Focal anteroapical myocardial infarction in swine altered regional and global patterns of sympathetic innervation, resulting in shorter mean activation recovery intervals (365 vs. 436 ms).
Does focal myocardial infarction alter global and regional patterns of sympathetic innervation and electrophysiological parameters in a swine model?
Focal distal anterior MI alters regional and global patterns of sympathetic innervation, leading to shorter ARIs, greater repolarization dispersion, and altered activation propagation, which may underlie arrhythmia mechanisms during enhanced sympathetic tone.
Absolute Event Rate: 365% vs 436%
p-value: p=<0.0001
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.
Ajijola et al. (Sat,) conducted a other in Myocardial Infarction (n=22). Focal anteroapical myocardial infarction vs. Control (no infarction) was evaluated on Mean activation recovery interval (ARI) at baseline (p=<0.0001). Focal anteroapical myocardial infarction in swine altered regional and global patterns of sympathetic innervation, resulting in shorter mean activation recovery intervals (365 vs. 436 ms).