Article

Can We Select Patients for Prophylactic VT Ablation?

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Correspondence Details:Theodoros Zografos, MD, PhD, Red Cross Hospital, Athens, Greece. E: theodoroszografos@gmail.com

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Dear Sir,

I read with great interest the elegant review by Mukherjee and colleagues on prophylactic VT ablation in the latest issue of the journal (AER 6(3)125-8).1 The concept is indeed revolutionary, and should extend the boundaries of interventional electrophysiology. However, such an approach cannot be feasible without rationalising patient selection. Current guidelines’ recommendations, based on the results of primary sudden cardiac death prevention trials, mainly the Multicenter Automatic Defibrillator Implantation Trial–II (MADIT-II)2 and the Sudden Cardiac Death in Heart Failure (SCD-Heft)3 trials, use the left ventricular ejection fraction (LVEF) as a sole criterion for the propensity to sudden cardiac death. However, LVEF alone has limited sensitivity,4 and low specificity5 for arrhythmic versus non-arrhythmic cardiac death.

Further risk stratification is crucial in this respect, and the issue of electrophysiology study (EPS) should not be ignored. In a recent review, the induction of sustained VT has been associated with a two- to three-fold increased risk of arrhythmia-related death in post-infarction patients with non-sustained VT.6 EPS has a sensitivity of 58.1 % and a specificity of 69.5 %, albeit with significant heterogeneity between the included studies. We think that in ischaemic patients with LVEF ≤35 %, EPS may be of value in identifying patients at high risk of future arrhythmic events, and should be useful as a risk stratifier in this setting. Such an approach might help focusing our attempts for prophylactic ablation on patients with a proven propensity, not just the substrate, for VT. If prophylactic VT ablation can ever become a clinical reality, effective selection of candidates is imperative.

Theodoros Zografos,

Red Cross Hospital, Athens, Greece

References

  1. Mukherjee RK, O’Neill L, O’Neill MD. Prophylactic catheter ablation for ventricular tachycardia: are we there yet? Arrhythm Electrophysiol Rev 2017;6:125–8.
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  2. Moss AJ, Zareba W, Hall WJ, et al.; Multicenter Automatic Defibrillator Implantation Trial II Investigators. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med 2002;346:877–83.
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  3. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med 2005;352:225–37.
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  4. Solomon SD, Zelenkofske S, McMurray JJ, et al. Sudden death in patients with myocardial infarction and left ventricular dysfunction, heart failure, or both. N Engl J Med 2005;352:2581–8.
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  5. Every N, Hallstrom A, McDonald KM, et al. Risk of sudden versus nonsudden cardiac death in patients with coronary artery disease. Am Heart J 2002;144:390–6.
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  6. Katritsis DG, Zografos T, Hindricks G. Electrophysiology testing for risk stratification of patients with ischemic cardiomyopathy: a call for action. Europace (In press)

 

Authors’ Reply:

We would like to thank Dr Zografos for his interest in our review ‘Prophylactic catheter ablation for ventricular tachycardia: are we there yet?

We agree with the author that risk predictive models for sudden cardiac death need to be improved in patients with ischaemic cardiomyopathy and that electrophysiology study (EPS) may have a crucial role to play in this regard. The value of EPS may not only be limited to improved risk stratification, but could also inform selection criteria for catheter ablation and assess the response to anti-tachycardia pacing, which could be useful for determination of future device programming.1

There is some evidence that in patients early after myocardial infarction, an LVEF ≤30 % or LVEF 31–35 % with NYHA II–III heart failure and inducible VT at EPS is associated with a decreased survival free of death or arrhythmia.2 However, in those patients who were EPS-negative with impaired LVEF, there was no significant difference compared with control patients with LVEF >40 %, suggesting the existence of a cohort of lower-risk patients with LVEF ≤30 % post myocardial infarction. The concern with EPS, however, has been its negative predictive value, with non-inducible patients in the Multicentre Automatic Defibrillator Implantation II population having a higher risk of VF than in inducible patients, although a combined arrhythmic endpoint of VT or VF was lower.3 The negative predictive value of EPS appears to be dependent on the VT induction protocol used.2

We also know that the addition of fibrosis detection by late gadolinium enhancement cardiac magnetic resonance may add value to risk stratification tools for the propensity of sudden cardiac death in this population. In a multivariate analysis of a large group of patients with sustained or non-sustained VT, the presence of LV fibrosis was an independent predictor of adverse outcomes (composite of cardiac death/arrest, new episode of sustained VT or appropriate implantable cardioverter defibrillator [ICD] discharge).4 Perhaps the best strategy for patient selection for prophylactic catheter ablation may be a personalised approach incorporating data from cardiac imaging and electrophysiological testing. A recent proof-of-concept report constructed personalised models of post-infarct hearts using MRI and computational modelling, and appeared to outperform several existing clinical metrics in assessing the propensity to future arrhythmic events.5

We agree with the author of the letter that further work is warranted investigating EPS as a risk stratification tool for sudden cardiac death and in selecting patients for prophylactic VT ablation; however, the primary outcomes of the major VT ablation clinical trials are survival from ICD therapies or time to VT/VF recurrence. Without more robust arrhythmic risk stratification tools it would be difficult to justify performing a prophylactic VT ablation, with its associated risks, in patients who either do not have an ICD or have never received any therapies from their device.

Rahul K Mukherjee, Division of Imaging Sciences and Biomedical Engineering, King’s College London, UK

Louisa O’Neill, Division of Imaging Sciences and Biomedical Engineering, King’s College London, UK

Mark D O’Neill, Department of Cardiology, Guy’s and St Thomas’ NHS Foundation Trust, London, UK

References

  1. Mitchell LB. The role of the transvenous catheter electrophysiology study in the evaluation and management of ventricular tachyarrhythmias associated with ischemic heart disease. Card Electrophysiol Rev 2002;6:458–62"
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  2. Zaman S, Narayan A, Thiagalingam A, et al. Long-term arrhythmia-free survival in patients with severe left ventricular dysfunction and no inducible ventricular tachycardia after myocardial infarction. Circulation 2014;129:848–54.
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  3. Daubert JP, Zareba W, Hall J, et al. Predictive value of ventricular arrhythmia inducibility for subsequent ventricular tachycardia or ventricular fibrillation in Multicenter Automatic Defibrillator Implantation Trial (MADIT) II patients. J Am Coll Cardiol 2006;47:98–107.
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  4. Dawson DK, Hawlisch K, Prescott G, et al. Prognostic role of CMR in patients presenting with ventricular arrhythmias. J Am Coll Cardiol Cardiovas Imag 2013;6:335–44.
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  5. Arevalo HJ, Vadakkumpadan F, Guallar E, et al. Arrhythmia risk stratification of patients after myocardial infarction using personalized heart models. Nat Commun 2016;7:11437.
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