trials randomized patients with a secondary prevention indication for an ICD and ischemic cardiomyopathy to ICD with VT catheter ablation or ICD without VT catheter ablation (Table 5).9-10

TABLE 66-5 Prophylactic VT Ablation to Minimize Appropriate ICD Therapy*


• The primary end point of the VTACH trial was time to first recurrence of VT, which was longer (18.6 months) in the ablation arm compared with the control arm with (5.9 months) (p = 0.051). Ablation resulted in a statistically significant improvement in the number of patients free from VT or VF at 2 years (47% in the ablation arm versus 29% of controls) (hazard ratio of 0.61 with 95% confidence interval [CI] of 0.37 to 0.99). The rate of appropriate ICD shocks per year during follow-up in the ablation group was 0.6% compared with 3.4% in the control group.9

• The primary endpoint in SMASH-VT was survival free from appropriate ICD therapy. The number of appropriate ICD therapies was significantly lower in the ablation arm (12%) compared with the control arm (33%) (hazard ratio 0.35 with 95% CI of 0.15 to 0.78 and p-value of 0.007). There was a 73% reduction in ICD shocks in the ablation group, as compared with controls. Overall survival was not different between treatment strategies.10

Timing of VT Ablation

• The optimal timing for VT ablation in patients with structural heart disease is unknown.

• Current guidelines give a class I recommendation for VT ablation in34:

Images Patients with sustained, monomorphic VT, who have failed an antiarrhythmic, do not tolerate an antiarrhythmic, or do not want to take long-term antiarrhythmic medications.

Images Patients with an ICD, who receive multiple shocks for sustained VT and are not willing to take long-term antiarrhythmic medications or are not controllable with reprogramming their ICD or adjusting antiarrhythmic medical therapy.

• Catheter ablation is also recommended for patients with incessant sustained monomorphic VT or electrical storm and patients with polymorphic VT or VF that is triggered by a targetable focus.35

• It has been suggested that earlier referral for VT ablation may result in more favorable outcomes, including lower rates of VT recurrence and reduced mortality, but this remains to be elucidated.

• One single center, retrospective analysis evaluated patients referred early after their first episode of VT (36 patients in early referral) compared with patients that had VT ablation after two or more VT episodes (62 patients in late referral).36

• Early referral patients had improved VT-free survival compared with the late referral group (p-value 0.01), and a multivariable analysis found that early referral was the only statistically significant, independent variable affecting VT-free survival.

• There are several ongoing randomized controlled studies investigating timing of ablation and/or comparing ablation with antiarrhythmic medications37:

Images Trial Comparing Ablation with Medical Therapy in Patients with Ventricular Tachycardia (VeTAMed).

Images Antiarrhythmic Medication versus MRI-Merge Ablation in the Treatment of Ventricular Tachycardia.

Images Early Ablation Therapy for the Treatment of Ischemic Ventricular Tachycardia in Patients with Implantable Cardioverter Defibrillators (ASPIRE).

Images Ventricular Tachycardia Ablation versus Enhanced Drug Therapy (VANISH).

Images A Study of Early Robotic Ablation by Substrate Elimination of Ventricular Tachycardia (ERASE-VT).

Images Pilot Study of Catheter Ablation for Ventricular Tachycardia in Patients with an Implantable Cardioverter Defibrillator (CALPYSO).

Images Does Timing of VT Ablation Affect Prognosis in Patients with an Implantable Cardioverter-Defibrillator? (PARTITA).


• ICD shocks for VT or VF are associated with poor prognosis and negative impact on quality of life.

• It is important to reassess the treatment plan for a patient after an appropriate ICD therapy.

• VT ablation can result in a low recurrence rate of VT or VF, and the procedure can decrease ICD therapies delivered in patients having frequent VT/VF episodes.

• Future studies should focus on understanding the long-term impact of this procedure on important outcomes like survival, health care utilization, and quality of life.

