Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Japan; Department of Advanced Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Japan.
Heart Rhythm. 2020 Nov;17(11):1870-1877. doi: 10.1016/j.hrthm.2020.05.031. Epub 2020 May 26.
Myocardial scarring is associated with nonresponse to cardiac resynchronization therapy (CRT) and conduction delay. Little is known about the significance and cause of left ventricular (LV) paced conduction disturbance (LPCD).
The purpose of this study was to investigate the clinical impact of paced interlead electrical delay and the difference in each conduction time from LV pace to right ventricular (RV) sense (LVp-RVs) and from RV pace to LV sense (RVp-LVs) [(LVp-RVs) - (RVp-LVs)], in CRT.
Among 137 patients who underwent CRT implantation, LVp-RVs and RVp-LVs were measured intraoperatively. The relationships between [(LVp-RVs) - (RVp-LVs)] and perfusion defects on myocardial perfusion single photon emission computed tomography (SPECT) imaging or [(LVp-RVs) - (RVp-LVs)] and clinical outcomes were assessed.
After CRT implantation, 81 patients (59%) responded to CRT. [(LVp-RVs) - (RVp-LVs)] was significantly longer in nonresponders than in responders (9.7 ± 47.3 ms vs -4.5 ± 33.2 ms; P = .041). Patients with LPCD [(LVp-RVs) > (RVp-LVs)] had higher perfusion defects in the anterolateral region (2.7 ± 2.7 vs 1.1 ± 1.6; P = .0015) on SPECT. Multivariate analysis showed that LPCD was the independent predictor of nonresponse to CRT (odds ratio 0.40; 95% confidence interval [CI] 0.17-0.90; P = .026). During median follow-up of 2.3 years (interquartile range 1.3-5.5), LPCD was the independent predictor of cardiac death and/or heart failure hospitalization in multivariate analysis (hazard ratio 2.04; 95% CI 1.19-3.55; P = .010).
LPCD could predict nonresponse to CRT and poor outcome. Further intervention, such as adjustment of pacing timing or multipoint/site pacing, may be needed in such patients.
心肌瘢痕与心脏再同步治疗（CRT）无反应和传导延迟有关。对于左心室（LV）起搏传导障碍（LPCD）的意义和原因知之甚少。
本研究旨在探讨 CRT 中起搏导联间电延迟和 LV 起搏至右心室（RV）感知（LVp-RVs）与 RV 起搏至 LV 感知（RVp-LVs）之间的每个传导时间差（LVp-RVs）-（RVp-LVs））的临床意义。
在 137 例行 CRT 植入术的患者中，术中测量 LVp-RVs 和 RVp-LVs。评估[(LVp-RVs)-(RVp-LVs)]与心肌灌注单光子发射计算机断层扫描（SPECT）成像上的灌注缺损之间的关系，或[(LVp-RVs)-(RVp-LVs)]与临床结局之间的关系。
CRT 植入后，81 例（59%）患者对 CRT 有反应。无反应者的[(LVp-RVs)-(RVp-LVs)]明显长于有反应者（9.7±47.3 ms 比-4.5±33.2 ms；P=0.041）。LPCD 患者[(LVp-RVs)＞(RVp-LVs)]的前外侧区域 SPECT 上的灌注缺损更高（2.7±2.7 比 1.1±1.6；P=0.0015）。多变量分析显示，LPCD 是 CRT 无反应的独立预测因子（优势比 0.40；95%置信区间 [CI] 0.17-0.90；P=0.026）。在中位随访 2.3 年（四分位间距 1.3-5.5）期间，LPCD 是多变量分析中心脏死亡和/或心力衰竭住院的独立预测因子（风险比 2.04；95%CI 1.19-3.55；P=0.010）。
LPCD 可预测 CRT 无反应和不良结局。此类患者可能需要进一步干预，如调整起搏时间或多点/位起搏。
