Lupi Gabriele, Sassone Biagio, Badano Luigi, Peraldo Carlo, Gaddi Oscar, Sitges Marta, Parthenakis Fragiskos, Molteni Santo, Pagliuca Maria Rosaria, Grovale Nicoletta, Menozzi Carlo, Brignole Michele
Department of Cardiology, Ospedali del Tigullio, Lavagna, Italy, and Department of Cardiology, University Hospital of Crete, Herakleion, Greece.
Am J Cardiol. 2006 Jul 15;98(2):219-22. doi: 10.1016/j.amjcard.2006.01.077. Epub 2006 May 11.
Some patients with right ventricular (RV) apical pacing show contractile asynchrony of the left ventricle. Whether the asynchrony is due to RV pacing or was a preexistimg condition remains unknown. The aim of this study was to evaluate how much pacing from the RV apex affects left ventricular (LV) electromechanical activation and to assess whether the extent of LV asynchrony during RV pacing can be predicted by clinical, electrocardiographic, or echocardiographic findings obtained during spontaneous rhythm. We evaluated 56 patients with narrow QRS and preserved atrioventricular conduction who received permanent backup RV pacing. Intra-LV electromechanical activation was assessed during spontaneous rhythm and during pacing using tissue Doppler echocardiography. An abnormal intra-LV electromechanical delay (EMD) (defined as a >41-ms difference between the faster and slower activated LV wall) was found in 15 patients (27%) during spontaneous rhythm and 28 patients (50%) during RV pacing (p<0.001). Of the 9 baseline variables (age, gender, history of heart failure, QRS duration in spontaneous rhythm and during pacing, LV end-diastolic and end-systolic diameters, LV ejection fraction, and intra-LV EMD in spontaneous rhythm), an abnormal baseline intra-LV EMD and QRS duration of >85 ms were independent predictors of an abnormal intra-LV delay during RV pacing. RV apical pacing induces asynchrony of LV contractions in a substantial percentage of patients but not in all. Although normal baseline intra-LV electromechanical activation cannot exclude the development of significant asynchrony during RV pacing, the presence of preimplant LV asynchrony predicts for a worsening of this detrimental effect.
一些右心室心尖部起搏的患者表现出左心室收缩不同步。这种不同步是由于右心室起搏所致还是先前就已存在的情况仍不清楚。本研究的目的是评估右心室心尖部起搏对左心室机电激活的影响程度,并评估右心室起搏期间左心室不同步的程度是否可通过自发心律时获得的临床、心电图或超声心动图检查结果来预测。我们评估了56例QRS波狭窄且房室传导功能保留的患者,这些患者接受了永久性备用右心室起搏。使用组织多普勒超声心动图在自发心律和起搏期间评估左心室内的机电激活情况。在15例患者(27%)的自发心律期间以及28例患者(50%)的右心室起搏期间发现左心室内存在异常的机电延迟(EMD)(定义为左心室壁激活较快与较慢部位之间的差异>41毫秒)(p<0.001)。在9个基线变量(年龄、性别、心力衰竭病史、自发心律和起搏时的QRS波时限、左心室舒张末期和收缩末期直径、左心室射血分数以及自发心律时的左心室内EMD)中,基线时左心室内EMD异常以及QRS波时限>85毫秒是右心室起搏期间左心室内延迟异常的独立预测因素。右心室心尖部起搏在相当比例的患者中会诱发左心室收缩不同步,但并非所有患者都会出现。虽然正常的基线左心室内机电激活不能排除右心室起搏期间出现显著不同步的情况,但植入前左心室存在不同步预示着这种有害效应会加重。