• Earlier referral for VT ablation has been suggested as a better approach to patients with VT and structural heart disease; however, more robust data on the optimal timing of VT ablation are needed.

• More data are also needed on selecting patients for VT ablation who are most likely to benefit from ablation.

• The data from current ongoing studies, future trials, and analyses of durability of VT ablation and long-term outcomes of ablation patients will likely influence future recommendations.


1. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. The Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. N Engl J Med. 1997;337(22):1576-1583.

2. Connolly SJ, Gent M, Roberts RS, et al. Canadian implantable defibrillator study (CIDS): a randomized trial of the implantable cardioverter defibrillator against amiodarone. Circulation. 2000;101(11):1297-1302.

3. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002;346(12):877-883.

4. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. 2005;352(3):225-237.

5. Kuck KH, Cappato R, Siebels J, Ruppel R. Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest: the Cardiac Arrest Study Hamburg (CASH). Circulation. 2000;102(7):748-754.

6. Mond HG, Proclemer A. The 11th world survey of cardiac pacing and implantable cardioverter-defibrillators: calendar year 2009—a World Society of Arrhythmia’s project. Pacing Clin Electrophysiol. 2011;34(8):1013-1027.

7. Daubert JP, Zareba W, Cannom DS, et al. Inappropriate implantable cardioverter-defibrillator shocks in MADIT II: frequency, mechanisms, predictors, and survival impact. J Am Coll Cardiol. 2008;51(14):1357-1365.

8. Poole JE, Johnson GW, Hellkamp AS, et al. Prognostic importance of defibrillator shocks in patients with heart failure. N Engl J Med. 2008;359(10):1009-1017.

9. 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(9708):31-40.

10. Reddy VY, Reynolds MR, Neuzil P, et al. Prophylactic catheter ablation for the prevention of defibrillator therapy. N Engl J Med. 2007;357(26):2657-2665.

11. Moss AJ, Greenberg H, Case RB, et al. Long-term clinical course of patients after termination of ventricular tachyarrhythmia by an implanted defibrillator. Circulation. 2004;110(25):3760-3765.

12. Schron EB, Exner DV, Yao Q, et al. Quality of life in the antiarrhythmics versus implantable defibrillators trial: impact of therapy and influence of adverse symptoms and defibrillator shocks. Circulation. 2002;105(5):589-594.

13. Yoshida K, Liu TY, Scott C, et al. The value of defibrillator electrograms for recognition of clinical ventricular tachycardias and for pace mapping of post-infarction ventricular tachycardia. J Am Coll Cardiol. 2010;56(12):969-979.

14. Tschabrunn CM, Anter E, Marchlinski FE. Identifying non-inducible ventricular tachycardia origin utilizing defibrillator electrograms. J Interv Card Electrophysiol. 2013;36(3):243-246.

15. Connolly SJ, Dorian P, Roberts RS, et al. Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: the OPTIC Study: a randomized trial. JAMA. 2006;295(2):165-171.

16. Hohnloser SH, Dorian P, Roberts R, et al. Effect of amiodarone and sotalol on ventricular defibrillation threshold: the optimal pharmacological therapy in cardioverter defibrillator patients (OPTIC) trial.Circulation. 2006;114(2):104-109.

17. Kozluk E, Gaj S, Kiliszek M, Lodzinski P, Piatkowska A, Opolski G. Efficacy of catheter ablation in patients with an electrical storm. Kardiol Pol. 2011;69(7):665-670.

18. Carbucicchio C, Santamaria M, Trevisi N, et al. Catheter ablation for the treatment of electrical storm in patients with implantable cardioverter-defibrillators: short- and long-term outcomes in a prospective single-center study. Circulation. 2008;117(4):462-469.

19. Arya A, Bode K, Piorkowski C, et al. Catheter ablation of electrical storm due to monomorphic ventricular tachycardia in patients with nonischemic cardiomyopathy: acute results and its effect on long-term survival. Pacing Clin Electrophysiol. 2010;33(12):1504-1509.

