“Ventricular fibrillation was generally viewed as a non-ablatable rhythm disturbance. However, several advances over the last decade have enabled electrophysiologists to successfully address this arrhythmia with ablation techniques,” writes Samuel J Asirvatham, Mayo Clinic, Rochester, USA. He will be discussing this topic at Heart Rhythm (Denver, USA, 8–11 May 2013).
To successfully ablate a cardiac rhythm disturbance, accurate mapping as a prerequisite for success was the norm. As a result, ventricular fibrillation was generally viewed as a non-ablatable rhythm disturbance. However, several advances, over the last decade, have enabled electrophysiologists to successfully address this arrhythmia with ablation techniques in patients both with and without structural heart disease:
2. Understanding that the inciting beats more frequently arise from identifiable anatomic sites that include the infrahisian conduction system, the perivalvar ventricular outflow tracts, and the papillary muscles;
3. A detailed understanding in mammalian hearts of the regional anatomy and distribution of the infrahisian conduction system.
In addition to these findings, the actual possibility of mapping ventricular fibrillation is also being increasingly considered. Percutaneously implantable temporary cardiac support devices3 that can support the circulation during rapid ventricular arrhythmias and arrhythmia occurring in patients with already permanently implanted left ventricular assist devices may allow this possibility. Important understanding of unique electroanatomic transition sites in the ventricular myocardium including the base of the papillary muscles and the perimitral valve region may help merge current mapping paradigms with the basic understanding of the electrophysiology behind the maintenance of ventricular fibrillation.4, 5 Thus, brief mapping and targeting signals that may represent primary rotors at sites like the base of the papillary muscle may address the ventricular fibrillation itself (rather than the triggering beat alone).
Currently, investigation has involved novel targets for ventricular fibrillation ablation and the development of mapping and able tools specifically designed to access the anatomic targets that have been identified as either triggers or maintainers of ventricular fibrillation. Cardiac telocytes or the Cajal-like cells initially identified for the first time in the heart in the peri-pulmonary vein tissue have now been found to occur in the ventricles including perivalvar regions and the papillary muscles. Their role in arrhythmogenesis, if any, is being investigated.6
Ablation techniques including direct current-based electroporation that creates widespread superficial lesions are being developed as a way of addressing arrhythmogenic ventricular fibrillogenic substrate and yet preserve ventricular function. These techniques aim to address the conduction tissue or the epicardial autonomic enervation without resulting in significant myocardial damage.
Investigations over the next decade will reveal which of these approaches and targets will result in a system for safe, quick, and effective ablation of ventricular fibrillation.
Samuel J Asirvatham, Division of Cardiovascular Diseases, Department of Medicine – Department of Pediatrics and Adolescent Medicine, Mayo Clinic, Rochester, USA.
1. Srivathsan K, Gami AS, Ackerman MJ, Asirvatham SJ. Treatment of ventricular fibrillation in a patient with prior diagnosis of long qt syndrome: Importance of precise electrophysiologic diagnosis to successfully ablate the trigger. Heart Rhythm. 2007;4:1090-1093
2. Haissaguerre M, Extramiana F, Hocini M, Cauchemez B, Jais P, Cabrera JA, Farre J, Leenhardt A, Sanders P, Scavee C, Hsu LF, Weerasooriya R, Shah DC, Frank R, Maury P, Delay M, Garrigue S, Clementy J. Mapping and ablation of ventricular fibrillation associated with long-qt and brugada syndromes. Circulation. 2003;108:925-928
3. Abuissa H, Roshan J, Lim B, Asirvatham SJ. Use of the impella microaxial blood pump for ablation of hemodynamically unstable ventricular tachycardia. J Cardiovasc Electrophysiol. 2010;21:458-461
4. Tabereaux PB, Dosdall DJ, Ideker RE. Mechanisms of vf maintenance: Wandering wavelets, mother rotors, or foci. Heart Rhythm. 2009;6:405-415
5. Pak HN, Kim YH, Lim HE, Chou CC, Miyauchi Y, Fang YH, Sun K, Hwang C, Chen PS. Role of the posterior papillary muscle and purkinje potentials in the mechanism of ventricular fibrillation in open chest dogs and swine: Effects of catheter ablation. J Cardiovasc Electrophysiol. 2006;17:777-783
6. Kapa S, McLeod CJ, Beyder A, Gomez Pinilla PJ, Farrugia F, Asirvatham SJ. Identification of interstitial cells of cajal and an ano1-encoded chloride channel in the heart may offer novel targets for cardiac dysrhythmias (abstract). Heart Rhythm. 2010;7:S161