The Ideal End Point for Ablation in Postinfarction Ventricular Tachycardia
One May Not Fit All
The end point of ventricular tachycardia (VT) ablation studies should ideally predict the target outcome—freedom from VT recurrence. VT in patients with previous myocardial infarction is often due to scar-related re-entry. This is supported, although not proven, by the fact that VT can be initiated by programmed electric stimulation (PES). Entrainment and resetting with fusion are strong arguments for re-entry but can be only performed during hemodynamically tolerated VT.
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The substrate for re-entry is characterized by regions of slow conduction, unidirectional conduction block that allows initiation of re-entry, and areas of conduction block that can define parts of the re-entry circuit. Conduction block can be anatomically fixed but also functional and thus only present during VT or at rapid rates. Catheter ablation aims to transect the critical isthmus of the re-entry circuit.
The ideal ablation candidate is inducible for the clinically documented, hemodynamically tolerated VT. This allows for detailed analysis of the mechanism involved and accurate delineation of the underlying substrate. Unfortunately, this scenario applies only to a minority (albeit an important number) of patients.
This first patient category was accepted for ablation in the early 1990s. Only the clinical VT was targeted and of importance, was, without exception reproducibly inducible from the right ventricle.1 Outcome was favorable if the clinical VT was abolished, a result achieved in 75% of the patients. Remarkably, 82% of them were noninducible for any VT after ablation. In 16% of these noninducible patients, ventricular arrhythmia (VA) recurred; in half of the patients early and often with the same VT morphology, perhaps due to lesion recovery. Patients presenting with a late recurrence either died suddenly, presumably (but not definitively) arrhythmic, or had a not previously documented VT. Patients with VA recurrence were more likely to be inducible for nonclinical VT. …