In recently published studies, modulation of rotors by ablation seems to be effective in termination of atrial fibrillation. Now, researchers are exploring the role of rotors in ventricular fibrillation. Siva K Mulpuru (Mayo Clinic, Rochester, USA), discusses the latest research in this field.
Sudden cardiac death occurs in about 225,000 individuals every year in the USA and the most common associated arrhythmia is ventricular fibrillation (VF). VF commonly occurs in patients with structural heart disease. Implantable cardioverter defibrillators (ICDs) are commonly used to prevent sudden cardiac death in patients who survived an episode or who are at risk. Although electrical therapies from ICDs terminate VF, the substrate remains unaltered and patients are in need of recurrent ICD therapies for treatment of ventricular arrhythmias.
Until now, recurrent VF is commonly managed by treatment of underlying heart disease and use of antiarrhythmic drugs. More recently, premature ventricular contractions that act as triggers are targeted with ablation procedures. These premature ventricular contractions seem to arise from the conduction system or near vicinity to the conduction system. In isolated heart muscle preparations and modelling experiments VF seems to be secondary to functional reentry, which occurs after an excitation wave encounters a wave break. This repetitive rotational form of reentry is commonly termed as a “rotor”. The core of the rotor is physiologically active and can drift with time. In recently published studies, modulation of rotors by ablation seems to be effective in termination of atrial fibrillation.
Krummen et al1 for the first time show mechanistic evidence of rotors due to functional reentry in a dog model of ventricular fibrillation. VF was induced by pacing in dogs and was recorded by multipolar basket catheters (Firmap, Topera) carefully placed in both ventricles. Analysis of the collected unipolar recordings was performed to identify patterns of repetitive rotational activity during VF. The dogs had 1.3±0.5 rotors identified (on average) in the endocardium of left ventricle. They went on to perform ablation in the region of rotor vs. sham ablation far away from identified rotors. Rotor ablation made VF non-inducible in two thirds of the dogs and in the remaining dogs VF was difficult to induce.
With this background knowledge the authors went on to map VF in a patient with ischaemic cardiomyopathy experiencing recurrent ICD therapies due to VF. Basket catheters were placed in both ventricles to record VF. Notably, the patient did not have consistent triggers for VF. Four rotors were mapped (two on each ventricle) during VF and were targeted with ablation during sinus rhythm. The rotors in the left ventricle coincided with the border zone between scar and normal tissue. Post-ablation, the patient remained VF free during one-year follow-up.
There are several points worth revisiting after examining this interesting paper. “Rotor” is a two dimensional representation of functional re-entry and the three dimensional equivalent is a scroll wave.
It is unclear how an ablation lesion would affect a scroll wave. The dogs studied in this model were healthy while the only human subject studied had ischaemic cardiomyopathy. If the results are validated by larger multicentre studies, it could potentially represent a paradigm shift in mapping and treatment of VF. Until then, treatment of underlying heart disease, ICDs, antiarrhythmic drugs and ablation of triggers are the cornerstone for management of recurrent VF.
References
- Krummen et al. J Cardiovasc Electrophysiol. 2015 Jul 14. doi: 10.1111/jce.12753
Siva K Mulpuru, assistant professor of Medicine, is a consultant at the Division of Cardiovascular Diseases at the Mayo Clinic, Rochester, USA
