Key result
Sympathetic nerve stimulation, but not norepinephrine, prolonged the T-peak to T-end interval (e.g., 40.4 to 92.4 ms during left stimulation; P<0.01) and increased dispersion of repolarization.
Why the study?
Does sympathetic nerve stimulation or circulating norepinephrine modulate T-peak to T-end interval and dispersion of repolarization in a porcine model?
Does sympathetic nerve stimulation or circulating norepinephrine modulate T-peak to T-end interval and dispersion of repolarization in a porcine model?
p-value: p=<0.01
Sympathetic nerve stimulation, but not circulating norepinephrine, prolongs the T-peak to T-end interval by increasing global dispersion of repolarization.
Neural sympathetic activation, unlike norepinephrine, may increase repolarization dispersion; leaves open human Tpe translation.
BACKGROUND: T-peak to T-end interval (Tp-e) is an independent marker of sudden cardiac death. Modulation of Tp-e by sympathetic nerve activation and circulating norepinephrine is not well understood. The purpose of this study was to characterize endocardial and epicardial dispersion of repolarization (DOR) and its effects on Tp-e with sympathetic activation. METHODS AND RESULTS: In Yorkshire pigs (n=13), a sternotomy was performed and the heart and bilateral stellate ganglia were exposed. A 56-electrode sock and 64-electrode basket catheter were placed around the epicardium and in the left ventricle (LV), respectively. Activation recovery interval, DOR, defined as variance in repolarization time, and Tp-e were assessed before and after left, right, and bilateral stellate ganglia stimulation and norepinephrine infusion. LV endocardial and epicardial activation recovery intervals significantly decreased, and LV endocardial and epicardial DOR increased during sympathetic nerve stimulation. There were no LV epicardial versus endocardial differences in activation recovery interval during sympathetic stimulation, and regional endocardial activation recovery interval patterns were similar to the epicardium. Tp-e prolonged during left (from 40.4±2.2 ms to 92.4±12.4 ms; P<0.01), right (from 47.7±2.6 ms to 80.7±11.5 ms; P<0.01), and bilateral (from 47.5±2.8 ms to 78.1±9.8 ms; P<0.01) stellate stimulation and strongly correlated with whole heart DOR during stimulation (P<0.001, R=0.86). Of note, norepinephrine infusion did not increase DOR or Tp-e. CONCLUSIONS: Regional patterns of LV endocardial sympathetic innervation are similar to that of LV epicardium. Tp-e correlated with whole heart DOR during sympathetic nerve activation. Circulating norepinephrine did not affect DOR or Tp-e.
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Yagishita et al. (2014) studied Sudden cardiac death markers (n=13). Stellate ganglia stimulation and norepinephrine infusion vs. Baseline (before stimulation/infusion) was evaluated on T-peak to T-end interval (Tp-e) and dispersion of repolarization (p=<0.01). Sympathetic nerve stimulation, but not norepinephrine, prolonged the T-peak to T-end interval (e.g., 40.4 to 92.4 ms during left stimulation; P<0.01) and increased dispersion of repolarization.
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