What factors lead to the acceleration of ventricular tachycardia during antitachycardia pacing?—Results from over 1000 episodes. Issue 1 (14th December 2017)

• Record Type: Journal Article
• Authors: Fang, Yin; Gu, Kai; Yang, Bing; Ju, Weizhu; Chen, Hongwu; Li, Mingfang; Liu, Hailei; Wang, Jiaxian; Yang, Gang; Chen, Minglong
• Is Part Of: Journal of arrhythmia. Volume 34:Issue 1(2017)
• Page Start: 36
• Page End: 45
• Publication Date: 2017-12-14
• Subjects: acceleration -- antitachycardia pacing -- degeneration -- implantable cardioverter defibrillator -- ventricular tachycardia; Arrhythmia -- Periodicals; Cardiac pacing -- Periodicals; Arrhythmias, Cardiac; Arrhythmia; Cardiac pacing; Periodicals; Electronic journals; Periodicals; 616.128
• DOI: 10.1002/joa3.12010
• Languages: English
• ISSNs: 1880-4276

Abstract

Abstract: Introduction: Ventricular tachycardia (VT) acceleration due to antitachycardia pacing (ATP) therapy could be often observed in patients with implantable cardioverter defibrillator (ICD), which usually results in additional shock. However, few studies focused on the risk factors for VT acceleration caused by ATP therapy. The purpose of this study was to investigate risk factors for VT acceleration due to ATP delivery. Methods: We retrospectively reviewed 1056 ATP episodes in 33 patients with structural heart diseases, of whom clinical characteristics and episodes details were evaluated. Results: At individual patient level, number of VT morphologies recorded in electrograms during follow‐up was a risk factor with cutoff point of 1 (AUC 0.79, sensitivity 72.7%, specificity 77.3%, P < .001) to predict ATP acceleration (OR 3.50, P = .008). From episode‐based analysis, VT cycle length (VTCL) and mean variation in VTCL were risk factors to predict ATP acceleration (OR 0.98, P < 0.001 vs OR 1.06, P < .001, respectively), with cutoff points of 347 ms (AUC 0.67, sensitivity 82.5%, specificity 47.6%, P < .001) and 7.3 ms (AUC 0.66, sensitivity 77.5%, specificity 56.7%, P < .001), respectively. In addition, VTs with cycle length less than 347 ms were more likely to be accelerated by burst stimulation with more pulse numbers (OR 3.31, P < .001). Conclusions: Number of VT morphologies, VTCL, and mean variation in VTCL are risk factors predicting ATP acceleration. Burst stimulation with less pulse numbers should be performed in VTs with cycle length less than 347 ms.