PO-05-056 FAILURE OF INTRINSIC ANTI-TACHYCARDIA PACING TO TERMINATE VENTRICULAR TACHYCARDIA AND POTENTIAL PROARRHYTHMIC EFFECTS

Abstract

Intrinsic anti-tachycardia pacing (iATP™) is a novel, automated ATP algorithm that provides individualized therapy to terminate ventricular tachycardia (VT). If the first ATP attempt is unsuccessful, the algorithm analyzes the tachycardia cycle length and the post-pacing interval (PPI) and adjusts the subsequent sequence to successfully terminate VT. This algorithm was effective in a single clinical study without a comparator arm and case reports have corroborated this success in clinical practice. Despite the previously presented data, iATP™ failure has not been well documented in the literature. We present the first case series of iATP™ failure in routine clinical practice with detailed episode analysis and the apprise the electrophysiology community of the potential proarrhythmic effect of the algorithm. We retrospectively evaluated 262 patients with Medtronic Cobalt XT defibrillators followed at Mayo Clinic campuses in Minnesota, Florida, and Arizona. 119 patients had devices with the iATP™ feature turned on. 4 out of 119 patients (3.36%) had an acceleration of their ventricular arrhythmias within our cohort. Illustrative Case: A 74-year-old male with a history of idiopathic, non-ischemic cardiomyopathy (LVEF) 21%) status post-cardiac resynchronization therapy (CRT)-defibrillator for primary prevention, subsequent VT, and atrial fibrillation presented to our heart rhythm clinic for evaluation of syncope. The patient was riding an all-terrain vehicle when he felt a sudden onset of dyspnea and pre-syncope. His device interrogation revealed a presenting rhythm of VT at 200 beats per minute (bpm). The patient underwent four unsuccessful rounds of ATP. The 4th round of ATP resulted in acceleration (figure 1A) and degeneration into ventricular fibrillation (VF), followed by a successful 39.5 J shock (figure 1B). Figure 1C shows the dot plot for the entire episode with the blue box highlighting the acceleration in ventricular rate after the 4th ATP sequence. Given concern for a proarrhythmic effect, iATP™ was turned off. The patient was treated with amiodarone and mexiletine and underwent endocardial ablation with substrate modification in the inferolateral LV. He is currently doing well without a subsequent need for VT therapies. While the novel adaptive algorithm and its underlying concepts are intriguing, clinicians should be aware of the potential for acceleration and degeneration of VT by iATP™ and prepared to turn off the feature when this occurs.