Ventricular Tachycardia Ablation in Ischemic Patients
Which of the two ablation approaches: 1) ablation limited to clinical ventricular tachycardia (VT) and mappable VT (“clinical ablation”), or 2) substrate-based ablation, results in lower rates of recurrent VT in patients with ischemic disease?
In a seven-center study, patients with ischemic cardiomyopathy and hemodynamically tolerated VT were randomized to clinical ablation (n = 60) versus substrate-based ablation that targeted all abnormal electrograms in the scar (n = 58). The primary endpoint was recurrence of VT. Secondary endpoints included periprocedural complications, 12-month mortality, and rehospitalizations.
At 12 months of follow-up, 16% and 48% of patients had VT recurrence in substrate-based and clinical VT ablation groups, respectively (log rank p < 0.001); 12% of patients with substrate ablation and 32% of patients with clinical ablation required rehospitalization (p = 0.014). Twelve-month mortality was 8.6% in substrate ablation and 15.0% in clinical ablation groups, respectively (log-rank p = 0.21). Combined incidence of rehospitalization and mortality was lower with substrate ablation (p = 0.003). Periprocedural complications were similar in both groups (p = 0.61).
The authors concluded that an extensive substrate-based ablation approach is superior to ablation targeting only clinical and stable VTs in ischemic cardiomyopathy patients presenting with tolerated VT.
The arrhythmogenic substrate in post-infarct patients consists of surviving myocardial bundles within and around the dense scar tissue. These surviving cardiac fibers constitute areas of slow conduction, which is implicated in re-entrant VT. There are usually a multitude of channels capable of activation; only some of these channels are implicated in inducible VT. Mapping of the induced VT in order to find the critical isthmus is a relatively complex process, and is limited by hemodynamic stability. On the other hand, substrate mapping relies on the identification of areas of slow conduction by analysis of the intracardiac electrograms recorded at the tip of the ablation catheter, usually during sinus rhythm, which is a less complex process. During substrate mapping, abnormal, fractionated, and late electrograms are identified. They are sensitive indicators of the arrhythmogenic substrate, albeit not very specific for clinical VT. The current study highlights the limitations of both inducibility and assigning a ‘clinical’ label to induced VTs (matching cycle length, 12-lead electrocardiogram [when available], and the intracardiac tracings from implantable cardioverter-defibrillator interrogation). ‘Carpet bombing’ of the scar tissue, more elegantly referred to as homogenization, allows for a more efficient elimination of as many channels within and around the scar as possible, and in this randomized study was found to be associated with a significant reduction in recurrent VT. Further work is needed to find the optimal method of substrate-based ablation.
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