Journal of Postgraduate Medicine
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Year : 2022  |  Volume : 68  |  Issue : 1  |  Page : 10-11  

Cardiac sympathetic denervation: A wonder solution to channelopathy-related ventricular tachycardia and much more

P Barwad 
 Department of Cardiology, Post Graduate Institute for Medical Education and Research (PGIMER), Chandigarh, India

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How to cite this article:
Barwad P. Cardiac sympathetic denervation: A wonder solution to channelopathy-related ventricular tachycardia and much more.J Postgrad Med 2022;68:10-11

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Barwad P. Cardiac sympathetic denervation: A wonder solution to channelopathy-related ventricular tachycardia and much more. J Postgrad Med [serial online] 2022 [cited 2022 Dec 2 ];68:10-11
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Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited channelopathy presenting with life-threatening ventricular dysrhythmias in a structurally normal heart. Channelopathy-related VT are a special group of dysrhythmias wherein the abnormal ionic fluxes cause imbalance of intracellular homeostasis causing polymorphic VT. CPVT is caused by mutation in the cardiac ryanodine receptor (RyR2)and calsequesterin (CASQ2) genes. These mutations cause rise in intracellular calcium leading to polymorphic VT and may also cause sudden cardiac death (SCD).

In the current issue Bansal et al.[1] describe a young individual with CPVT who was managed successfully by cardiac sympathetic denervation (CSD). However, there are various aspects of this case that needs further discussion. The diagnosis of CPVT is not always straightforward. It requires a detailed evaluation and many a time, one may have to rely predominantly on the history of the patient, as in this case. One among the important points to consider is that in 40% of cases of CPVT no genetic abnormality is diagnosed as classically described in the literature. Moreover, there are at least five different variants of CPVT and other related entities [Andersen-Tawil syndrome (ATS), also known as long QT syndrome type 7 (LQT7)]. The classical description of bidirectional VT (BVT) is also not very common in all cases of CPVT and it may also present as junctional tachycardia, premature ventricular complex (PVC) with quadrigeminy, trigeminy or bigeminy, and short salvos of BVT. However, as classically described, the inciting event is always an exercise or any other catecholamine stimulation. In order to to maintain uniformity of diagnosis, Priori et al.[2] in 2013 have laid down certain criteria. Also, a high index of suspicion and detailed evaluation is a must in these cases, as early recognition can lead to prevention of SCD.

Exercise-induced syncope is also a manifestation in other disease entities with a structurally normal heart, such as LQT syndrome, ATS, congenital coronary anomalies, and hypertrophic cardiomyopathy, and it is also important to differentiate these from CPVT in order to formulate the right management plan.

Treatment of CPVT should also be tailored to the patient as described in the case by Bansal et al.[1]. It involves the removal of triggers for sympathetic stimulation, medications, and CSD. Patients should be counselled against any vigorous physical activity or competitive sports. Drugs that have been found to be effective in the treatment of CPVT are beta blockers, calcium channel blockers, and flecainide. In the referenced case,[1] the authors describe a patient being started on maximum dosages of beta blockers and considered for CSD ahead of any other therapeutic options. Although it appears to be a matter of debate, I would like to congratulate the authors for the same. As the patient had a history of exercise-induced syncope in the past, the most likely mechanism in this patient would be polymorphic VT. And CSD is a very effective long-term therapeutic option. It acts as a critical adjunct to medical therapy and should be performed in patients of CPVT with malignant dysrhythmias despite maximum medical therapy.

The effectiveness of implantable cardioverter-defibrillator (ICD) therapy in patients with CPVT is also a matter of debate. If the dysrhythmias are not adequately controlled on medical therapy, these patients have a high likelihood of experiencing an electric storm if implanted with an ICD. Thus, ICD in CPVT should be implanted in patients when they have infrequent recurrences of malignant dysrhythmia despite being on maximal medical therapy and after CSD.

CSD is now being considered as a one-hit wonder in patients with refractory VT or VT storm.[3] Though it has an established role in CPVT and long QT syndrome, the data supporting its role in VT in structural heart disease is increasing. A latest systematic review[4] has described it to be highly efficacious in reducing the number of shocks in patients with multiple failed prior ablations. Another recent study[5] has demonstrated that CSD can be considered ahead of catheter-based ablation in the management of refractory VT. As our understanding of neuromodulation of the heart is increasing with time, we shall see a wider use of CSD in cardiac ailments such as heart failure and cardiac dysrhythmias.


1Bansal R, Mahajan A, Vichare S, Lokhandwala Y. Cardiac sympathetic denervation for catecholaminergic polymorphic ventricular tachycardia. J Postgrad Med 2022;68:41-3.
2Priori SG, Wilde AA, Horie M, Cho Y, Behr ER, Berul C, et al. Executive summary: HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes. Heart Rhythm 2013;10:e85-108.
3Assis FR, Tandri H. Sympathectomy: A “one hit wonder” for life? J Cardiovasc Electrophysiol 2021;32:1075-6.
4Shah R, Assis F, Alugubelli N, Okada DR, Cardoso R, Shivkumar K, et al. Cardiac sympathetic denervation for refractory ventricular arrhythmias in patients with structural heart disease: A systematic review. Heart Rhythm 2019;16:1499-505.
5Barwad P, Sinkar K, Bachani N, Shah R, Shah V, Kumar B, et al. Long-term clinical outcomes of cardiac sympathetic denervation in patients with refractory ventricular arrhythmias. J Cardiovasc Electrophysiol 2021;32:1065-74.

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