Rossi Stefano, Baruffi Silvana, Bertuzzi Andrea, Miragoli Michele, Corradi Domenico, Maestri Roberta, Alinovi Rossella, Mutti Antonio, Musso Ezio, Sgoifo Andrea, Brisinda Donatella, Fenici Riccardo, Macchi Emilio
Dipartimento di Biologia Evolutiva e Funzionale, Sezione Fisiologia, Università degli Studi, Viale Gian Paolo Usberti, 11/A, 43100 Parma, Italy.
Am J Physiol Heart Circ Physiol. 2008 Dec;295(6):H2336-47. doi: 10.1152/ajpheart.00517.2008. Epub 2008 Oct 10.
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.
室性心律失常在老年人群中经常出现，这继发于心电生理特性的改变，而这种改变随着心脏正常衰老过程而发生。然而，其潜在机制仍知之甚少。本研究的目的是确定心室电生理特性和心肌结构中与年龄相关的特定变化，这些变化可能与结构 - 功能致心律失常基质有关。在正常窦性心律和心室起搏期间，在4只对照大鼠和7只老年大鼠的心室前表面体内记录多个单极电图。电数据与潜在心室心肌的形态计量学和免疫组织化学参数相关。在老年心脏中，总心室激活时间显著延迟（QRS波时限：增加69%），而与对照心脏相比，心室传导速度没有显著变化。此外，心室激活模式显示出数量可变的心外膜突破点，其出现可能随时间变化。老年大鼠的形态学分析表明，心脏重量和心肌细胞横径显著增加，散在的间质纤维化微灶主要存在于心室心内膜下，与对照大鼠相比，心室心肌中的缝隙连接连接蛋白表达显著降低。我们的结果表明，在老年心脏中，总心室激活时间延迟和异常激活模式并非由于心肌传导延迟，提示通过传导系统的冲动传播受损，导致心肌兴奋不协调。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，导致老年人群室性心律失常的发生率更高。
