Yu Cheuk-Man, Yang Hua, Lau Chu-Pak, Wang Qiong, Wang Shelley, Lam Linda, Sanderson John E
Division of Cardiology, Department of Medicine, Queen Mary Hospital, University of Hong Kong.
Pacing Clin Electrophysiol. 2003 Feb;26(2 Pt 1):562-70. doi: 10.1046/j.1460-9592.2003.00095.x.
LV electromechanical delay results in asynchronized contraction. However, it is not known if the presence of cardiac diseases without QRS prolongation may result in inter- or intraventricular asynchrony. This study investigated the occurrence of systolic mechanical delay in different regions of the LV in patients with underlying heart diseases and normal QRS duration. Tissue Doppler imaging (TDI) was performed in 141 patients (age 63.7 +/- 11.5 years) with underlying heart diseases (82% had ischemic heart disease) and 92 normal healthy volunteers (age 63.9 +/- 9.8 years) based on the four-basal and four-mid-segment model by apical views. Of these, 124 patients had normal QRS duration (< or = 120 ms) while 17 were prolonged due to LBBB or intraventricular conduction defect. Patients with normal QRS duration had significantly lower peak myocardial isovolumic contraction velocity (IVCM), sustained systolic velocity (SM), and prolonged time to peak IVCM and SM in almost all myocardial segments when compared to controls. The time to peak IVCM (basal lateral vs basal septal segment: 61.0 +/- 29.4 vs 53.3 +/- 24.1 ms, P < 0.005) and SM (basal lateral vs basal septal segment: 174 +/- 44 vs 154 +/- 36 ms, P < 0.001) was further delayed in the LV free-wall segments. Mechanical delay was also evident in the LV free-wall segments in patients with preserved or impaired systolic function, in patients with or without previous myocardial infarction, and in patients with prolonged QRS duration. Patients with prolonged QRS had a higher prevalence of LV free-wall delay of > 50 ms (47 vs 24%, chi-square = 4.6, P < 0.05). In conclusion, the presence of cardiac diseases was characterized by LV global mechanical delay; and, intraventricular asynchronized contraction characterized mostly by further mechanical delay in the free-wall region. These changes occur even in those with normal QRS duration.
左心室机电延迟会导致收缩不同步。然而,尚不清楚无QRS波增宽的心脏病患者是否会导致心室内或心室内不同步。本研究调查了QRS波时限正常的心脏病患者左心室不同区域收缩期机械延迟的发生情况。基于心尖视图的四基底节段和四中段模型,对141例(年龄63.7±11.5岁)患有心脏病(82%患有缺血性心脏病)的患者和92名正常健康志愿者(年龄63.9±9.8岁)进行了组织多普勒成像(TDI)检查。其中,124例患者QRS波时限正常(≤120毫秒),17例因左束支传导阻滞或心室内传导缺陷而延长。与对照组相比,QRS波时限正常的患者几乎在所有心肌节段的心肌等容收缩峰值速度(IVCM)、持续收缩速度(SM)均显著降低,且IVCM和SM达到峰值的时间延长。左心室游离壁节段IVCM达到峰值的时间(基底外侧节段与基底间隔节段:分别为61.0±29.4毫秒和53.3±24.1毫秒,P<0.005)和SM达到峰值的时间(基底外侧节段与基底间隔节段:分别为174±44毫秒和154±36毫秒,P<0.001)进一步延迟。在收缩功能保留或受损的患者、有或无既往心肌梗死的患者以及QRS波时限延长的患者中,左心室游离壁节段也存在明显的机械延迟。QRS波时限延长的患者左心室游离壁延迟>50毫秒的患病率更高(47%对24%,卡方检验=4.6,P<0.05)。总之,心脏病患者的特征是左心室整体机械延迟;而心室内不同步收缩主要表现为游离壁区域进一步的机械延迟。即使在QRS波时限正常的患者中也会出现这些变化。