Fang Fang, Chan Joseph Yat-Sun, Yip Gabriel Wai-Kwok, Xie Jun-Min, Zhang Qing, Fung Jeffrey Wing-Hong, Lam Yat-Yin, Yu Cheuk-Man
Division of Cardiology, Department of Medicine and Therapeutics, Institute of Vascular Medicine, SH Ho Cardiovascular and Stroke Centre, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong, China.
Eur J Echocardiogr. 2010 Mar;11(2):109-18. doi: 10.1093/ejechocard/jep171. Epub 2009 Nov 20.
Right ventricular apical (RVA) pacing may induce mechanical dyssynchrony. However, its impact on patients with normal ejection fraction (EF) is not fully understood. This study examined the prevalence and predictors of RVA pacing-induced systolic dyssynchrony by real-time three-dimensional echocardiography (RT3DE), and evaluated its impact on left ventricular (LV) function.
Ninety-three patients with sinus node dysfunction and normal EF (>50%) received RVA-based dual-chamber pacing were assessed by RT3DE during RVA pacing (V-pace) and intrinsic conduction (V-sense). Systolic dyssynchrony was evaluated using the standard deviation of the time to minimal regional volume of 16 LV segments (Tmsv-16SD), and a cutoff value of 16 ms was determined from 93 normal controls. Systolic dyssynchrony was induced in 49.5% of patients at V-pace with significant increase in LV end-systolic volume (LVESV), decrease in EF, and worsening of Tmsv-16SD (all P < 0.001). Furthermore, patients who developed dyssynchrony had larger LVESV (P < 0.001), lower EF (P < 0.001) at V-pace mode, and higher cumulative percentage of RVA pacing in the past 6 months (P < 0.001) than those without systolic dyssynchrony. In multivariate logistic regression analysis, independent predictors of developing LV systolic dyssynchrony during V-pace included a low normal EF at V-sense, pre-existing LV hypertrophy, and cumulative RVA pacing >40% in the past 6 months.
For patients with preserved EF received RVA pacing, half of them would develop systolic dyssynchrony which was associated with EF deterioration and LV enlargement. A low normal EF, a high cumulative percentage of RVA pacing, and pre-existing LV hypertrophy were predictors of developing dyssynchrony.
右心室心尖部（RVA）起搏可能会诱发机械性不同步。然而，其对射血分数（EF）正常的患者的影响尚未完全明确。本研究通过实时三维超声心动图（RT3DE）检查RVA起搏诱发的收缩期不同步的发生率及预测因素，并评估其对左心室（LV）功能的影响。
93例窦房结功能障碍且EF正常（>50%）并接受基于RVA的双腔起搏的患者，在RVA起搏（V起搏）和自身传导（V感知）期间通过RT3DE进行评估。使用16个左心室节段最小区域容积时间的标准差（Tmsv-16SD）评估收缩期不同步，并从93名正常对照中确定16毫秒的临界值。49.5%的患者在V起搏时诱发收缩期不同步，左心室收缩末期容积（LVESV）显著增加，EF降低，Tmsv-16SD恶化（均P<0.001）。此外，发生不同步的患者在V起搏模式下LVESV更大（P<0.001），EF更低（P<0.001），且过去6个月RVA起搏的累积百分比更高（P<0.001），高于无收缩期不同步的患者。在多因素逻辑回归分析中，V起搏期间发生左心室收缩期不同步的独立预测因素包括V感知时EF略低、既往存在左心室肥厚以及过去6个月RVA起搏累积>40%。
对于EF保留且接受RVA起搏的患者，其中一半会发生收缩期不同步，这与EF恶化和左心室扩大有关。EF略低、RVA起搏的累积百分比高以及既往存在左心室肥厚是发生不同步的预测因素。
