Verbeek Xander A A M, Vernooy Kevin, Peschar Maaike, Cornelussen Richard N M, Prinzen Frits W
Department of Physiology, Cardiovascular Research Institute, Maastricht University, Maastricht, The Netherlands.
J Am Coll Cardiol. 2003 Aug 6;42(3):558-67. doi: 10.1016/s0735-1097(03)00641-7.
We sought to investigate to what extent intra-ventricular asynchrony (intraVA) and inter-ventricular asynchrony (interVA) determine left ventricular (LV) function in canine hearts with left bundle branch block (LBBB) during ventricular pacing.
Pacing therapy improves LV pump function in patients with heart failure and abnormal ventricular conduction supposedly due to resynchronization. However, the relationship between LV pump function and measures of asynchrony is not well established.
In 15 experiments, LV (various sites) and biventricular (BiV) pacing was performed at atrioventricular (AV) delays of 20 to 140 ms. Measured were the maximum rate of increase (dP/dt(max)) of LV pressure and LV stroke work (SW) (conductance catheter), interVA (time delay between the upslope of LV and RV pressures), and intraVA (from endocardial electrical activation maps).
Induction of LBBB increased interVA (-6.4 +/- 8.6 to -28.4 +/- 8.5 ms [RV earlier]) and intraVA (4.9 +/- 2.4 to 18.0 +/- 3.3 ms), whereas LV dP/dt(max) and SW decreased (-13 +/- 18% and -39 +/- 24%, respectively). During LBBB, LV and BiV pacing increased LV dP/dt(max) and SW (mean increases 14% to 21% and 11% to 15%, respectively) without changing diastolic function or preload. Optimal improvement in LV function was obtained consistently when intraVA returned to pre-LBBB values, while interVA remained elevated. Normalization of intraVA required AV delays shorter than the baseline PQ time during LV apex and BiV pacing, thus excluding endogenous LV activation, but AV delays virtually equal to the baseline PQ time (difference 4 +/- 9 ms, p = NS) during pacing at (mid)lateral LV sites to obtain fusion between pacing-induced and endogenous activation.
In LBBB hearts, optimal restoration of LV systolic function by pacing requires intra-ventricular resynchronization. The optimal AV delay to achieve this depends on both the site of pacing and baseline PQ time.
我们试图研究在心室起搏期间,左束支传导阻滞(LBBB)犬心室内非同步性(intraVA)和心室间非同步性(interVA)在多大程度上决定左心室(LV)功能。
起搏治疗可改善心力衰竭和心室传导异常患者的左心室泵功能,推测是由于再同步化。然而,左心室泵功能与非同步性测量指标之间的关系尚未完全明确。
在15项实验中,以20至140毫秒的房室(AV)延迟进行左心室(不同部位)和双心室(BiV)起搏。测量左心室压力最大上升速率(dP/dt(max))和左心室搏功(SW)(电导导管)、心室间非同步性(左心室和右心室压力上升斜率之间的时间延迟)和心室内非同步性(来自心内膜电激动图)。
诱发LBBB增加了心室间非同步性(从-6.4±8.6毫秒至-28.4±8.5毫秒[右心室更早])和心室内非同步性(从4.9±2.4毫秒至18.0±3.3毫秒),而左心室dP/dt(max)和SW降低(分别降低-13±18%和-39±24%)。在LBBB期间,左心室和双心室起搏增加了左心室dP/dt(max)和SW(平均增加分别为14%至21%和11%至15%),而不改变舒张功能或前负荷。当心室内非同步性恢复到LBBB前的值,而心室间非同步性仍升高时,始终能获得左心室功能的最佳改善。在左心室心尖和双心室起搏期间,心室内非同步性的正常化需要房室延迟短于基线PQ时间,从而排除内源性左心室激动,但在左心室(中)外侧部位起搏期间,房室延迟实际上等于基线PQ时间(差异4±9毫秒,p = 无显著性差异),以获得起搏诱发激动和内源性激动之间的融合。
在LBBB心脏中,起搏实现左心室收缩功能的最佳恢复需要心室内再同步化。实现这一目标的最佳房室延迟取决于起搏部位和基线PQ时间。