Objectives The purpose of this study was to investigate how LBBB and CRT modify RV free wall function by direct ventricular interaction. Background Right ventricular (RV) function influences prognosis in patients with left bundle branch block (LBBB) and cardiac resynchronization therapy (CRT). There is, however, limited insight into how LBBB and CRT affect RV function. Methods In 24 patients with LBBB with nonischemic cardiomyopathy, RV and left ventricular (LV) strain by speckle-tracking echocardiography was measured before and after CRT. Underlying mechanisms were studied in 16 anesthetized dogs with ultrasonic dimension crystals and micromanometers. Results Patients with LBBB demonstrated distinct early systolic shortening in the RV free wall, which coincided with the typical abnormal early systolic septal shortening. In animals, this RV free wall contraction pattern resulted in reduced myocardial work as a large portion of the shortening occurred against low pressure during early systole, coinciding with abnormal leftward septal motion. RV systolic function was maintained by vigorous contraction in the late-activated LV lateral wall, which pushed the septum toward the RV. CRT reduced abnormal septal motion and increased RV free wall work because there was less inefficient shortening against low pressure. Conclusions LBBB reduces workload on the RV free wall because of abnormal septal motion and delayed activation of the LV lateral wall. Restoring septal and LV function by CRT increases workload in RV free wall and may explain why patients with RV failure respond poorly to CRT. (Contractile Reserve in Dyssynchrony: A Novel Principle to Identify Candidates for Cardiac Resynchronization Therapy [CRID-CRT]; [NCT02525185][1]) [1]: https://clinicaltrials.gov/ct2/show/NCT02525185?term=NCT02525185&draw=1&rank=1

中文翻译：

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左束支传导阻滞和心脏再同步治疗对右心室功能的机械作用。

目的 本研究的目的是研究 LBBB 和 CRT 如何通过直接心室相互作用改变 RV 游离壁功能。背景右心室 (RV) 功能影响左束支传导阻滞 (LBBB) 和心脏再同步治疗 (CRT) 患者的预后。然而，对 LBBB 和 CRT 如何影响 RV 功能的了解有限。方法在24例LBBB合并非缺血性心肌病患者中，通过斑点追踪超声心动图测量CRT前后的RV和左心室（LV）应变。使用超声波尺寸晶体和微压计在 16 只麻醉的狗中研究了潜在机制。结果 LBBB 患者右室游离壁有明显的早期收缩期缩短，这与典型的早期收缩期间隔缩短异常一致。在动物中，这种 RV 游离壁收缩模式导致心肌做功减少，因为在收缩早期，大部分收缩发生在低压下，与向左室间隔异常运动相吻合。RV 收缩功能是通过晚期激活的 LV 侧壁的剧烈收缩来维持的，这将隔膜推向 RV。CRT 减少了异常的间隔运动并增加了 RV 游离壁工作，因为在低压下缩短的效率较低。结论 LBBB 减少了 RV 游离壁的工作量，因为间隔运动异常和 LV 侧壁延迟激活。通过 CRT 恢复室间隔和 LV 功能会增加 RV 游离壁的工作量，这可以解释为什么 RV 衰竭患者对 CRT 反应不佳。（不同步中的收缩储备：确定心脏再同步治疗候选者的新原则 [CRID-CRT]；[NCT02525185][1]) [1]：https://clinicaltrials.gov/ct2/show/NCT02525185?term=NCT02525185&draw=1&rank=1