Varma Niraj
Cleveland Clinic, Cleveland, OH, USA.
J Electrocardiol. 2015 Jan-Feb;48(1):53-61. doi: 10.1016/j.jelectrocard.2014.09.002. Epub 2014 Sep 16.
Assess effect of right ventricular pacing (RVP) on left ventricular (LV) activation in heart failure patients with left bundle branch block (LBBB).
LV activation during RVP is regarded as similar to LBBB; hence novel CRT algorithms may avoid RVP by adopting "fusion" pacing with intrinsic RBB-mediated conduction. However, other CRT techniques demand RV paced wavefronts for optimal resynchronization. Appropriate selection may require attention to interaction between RVP-generated wavefronts with preexisting conduction abnormalities posed by LBBB i.e. transseptal delay and LV activation. We hypothesized that LV activation during RVP would differ to LBBB.
Eleven patients (59±19years, 8 male, LV ejection fraction 25±10%; ischemic etiology 45%) were studied 5.4±5months after CRT implant. All had intact AV conduction with LBBB (PR interval 204±55; QRS 167±27ms) prior to CRT. None had mid-septal/outflow tract lead positions. Using non-invasive electrocardiographic imaging (ECGI), LV activation was contrasted in each patient between intrinsic conduction and RVP with minimized AV interval (i.e. committing ventricular excitation to the paced wavefront).
RVP affected LV activation variably. Transseptal time decreased in 64% of patients. More LV conduction barriers were created than resolved, slowing LV free wall activation from 67±29ms during intrinsic conduction to 104±24ms with RVP (p=0.025). The load of late-activated LV myocardium increased in 73% but decreased in 27% patients. Changes were not reflected by QRS duration. Ultimate action of RVP in any patient depended on summary effects of transseptal breakthrough and following LV activation. If both were enhanced then LV preexcitation occurred. If one was delayed but other accelerated, then the outcome of their balance determined the ultimate effect on LV depolarization.
RVP may aggravate or resolve LBBB-induced conduction problems at one or more levels. Its avoidance vs integration (or timing relative to LV pacing) during CRT depends on its electrical action in any particular individual.
评估右心室起搏(RVP)对左束支传导阻滞(LBBB)心力衰竭患者左心室(LV)激活的影响。
RVP期间的LV激活被认为与LBBB相似;因此,新型心脏再同步治疗(CRT)算法可通过采用与固有右束支介导传导的“融合”起搏来避免RVP。然而,其他CRT技术需要右心室起搏波前以实现最佳再同步。合适的选择可能需要关注RVP产生的波前与LBBB引起的既有传导异常之间的相互作用,即经间隔延迟和LV激活。我们假设RVP期间的LV激活与LBBB不同。
对11例患者(年龄59±19岁,男性8例,LV射血分数25±10%;缺血性病因45%)在CRT植入后5.4±5个月进行研究。所有患者在CRT植入前均有完整的房室传导伴LBBB(PR间期204±55;QRS 167±27ms)。无一例患者有中隔/流出道导联位置。使用无创心电图成像(ECGI),在每位患者中对比固有传导和RVP(房室间期最小化,即将心室激动托付给起搏波前)时的LV激活情况。
RVP对LV激活的影响各不相同。64%的患者经间隔时间缩短。产生的LV传导障碍多于解决的传导障碍,LV游离壁激活从固有传导时的67±29ms减慢至RVP时的104±24ms(p=0.025)。73%的患者晚期激活的LV心肌负荷增加,但27%的患者减少。这些变化未通过QRS时限反映出来。RVP在任何患者中的最终作用取决于经间隔突破和随后LV激活的综合效应。如果两者均增强,则发生LV预激。如果一个延迟而另一个加速,则它们平衡后的结果决定对LV去极化的最终影响。
RVP可能在一个或多个层面加重或解决LBBB引起的传导问题。CRT期间对其避免与整合(或相对于LV起搏的时机)取决于其在任何特定个体中的电作用。