Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland.
Heart Rhythm. 2013 Dec;10(12):1800-6. doi: 10.1016/j.hrthm.2013.08.003. Epub 2013 Aug 6.
The acute response to cardiac resynchronization therapy (CRT) has been shown to be due to 3 mechanisms: resynchronization of ventricular contraction, efficient preloading of the ventricles by a properly timed atrial contraction, and mitral regurgitation reduction. However, the contribution of each of the 3 mechanisms to the acute response to CRT, specifically stroke work improvement, has not been quantified.
To use a magnetic resonance image-based anatomically accurate 3-dimensional model of failing canine ventricular electromechanics to quantify the contribution of each of the 3 mechanisms to stroke work improvement and identify the predominant mechanisms.
An MRI-based electromechanical model of the failing canine ventricles assembled previously by our group was further developed and modified. Three different protocols were used to dissect the contribution of each of the 3 mechanisms to stroke work improvement.
Resynchronization of ventricular contraction did not lead to a significant stroke work improvement. Efficient preloading of the ventricles by a properly timed atrial contraction was the predominant mechanism underlying stroke work improvement. Stroke work improvement peaked at an intermediate atrioventricular delay, as it allowed ventricular filling by atrial contraction to occur at a low diastolic left ventricular pressure but also provided adequate time for ventricular filling before ventricular contraction. Reduction of mitral regurgitation by CRT led to stroke work worsening instead of improvement.
Efficient preloading of the ventricles by a properly timed atrial contraction is responsible for a significant stroke work improvement in the acute CRT response.
心脏再同步治疗(CRT)的急性反应归因于 3 种机制:心室收缩的再同步、通过适时的心房收缩有效预充心室以及二尖瓣反流减少。然而,这 3 种机制中每一种对 CRT 急性反应(特别是改善每搏功)的贡献尚未量化。
使用基于 MRI 的衰竭犬心室机电学的解剖学精确 3 维模型来量化这 3 种机制中每一种对改善每搏功的贡献,并确定主要机制。
我们小组先前组装的基于 MRI 的衰竭犬心室机电学模型得到进一步开发和修改。使用 3 种不同的方案来剖析每一种机制对改善每搏功的贡献。
心室收缩的再同步不会导致显著的每搏功改善。通过适时的心房收缩有效预充心室是改善每搏功的主要机制。中间房室延迟时每搏功改善达到峰值,因为它允许心房收缩在较低的舒张期左心室压力下进行心室充盈,同时也为心室收缩前提供足够的时间进行充盈。CRT 导致的二尖瓣反流减少反而导致每搏功恶化而非改善。
通过适时的心房收缩有效预充心室是 CRT 急性反应中显著改善每搏功的原因。