Sympathetic modulation of electrical activation in normal and infarcted myocardium: implications for arrhythmogenesis
Sympathetic modulation of electrical activation in normal and infarcted myocardium: implications for arrhythmogenesis
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DOI：
10.1152/ajpheart.00575.2016
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发表时间：
2017-03-01
影响因子：
4.8
通讯作者：
Shivkumar, Kalyanam
中科院分区：
文献类型：
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作者：
Ajijola, Olujimi A.;Lux, Robert L.;Shivkumar, Kalyanam
心脏交感神经支配对正常和慢性梗塞心室心肌电激活的影响尚不清楚。心脏正常（NL，n = 12）或前壁心肌梗死（MI，n = 9）的约克夏猪在基线时和左右星状神经节刺激期间（分别为 LSGS 和 RSGS）接受了前心尖左心室的高分辨率测绘。测量了传导速度 (CV)、激活时间 (AT) 和传播方向性。使用扩散张量成像和组织学确定心肌纤维方向。 RSGS 增加了纵向 CV (CVL)（0.98 +/- 0.11 对比 1.2 +/- 0.14m/s，P < 0.001），但横向 CV (CVT) 没有增加。这种增加被β-肾上腺素受体和间隙连接（GJ）阻断所消除。 LSGS 并未增加 CVL 和 CVT。在梗死周围区域，RSGS 和 LSGS 均缩短了窦性心律中的 ARI（分别为 423 +/- 37 与 322 +/- 30 毫秒，P < 0.001，以及 423 +/- 36 与 398 +/- 36 毫秒，P = 0.035），并改变了所有动物的激活模式。根据平均 AT 估计，CV 通过 RSGS 以方向依赖方式增加（14.6 +/- 1.2 与 17.3 +/- 1.6 ms，P = 0.015），与 GJ 偏侧化相关。 RSGS 和 LSGS 不均匀地调节 AT，并在 MI 动物中分别诱导 75% 和 67% 的映射区域的相对或绝对功能激活延迟，在对照动物中分别为 0 和 15%（两者 P < 0.001）。总之，交感神经兴奋增加正常心肌的CV并调节梗塞周围心室心肌的激活传播。这些数据证明了交感神经对心律失常梗塞周围基质的功能控制，并部分解释了心律失常发生的时间性质。新的和值得注意的这项研究证明了交感神经对正常心脏传导速度的区域控制。然而，在梗塞心脏中，不仅传播调节不均匀，而且某些区域表现出矛盾的传导减慢。交感神经兴奋改变了所研究的所有梗塞心脏的传播，我们描述了这些发现的暂时性心律失常潜力。请收听本文的相应播客：http://ajpheart。 podbean.com/e/sympathetic-nerves-and-cardiac-propagation/.自主神经系统；交感神经；传导速度；电传播；室性心律失常
The influence of cardiac sympathetic innervation on electrical activation in normal and chronically infarcted ventricular myocardium is not understood. Yorkshire pigs with normal hearts (NL, n = 12) or anterior myocardial infarction (MI, n = 9) underwent high-resolution mapping of the anteroapical left ventricle at baseline and during left and right stellate ganglion stimulation (LSGS and RSGS, respectively). Conduction velocity (CV), activation times (ATs), and directionality of propagation were measured. Myocardial fiber orientation was determined using diffusion tensor imaging and histology. Longitudinal CV (CVL) was increased by RSGS (0.98 +/- 0.11 vs. 1.2 +/- 0.14m/s, P < 0.001) but not transverse CV (CVT). This increase was abrogated by beta-adrenergic receptor and gap junction (GJ) blockade. Neither CVL nor CVT was increased by LSGS. In the peri-infarct region, both RSGS and LSGS shortened ARIs in sinus rhythm (423 +/- 37 vs. 322 +/- 30 ms, P < 0.001, and 423 +/- 36 vs. 398 +/- 36 ms, P = 0.035, respectively) and altered activation patterns in all animals. CV, as estimated by mean ATs, increased in a directionally dependent manner by RSGS (14.6 +/- 1.2 vs. 17.3 +/- 1.6 ms, P = 0.015), associated with GJ lateralization. RSGS and LSGS inhomogeneously modulated AT and induced relative or absolute functional activation delay in parts of the mapped regions in 75 and 67%, respectively, in MI animals, and in 0 and 15%, respectively, in control animals ( P < 0.001 for both). In conclusion, sympathoexcitation increases CV in normal myocardium and modulates activation propagation in peri-infarcted ventricular myocardium. These data demonstrate functional control of arrhythmogenic periinfarct substrates by sympathetic nerves and in part explain the temporal nature of arrhythmogenesis.NEW & NOTEWORTHY This study demonstrates regional control of conduction velocity in normal hearts by sympathetic nerves. In infarcted hearts, however, not only is modulation of propagation heterogeneous, some regions showed paradoxical conduction slowing. Sympathoexcitation altered propagation in all infarcted hearts studied, and we describe the temporal arrhythmogenic potential of these findings.Listen to this article's corresponding podcast at http://ajpheart. podbean.com/e/sympathetic-nerves-and-cardiac-propagation/.autonomic nervous system; sympathetic nerves; conduction velocity; electrical propagation; ventricular arrhythmias