Boe Espen, Russell Kristoffer, Remme Espen W, Gjesdal Ola, Smiseth Otto A, Skulstad Helge
Institute for Surgical Research, 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; Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; and.
Am J Physiol Heart Circ Physiol. 2014 Aug 1;307(3):H370-8. doi: 10.1152/ajpheart.00089.2014. Epub 2014 Jun 6.
Cardiac resynchronization therapy (CRT) has been proposed in heart failure patients with narrow QRS, but the mechanism of a potential beneficial effect is unknown. The present study investigated the hypothesis that left ventricular (LV) pacing increases LV end-diastolic volume (LVEDV) by allowing the LV to start filling before the right ventricle (RV) during narrow QRS in an experimental model. LV and biventricular pacing were studied in six anesthetized dogs before and after the induction of LV failure. Function was evaluated by pressures and dimensions, and dyssynchrony was evaluated by electromyograms and deformation. In the nonfailing heart, LV pacing gave the LV a head start in filling relative to the RV (P < 0.05) and increased LVEDV (P < 0.05). The response was similar during LV failure when RV diastolic pressure was elevated. The pacing-induced increase in LVEDV was attributed to a rightward shift of the septum (P < 0.01) due to an increased left-to-right transseptal pressure gradient (P < 0.05). LV pacing, however, also induced dyssynchrony (P < 0.05) and therefore reduced LV stroke work (P < 0.05) during baseline, and similar results were seen in failing hearts. Biventricular pacing did not change LVEDV, but systolic function was impaired. This effect was less marked than with LV pacing. In conclusion, pacing of the LV lateral wall increased LVEDV by displacing the septum rightward, suggesting a mechanism for a favorable effect of CRT in narrow QRS. The pacing, however, induced dyssynchrony and therefore reduced LV systolic function. These observations suggest that detrimental effects should be considered when applying CRT in patients with narrow QRS.
心脏再同步治疗（CRT）已被应用于QRS波狭窄的心力衰竭患者，但潜在有益作用的机制尚不清楚。本研究调查了这样一个假设：在实验模型中，左心室（LV）起搏通过在QRS波狭窄时使左心室在右心室（RV）之前开始充盈，从而增加左心室舒张末期容积（LVEDV）。在诱导左心室衰竭前后，对6只麻醉犬进行了左心室和双心室起搏研究。通过压力和尺寸评估功能，通过肌电图和变形评估不同步性。在未发生衰竭的心脏中，左心室起搏使左心室相对于右心室在充盈方面有一个领先优势（P<0.05），并增加了左心室舒张末期容积（P<0.05）。当右心室舒张压升高时，在左心室衰竭期间的反应相似。起搏诱导的左心室舒张末期容积增加归因于由于左向右跨间隔压力梯度增加（P<0.05）导致的间隔向右移位（P<0.01）。然而，左心室起搏在基线时也会诱导不同步性（P<0.05），因此会降低左心室搏功（P<0.05），在衰竭心脏中也观察到了类似结果。双心室起搏并没有改变左心室舒张末期容积，但收缩功能受损。这种影响不如左心室起搏明显。总之，左心室侧壁起搏通过使间隔向右移位增加了左心室舒张末期容积，提示了CRT对QRS波狭窄患者产生有利作用的一种机制。然而，起搏会诱导不同步性，因此会降低左心室收缩功能。这些观察结果表明，在QRS波狭窄的患者中应用CRT时应考虑到有害影响。
