Cardiology Department, Guy's and St Thomas' NHS Foundation Trust, London, UK.
School of Biomedical Engineering and Imaging Sciences, King's College London, London, UK.
Pacing Clin Electrophysiol. 2020 Jul;43(7):737-745. doi: 10.1111/pace.13969. Epub 2020 Jun 21.
Antitachycardia pacing (ATP), which may avoid unnecessary implantable cardioverter-defibrillator (ICD) shocks, does not always terminate ventricular arrhythmias (VAs). Mean entropy calculated using cardiac magnetic resonance texture analysis (CMR-TA) has been shown to predict appropriate ICD therapy. We examined whether scar heterogeneity, quantified by mean entropy, is associated with ATP failure and explore potential mechanisms using computer modeling.
A subanalysis of 114 patients undergoing CMR-TA where the primary endpoint was delivery of appropriate ICD therapy (ATP or shock therapy) was performed. Patients receiving appropriate ICD therapy (n = 33) were dichotomized into "successful ATP" versus "shock therapy" groups. In silico computer modeling was used to explore underlying mechanisms.
A total of 16 of 33 (48.5%) patients had successful ATP to terminate VA, and 17 of 33 (51.5%) patients required shock therapy. Mean entropy was significantly higher in the shock versus successful ATP group (6.1 ± 0.5 vs 5.5 ± 0.7, P = .037). Analysis of patients receiving ATP (n = 22) showed significantly higher mean entropy in the six of 22 patients that failed ATP (followed by rescue ICD shock) compared to 16 of 22 that had successful ATP (6.3 ± 0.7 vs 5.5 ± 0.7, P = .048). Computer modeling suggested inability of the paced wavefront in ATP to successfully propagate from the electrode site through patchy fibrosis as a possible mechanism of failed ATP.
Our findings suggest lower scar heterogeneity (mean entropy) is associated with successful ATP, whereas higher scar heterogeneity is associated with more aggressive VAs unresponsive to ATP requiring shock therapy that may be due to inability of the paced wavefront to propagate through scar and terminate the VA circuit.
抗心动过速起搏(ATP)可以避免不必要的植入式心脏复律除颤器(ICD)电击,但其并不总能终止室性心律失常(VA)。使用心脏磁共振纹理分析(CMR-TA)计算的平均熵已被证明可预测适当的 ICD 治疗。我们检查了由平均熵量化的瘢痕异质性是否与 ATP 失败相关,并使用计算机建模探索了潜在机制。
对 114 例行 CMR-TA 的患者进行了亚分析,主要终点是给予适当的 ICD 治疗(ATP 或电击治疗)。接受适当 ICD 治疗的患者(n=33)分为“成功的 ATP”与“电击治疗”组。使用计算机模拟来探索潜在的机制。
共有 33 例患者中的 16 例(48.5%)通过 ATP 成功终止 VA,33 例患者中的 17 例(51.5%)需要电击治疗。与成功的 ATP 组相比,电击组的平均熵明显更高(6.1±0.5 vs 5.5±0.7,P=0.037)。对接受 ATP 治疗的患者(n=22)进行分析,发现 22 例患者中有 6 例 ATP 治疗失败(随后进行 ICD 电击抢救)的患者平均熵明显高于 22 例成功的 ATP 患者(6.3±0.7 vs 5.5±0.7,P=0.048)。计算机建模表明,ATP 中起搏波阵面无法从电极部位成功传播到斑片状纤维化,这可能是 ATP 治疗失败的一种机制。
我们的研究结果表明,较低的瘢痕异质性(平均熵)与成功的 ATP 相关,而较高的瘢痕异质性与更具侵袭性的 VA 相关,ATP 治疗反应不佳需要电击治疗,这可能是由于起搏波阵面无法通过瘢痕传播并终止 VA 回路所致。