Korean Circ J.  2020 Mar;50(3):203-219. 10.4070/kcj.2019.0292.

Ventricular Tachycardia Ablation in Non-ischemic Cardiomyopathy

Affiliations
  • 1Department of Cardiology, Westmead Hospital, Sydney, NSW, Australia. saurabh.kumar@health.nsw.gov.au
  • 2Westmead Applied Research Centre, University of Sydney, Sydney, NSW, Australia.
  • 3Centre for Heart Research, The Westmead Institute for Medical Research, Westmead, NSW, Australia.

Abstract

Non-ischemic cardiomyopathies are a heterogeneous group of diseases of the myocardium that have a distinct proclivity to ventricular arrhythmias. Of these, ventricular tachycardias pose significant management challenges with the risk of sudden cardiac death and morbidity from multiple causes. Catheter ablation of ventricular tachycardias is becoming an increasingly utilised intervention that has been found to have significant benefits with improving symptoms, reducing anti-arrhythmic drug burden and debilitating device therapies, thereby improving quality of life. Nonetheless, the approach to the ablation of ventricular tachycardias in non-ischemic cardiomyopathies is governed heavily by the disease process, with several distinct differences from ischemic cardiomyopathy including a preponderance to epicardial and deep intramural substrate. This contemporary review aims to present the various disease processes within non-ischemic cardiomyopathies, catheter ablation techniques which have been developed to target ventricular tachycardia and more novel adjunctive therapeutic measures.

Keyword

Ventricular tachycardia; Catheter ablation; Cardiomyopathies

MeSH Terms

Arrhythmias, Cardiac
Cardiomyopathies*
Catheter Ablation
Death, Sudden, Cardiac
Myocardium
Quality of Life
Tachycardia, Ventricular*

Figure

  • Figure 1 Electroanatomic voltage maps in nonischemic cardiomyopathy by disease aetiology. (A) Bipolar (top) and unipolar (bottom) electroanatomic voltage maps of the LV in a patient with Lamin A/C cardiomyopathy showing deep intramural anteroseptal substrate (light green, yellow, and red). Red dots mark points of radiofrequency ablation. (B) Epicardial voltage maps demonstrating extensive inferolateral low-voltage substrate (red) in the RAO (top) and LAO (bottom) views. (C) Bipolar voltage map (top) of the LV of a patient with sarcoidosis demonstrating low-voltage substrate (red) in the basal peri-valvular region and focal substrate in the anteroseptum. Unipolar mapping (bottom) showing more extensive deep intramural anteroseptal substrate (light-green, yellow, and red). (D) Superior view of both endocardial & epicardial voltage maps of the RV & LV showing significant basal-perivalvular, septal and inferolateral epicardial substrate (red) (top). Bottom panel shows confluent and patchy low-voltage inferolateral epicardial substrate from an inferior view due to the patchy inflammatory involvement of the myocardium in sarcoidosis (light green, yellow, and red). (E) Endocardial bipolar voltage map (top panels) of the RV in the RL and PA (F) views showing low-voltage substrate (red) at the superior aspect of the TA and free wall of the RVOT in a patient with ARVC. Unipolar voltage mapping (bottom panels) showing more extensive low-voltage (light-green) extending from the TA to the RVOT, indicating a larger area of far-field scar, likely to be epicardial given the natural history of ARVC. ARVC = arrhythmogenic right ventricular cardiomyopathy; INF = inferior; LAO = left anterior oblique; LMNA = lamin A/C cardiomyopathy; LV = left ventricle; LVOT = left ventricular outflow tract; MA = mitral annulus; PA = postero-anterior; RAO = right anterior oblique; RL = right lateral; RV = right ventricle; RVOT = right ventricular outflow tract; TA = tricuspid annulus.


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