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首页> 外文期刊>Journal of cardiovascular electrophysiology >Acute pacing-induced dyssynchronous activation of the left ventricle creates systolic dyssynchrony with preserved diastolic synchrony.
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Acute pacing-induced dyssynchronous activation of the left ventricle creates systolic dyssynchrony with preserved diastolic synchrony.

机译:急性起搏诱导的左心室不同步激活会导致收缩性不同步,并伴有舒张期同步性。

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INTRODUCTION: Patients with heart block have conventionally received a pacemaker that stimulates the right ventricular apex (RVA) to restore heart rate control. While RVA pacing has been shown to create systolic dyssynchrony acutely, dyssynchrony can also occur in diastole. The effects of acute RVA pacing on diastolic synchrony have not been investigated. RVA pacing acutely impairs diastolic function by increasing the time constant of relaxation, decreasing the peak lengthening rate and decreasing peak negative dP/dt. We therefore hypothesized that acute RVA pacing would cause diastolic dyssynchrony in addition to creating systolic dyssynchrony. METHODS AND RESULTS: Fourteen patients (13 +/- 4 years old) with non-preexcited supraventricular tachycardia underwent ablation therapy with subsequent testing to confirm elimination of the tachycardia substrate. Normal cardiac structure and function were then documented on two-dimensional echocardiography and 12-lead electrocardiography prior to enrollment. Tissue Doppler images were collected during normal sinus rhythm (NSR), right atrial appendage pacing (AAI), and VVI-RVA pacing during the postablation waiting interval. Systolic and diastolic dyssynchrony were quantified using cross-correlation analysis of tissue Doppler velocity curves. Systolic dyssynchrony increased 81% during RVA pacing relative to AAI and NSR (P < 0.01). Diastolic synchrony was not affected by the different pacing modes (P = 0.375). CONCLUSION: Acute dyssynchronous activation of the LV created by RVA pacing resulted in systolic dyssynchrony with preserved diastolic synchrony in pediatric patients following catheter ablation for treatment of supraventricular tachycardia. Our results suggest that systolic and diastolic dyssynchrony are not tightly coupled and may develop through separate mechanisms.
机译:简介:患有心脏传导阻滞的患者通常接受起搏器,以刺激右心尖(RVA)恢复心律。虽然RVA起搏已被证明可引起急性收缩不同步,但不同步也可能发生在舒张期。尚未研究急性RVA起搏对舒张同步性的影响。 RVA起搏会通过增加松弛时间常数,降低峰延长速率并降低峰负dP / dt来严重损害舒张功能。因此,我们假设急性RVA起搏除了会导致收缩不同步外,还会引起舒张不同步。方法和结果:14例非早发性室上性心动过速的患者(13 +/- 4岁)接受了消融治疗,随后进行了测试,以确认消除了心动过速。然后在入组前通过二维超声心动图和12导联心电图记录正常的心脏结构和功能。在消融后的等待间隔期间,在正常窦性心律(NSR),右心耳起搏(AAI)和VVI-RVA起搏期间收集组织多普勒图像。使用组织多普勒速度曲线的互相关分析对收缩和舒张不同步进行定量。相对于AAI和NSR,在RVA起搏期间收缩不同步增加了81%(P <0.01)。舒张同步性不受不同起搏模式的影响(P = 0.375)。结论:RVA起搏引起的LV急性不同步激活导致小儿导管消融治疗室上性心动过速的收缩期不同步和舒张同步性得以维持。我们的研究结果表明收缩和舒张不同步不是紧密耦合的,可能通过不同的机制发展。

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