Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
JACC Cardiovasc Imaging. 2020 Jul;13(7):1475-1484. doi: 10.1016/j.jcmg.2019.11.016. Epub 2020 Jan 15.
The purpose of this study was to investigate how LBBB and CRT modify RV free wall function by direct ventricular interaction.
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.
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.
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.
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).
本研究旨在探讨左束支传导阻滞(LBBB)和心脏再同步治疗(CRT)如何通过直接心室相互作用改变右心室(RV)游离壁功能。
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,对于 LBBB 和 CRT 如何影响 RV 功能,人们的了解有限。
在 24 例非缺血性心肌病伴 LBBB 的患者中,使用斑点追踪超声心动图测量 CRT 前后 RV 和左心室(LV)应变。在 16 只麻醉犬中使用超声维度晶体和微压力计研究潜在机制。
LBBB 患者 RV 游离壁出现明显的早期收缩缩短,与典型的异常早期收缩间隔缩短相对应。在动物中,这种 RV 游离壁收缩模式导致心肌做功减少,因为大部分缩短发生在早期收缩期间的低压下,与异常的左隔运动相对应。RV 收缩功能通过晚期激活的 LV 外侧壁的有力收缩来维持,该收缩将间隔推向 RV。CRT 减少了异常的间隔运动并增加了 RV 游离壁的做功,因为低压下效率较低的缩短减少了。
由于异常的间隔运动和 LV 外侧壁延迟激活,LBBB 减少了 RV 游离壁的工作量。通过 CRT 恢复间隔和 LV 功能会增加 RV 游离壁的工作量,这可能解释了为什么 RV 衰竭患者对 CRT 反应不佳。(不同步中的收缩储备:一种识别心脏再同步治疗候选者的新原理 [CRID-CRT];NCT02525185)。