Sinus Rhythm Targeting of Channels for Ablation of Postinfarction Ventricular Tachycardia

Abstract

Scar-related reentry is the most common cause of sustained monomorphic ventricular tachycardia (VT) in patients with structural heart disease. These scars are comprised not only of dense fibrosis but also contain surviving myocyte bundles that support reentry. The separation of myocytes creates a circuitous path (zig-zag conduction) that slows conduction despite the presence of relatively normal action potential upstrokes.1,2 Gap junction remodeling and ion channel alterations may also contribute to slow conduction.3 After myocardial infarction, the scar evolves as part of the ventricular remodeling process, and acute reperfusion favorably influences this process. Article see p 90 Of 689 patients with acute ST elevation myocardial infarction who received acute percutaneous intervention for reperfusion reported by Zaman et al,4 only 17% had a left ventricular ejection fraction <40%, and of these, only 32 (≈5% of the total group) had inducible VT when studied early after the infarction. By 1 year, only 19% of the patients with inducible VT had spontaneous VT. Interestingly, the VTs that occurred spontaneously (a mean of 11 months after the infarct) were substantially slower as compared with those that were induced early after infarction. Thus, it seems likely that the ongoing remodeling efforts result in conduction slowing in or around the channels of surviving myocytes in the infarct that foster reentrant VT. The risk of VT may increase over years. The time between infarction and referral for VT ablation was an average of 16 years for patients who receive acute infarct reperfusion in one study.5 Once VT is clinically manifest, the reentry substrate is relatively stable, such that the risk of recurrence exceeds 40% by 2 years. An implantable defibrillator is protection against sudden death, but recurrent VT is associated with worse outcomes.6 Catheter ablation has an important role in reducing …