Invasive electrophysiology (EP) mapping and catheter ablation has increasingly become the standard of care for many cardiac arrhythmias like supraventricular tachycardias, atrial fibrillation, premature ventricular complexes (PVC), and monomorphic ventricular tachycardia. In this review, we discuss the recent progress made in the mapping and ablation of ventricular fibrillation (VF). Ventricular activation during VF is apparently disorganized, making mapping and interpretation difficult. Prolonged mapping during VF would require mechanical circulatory support as VF causes complete hemodynamic collapse. These limitations have been addressed by the realization that there is often a reliable trigger arrhythmia that initiates the clinical VF episodes, and an approach to map and ablate this trigger can be successful. Such triggers can be PVCs localizing to the Purkinje/fascicular system, and in other cases can be ectopy from outflow tracts or intracavitary structures like papillary muscles, false tendons or moderator band, or can be monomorphic VT or preexcited atrial fibrillation that degenerate into VF. More recently, approaches beyond trigger elimination directly targeting the VF substrate have been devised. This includes elimination of the arrhythmogenic substrate localizing to the epicardial right ventricular outflow tract in patients with Brugada syndrome, akin to elimination of the arrhythmogenic substrate harbored by regions within scar in ischemic and non-ischemic cardiomyopathies. Further, recent attempts have been made to try to identify and ablate rotors during VF that may be important in perpetuating the VF episode. Such exciting advances in “curing” VF are proving to be life saving for resuscitated survivors of arrhythmic death.
|Journal||Current Treatment Options in Cardiovascular Medicine|
|State||Published - Mar 1 2018|
- Premature ventricular complexes
- Ventricular fibrillation