20. Deneke T, Shin DI, Lawo T, et al. Catheter ablation of electrical storm in a collaborative hospital network. Am J Cardiol. 2011;108(2):233-239.

21. Brugada J, Berruezo A, Cuesta A, et al. Nonsurgical transthoracic epicardial radiofrequency ablation. J Am Coll Cardiol. 2003;41(11):2036-2043.

22. Cao K, Gonska BD. Catheter ablation of incessant ventricular tachycardia: acute and long-term results. Eur Heart J. 1996;17(5):756-763.

23. Sauer WH, Zado E, Gerstenfeld EP, Marchlinski FE, Callans DJ. Incidence and predictors of mortality following ablation of ventricular tachycardia in patients with an implantable cardioverter-defibrillator. Heart Rhythm. 2010;7(1):9-14.

24. Inada K, Roberts-Thomson KC, Seiler J, et al. Mortality and safety of catheter ablation for antiarrhythmic drug-refractory ventricular tachycardia in elderly patients with coronary artery disease. Heart Rhythm. 2010;7(6):740-744.

25. Segal OR, Chow AW, Markides V, Schilling RJ, Peters NS, Davies DW. Long-term results after ablation of infarct-related ventricular tachycardia. Heart Rhythm. 2005;2(5):474-482.

26. O’Callaghan PA, Poloniecki J, Sosa-Suarez G, Ruskin JN, McGovern BA, Garan H. Long-term clinical outcome of patients with prior myocardial infarction after palliative radiofrequency catheter ablation for frequent ventricular tachycardia. Am J Cardiol. 2001;87(8):975-979;A4.

27. Kim YH, Sosa-Suarez G, Trouton TG, et al. Treatment of ventricular tachycardia by transcatheter radiofrequency ablation in patients with ischemic heart disease. Circulation. 1994;89(3):1094-1102.

28. Alzand BS, Timmermans CC, Wellens HJ, et al. Unmappable ventricular tachycardia after an old myocardial infarction. Long-term results of substrate modification in patients with an implantable cardioverter defibrillator. J Interv Card Electrophysiol. 2011;31(2):149-156.

29. Jais 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.

30. Calkins H, Epstein A, Packer D, et al. Catheter ablation of ventricular tachycardia in patients with structural heart disease using cooled radiofrequency energy: results of a prospective multicenter study. Cooled RF Multi Center Investigators Group. J Am Coll Cardiol. 2000;35(7):1905-1914.

31. Stevenson WG, Wilber DJ, Natale A, et al. Irrigated radiofrequency catheter ablation guided by electroanatomic mapping for recurrent ventricular tachycardia after myocardial infarction: the multicenter thermocool ventricular tachycardia ablation trial. Circulation. 2008;118(25):2773-2782.

32. Tanner H, Hindricks G, Volkmer M, et al. Catheter ablation of recurrent scar-related ventricular tachycardia using electroanatomical mapping and irrigated ablation technology: results of the prospective multicenter Euro-VT-study. J Cardiovasc Electrophysiol. 2010;21(1):47-53.

33. Henz BD, do Nascimento TA, Dietrich Cde O, et al. Simultaneous epicardial and endocardial substrate mapping and radiofrequency catheter ablation as first-line treatment for ventricular tachycardia and frequent ICD shocks in chronic chagasic cardiomyopathy. J Interv Card Electrophysiol. 2009;26(3):195-205.

34. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death—executive summary: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Eur Heart J. 2006;27(17):2099-2140.

35. 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(6):771-817.

36. Frankel DS, Mountantonakis SE, Robinson MR, Zado ES, Callans DJ, Marchlinski FE. Ventricular tachycardia ablation remains treatment of last resort in structural heart disease: argument for earlier intervention. J Cardiovasc Electrophysiol. 2011;22(10):1123-1128.

37. National Institutes of Health Clinical Trials Website. Accessed March 10, 2014.