International Centre for Circulatory Health, National Heart and Lung Institute, Imperial College London, UK.
International Centre for Circulatory Health, National Heart and Lung Institute, Imperial College London, UK.
Int J Cardiol. 2014 Feb 1;171(2):144-52. doi: 10.1016/j.ijcard.2013.10.026. Epub 2013 Oct 16.
The mechanoenergetic effects of atrioventricular delay optimization during biventricular pacing ("cardiac resynchronization therapy", CRT) are unknown.
Eleven patients with heart failure and left bundle branch block (LBBB) underwent invasive measurements of left ventricular (LV) developed pressure, aortic flow velocity-time-integral (VTI) and myocardial oxygen consumption (MVO2) at 4 pacing states: biventricular pacing (with VV 0 ms) at AVD 40 ms (AV-40), AVD 120 ms (AV-120, a common nominal AV delay), at their pre-identified individualised haemodynamic optimum (AV-Opt); and intrinsic conduction (LBBB).
AV-120, relative to LBBB, increased LV developed pressure by a mean of 11(SEM 2)%, p=0.001, and aortic VTI by 11(SEM 3)%, p=0.002, but also increased MVO2 by 11(SEM 5)%, p=0.04. AV-Opt further increased LV developed pressure by a mean of 2(SEM 1)%, p=0.035 and aortic VTI by 4(SEM 1)%, p=0.017. MVO2 trended further up by 7(SEM 5)%, p=0.22. Mechanoenergetics at AV-40 were no different from LBBB. The 4 states lay on a straight line for Δexternal work (ΔLV developed pressure × Δaortic VTI) against ΔMVO2, with slope 1.80, significantly >1 (p=0.02).
Biventricular pacing and atrioventricular delay optimization increased external cardiac work done but also myocardial oxygen consumption. Nevertheless, the increase in cardiac work was ~80% greater than the increase in oxygen consumption, signifying an improvement in cardiac mechanoenergetics. Finally, the incremental effect of optimization on external work was approximately one-third beyond that of nominal AV pacing, along the same favourable efficiency trajectory, suggesting that AV delay dominates the biventricular pacing effect - which may therefore not be mainly "resynchronization".
房室延迟优化在双心室起搏（“心脏再同步治疗”，CRT）中的机械能量效应尚不清楚。
11 例心力衰竭伴左束支传导阻滞（LBBB）患者在 4 种起搏状态下进行左心室（LV）发展压、主动脉血流速度时间积分（VTI）和心肌耗氧量（MVO2）的侵入性测量：双心室起搏（VV 0 ms）时房室延迟 40 ms（AV-40）、房室延迟 120 ms（AV-120，常用的标称房室延迟）、其预先确定的个体最佳血流动力学状态（AV-Opt）；以及固有传导（LBBB）。
与 LBBB 相比，AV-120 平均增加 LV 发展压 11（SEM 2）%，p=0.001，增加主动脉 VTI 11（SEM 3）%，p=0.002，但也增加 MVO2 11（SEM 5）%，p=0.04。AV-Opt 进一步使 LV 发展压平均增加 2（SEM 1）%，p=0.035，主动脉 VTI 增加 4（SEM 1）%，p=0.017。MVO2 进一步增加 7（SEM 5）%，p=0.22。AV-40 的机械能量与 LBBB 无差异。4 种状态的Δ外部功（ΔLV 发展压×Δ主动脉 VTI）与ΔMVO2 呈直线关系，斜率为 1.80，明显大于 1（p=0.02）。
双心室起搏和房室延迟优化增加了外部心脏做功，但也增加了心肌耗氧量。然而，心脏做功的增加约为耗氧量增加的 80%，表明心脏机械能量得到改善。最后，优化对外功的增量效应大约是标称 AV 起搏的三分之一，沿着相同有利的效率轨迹，这表明 AV 延迟主导了双心室起搏效应——这可能不是主要的“再同步化”。
Zotero 插件
