Focal myocardial infarction induces global remodeling of cardiac sympathetic innervation: neural remodeling in a spatial context
Focal myocardial infarction induces global remodeling of cardiac sympathetic innervation: neural remodeling in a spatial context
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DOI：
10.1152/ajpheart.00434.2013
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发表时间：
2013-10-01
影响因子：
4.8
通讯作者：
Shivkumar, Kalyanam
中科院分区：
文献类型：
--
作者：
Ajijola, Olujimi A.;Yagishita, Daigo;Shivkumar, Kalyanam
心肌梗死(MI)会导致瘢痕边缘区域的神经和电重构。局灶性心肌梗死对整体功能神经重构的影响尚不清楚。交感神经刺激在9只前心尖梗死(MI；n=9)和9只对照猪(n=9)上进行。一只56电极的袜子被放置在两个脑室上，以记录基线时以及刺激左侧、右侧和双侧星状神经节时的心电图。从心电图测量激活恢复间期(ARI)。在交感神经刺激前和刺激期间评估整体和局部ARI缩短、复极离散度和激活传播。心肌梗死组较对照组平均ARI短(356±/-8比436+/-9ms，P=0.0001)，复极离散度较对照组大(734±/-123vs.362+/-32ms，P=0.02)，心肌梗死区较非梗死区长(406±/-14比365+/-8ms，P=0.027)。在对照组动物中，刺激右侧星状神经节时，前壁ARI缩短的百分比大于后壁(P=0.0001)，而刺激左侧星状神经节时则相反(P=0.0003)。在脑梗塞的动物中，这种模式完全消失了。在所研究的50%的动物中，与基线相比，交感神经刺激显著改变了起搏期间从心肌内疤痕发出的激活传播的方向。总之，局灶性前壁心肌梗死改变了交感神经支配的局部和整体模式，导致梗死心脏ARI缩短，复极离散度增大，激活传播改变。这些情况可能是交感神经张力增强时引发心律失常的机制的基础。
Myocardial infarction (MI) induces neural and electrical remodeling at scar border zones. The impact of focal MI on global functional neural remodeling is not well understood. Sympathetic stimulation was performed in swine with anteroapical infarcts (MI; n = 9) and control swine (n = 9). A 56-electrode sock was placed over both ventricles to record electrograms at baseline and during left, right, and bilateral stellate ganglion stimulation. Activation recovery intervals (ARIs) were measured from electrograms. Global and regional ARI shortening, dispersion of repolarization, and activation propagation were assessed before and during sympathetic stimulation. At baseline, mean ARI was shorter in MI hearts than control hearts (365 +/- 8 vs. 436 +/- 9 ms, P < 0.0001), dispersion of repolarization was greater in MI versus control hearts (734 +/- 123 vs. 362 +/- 32 ms(2), P = 0.02), and the infarcted region in MI hearts showed longer ARIs than noninfarcted regions (406 +/- 14 vs. 365 +/- 8 ms, P = 0.027). In control animals, percent ARI shortening was greater on anterior than posterior walls during right stellate ganglion stimulation (P = 0.0001), whereas left stellate ganglion stimulation showed the reverse (P = 0.0003). In infarcted animals, this pattern was completely lost. In 50% of the animals studied, sympathetic stimulation, compared with baseline, significantly altered the direction of activation propagation emanating from the intramyocardial scar during pacing. In conclusion, focal distal anterior MI alters regional and global pattern of sympathetic innervation, resulting in shorter ARIs in infarcted hearts, greater repolarization dispersion, and altered activation propagation. These conditions may underlie the mechanisms by which arrhythmias are initiated when sympathetic tone is enhanced.