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Ventricular activation is impaired in aged rat hearts

机译:老年大鼠心脏的心室激活受损

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Ventricular activation is impaired in aged rat hearts. Am J Physiol Heart Circ Physiol 295: H2336-H2347, 2008. First published October 10, 2008; doi:10.1152/ajpheart.00517.2008.-Ventricular arrhythmias are frequently observed in the elderly population secondary to alterations of electrophysiological properties that occur with the normal aging process of the heart. However, the underlying mechanisms remain poorly understood. The aim of the present study was to determine specific age-related changes in electrophysiological properties and myocardial structure in the ventricles that can be related to a structural-functional arrhythmogenic substrate. Multiple unipolar electrograms were recorded in vivo on the anterior ventricular surface of four control and seven aged rats during normal sinus rhythm and ventricular pacing. Electrical data were related to morphometric and immunohistochemical parameters of the underlying ventricular myocardium. In aged hearts total ventricular activation time was significantly delayed (QRS duration: +69%), while ventricular conduction velocity did not change significantly compared with control hearts. Moreover, ventricular activation patterns displayed variable numbers of epicardial breakthrough points whose appearance could change with time. Morphological analysis in aged rats revealed that heart weight and myocyte transverse diameter increased significantly, scattered microfoci of interstitial fibrosis were mostly present in the ventricular subendocardium, and gap junction connexin expression decreased significantly in ventricular myocardium compared with control rats. Our results show that in aged hearts delayed total ventricular activation time and abnormal activation patterns are not due to delayed myocardial conduction and suggest the occurrence of impaired impulse propagation through the conduction system leading to uncoordinated myocardial excitation. Impaired interaction between the conduction system and ventricular myocardium might create a potential reentry substrate, contributing to a higher incidence of ventricular arrhythmias in the elderly population
机译:在老年大鼠心脏中,心室激活受损。 Am J Physiol Heart Circ Physiol 295:H2336-H2347,2008年。2008年10月10日首次发布; doi:10.1152 / ajpheart.00517.2008.-老年人的室性心律失常通常是继心脏正常衰老过程后发生的电生理特性改变后继发的。但是,基本机制仍然知之甚少。本研究的目的是确定脑室中与结构功能性心律失常底物相关的特定年龄相关的电生理特性和心肌结构变化。在正常窦性心律和心室起搏期间,在四只对照组和七只老年大鼠的前室前表面体内记录了多个单极电描记图。电学数据与基础心室心肌的形态计量学和免疫组化参数有关。在老年心脏中,总心室激活时间明显延迟(QRS持续时间:+ 69%),而与对照组相比,心室传导速度没有明显改变。此外,心室激活模式显示出不同数量的心外膜突破点,其出现可能随时间变化。老年大鼠的形态学分析表明,与对照组相比,心室心内膜下层的心脏重量和心肌细胞横径显着增加,间质纤维化的散在微灶主要存在,并且心室间隙连接蛋白的表达明显降低。我们的研究结果表明,在老年心脏中,延迟的总心室激活时间和异常的激活模式不是由于延迟的心肌传导而引起的,并且表明通过传导系统发生的冲动传播受损会导致不协调的心肌兴奋。传导系统与心室心肌之间的相互作用受损可能会形成潜在的折返基质,从而导致老年人口心律失常的发生率更高

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