Electrophysiological effects of right and left vagal nerve stimulation on the ventricular myocardium

Abstract

(VNS) has been proposed as a cardioprotective intervention. However, regional ventricular electrophysiological effects of VNS are not well characterized. The purpose of this study was to evaluate effects of right and left VNS on electrophysiological properties of the ventricles and hemodynamic parameters. In Yorkshire pigs, a 56-electrode sock was used for epicardial (n ϭ 12) activation recovery interval (ARI) recordings and a 64-electrode catheter for endocardial (n ϭ 9) ARI recordings at baseline and during VNS. Hemodynamic recordings were obtained using a conductance catheter. Right and left VNS decreased heart rate (84 Ϯ 5 to 71 Ϯ 5 beats/min and 84 Ϯ 4 to 73 Ϯ 5 beats/min), left ventricular pressure (89 Ϯ 9 to 77 Ϯ 9 mmHg and 91 Ϯ 9 to 83 Ϯ 9 mmHg), and dP/dt max (1,660 Ϯ 154 to 1,490 Ϯ 160 mmHg/s and 1,595 Ϯ 155 to 1,416 Ϯ 134 mmHg/s) and prolonged ARI (327 Ϯ 18 to 350 Ϯ 23 ms and 327 Ϯ 16 to 347 Ϯ 21 ms, P Ͻ 0.05 vs. baseline for all parameters and P ϭ not significant for right VNS vs. left VNS). No anteriorposterior-lateral regional differences in the prolongation of ARI during right or left VNS were found. However, endocardial ARI prolonged more than epicardial ARI, and apical ARI prolonged more than basal ARI during both right and left VNS. Changes in dP/dt max showed the strongest correlation with ventricular ARI effects (R 2 ϭ 0.81, P Ͻ 0.0001) than either heart rate (R 2 ϭ 0.58, P Ͻ 0.01) or left ventricular pressure (R 2 ϭ 0.52, P Ͻ 0.05). Therefore, right and left VNS have similar effects on ventricular ARI, in contrast to sympathetic stimulation, which shows regional differences. The decrease in inotropy correlates best with ventricular electrophysiological effects.vagal nerve stimulation; ventricle; repolarization THE AUTONOMIC NERVOUS SYSTEM plays a significant role in the genesis and persistence of ventricular arrhythmias (54, 59). Sympathetic activation is proarrhythmic (16,32,53), whereas parasympathetic activation is thought to be cardioprotective (17, 31). The vagal nerve trunk provides important cardiomotor efferent fibers to the heart and also carries afferent signals from the heart. Vagal nerve stimulation (VNS) has been shown to decrease infarct size (48), reduce the ventricular fibrillation (VF) threshold (39), and decrease the incidence of ventricular arrhythmias and mortality during ischemia (13,27,38,52). Furthermore, a preserved parasympathetic reflex has been reported to be protective during myocardial infarction (46). Stimulation of the right vagal nerve (RVN) has shown benefits in a series of patients with cardiomyopathy and is undergoing evaluation in clinical trials (20,47). The mechanisms of the antiarrhythmic effects of VNS are less clear and are thought to be multifactorial, with a decrease in heart rate (HR) (15), release of nitric oxide (9), and antagonism of the sympathetic nervous system all thought to play a role (8,30,49).Modulation of repolarization by sympathetic nerve stimulation has been well characterized (1,25,41,55,58). However, the effects of parasympatheti...

Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction

“…In addition, in infarcted hearts, bipolar voltage electroanatomic mapping was performed as described above, and location of each electrode overlying scar, border zone, or viable myocardium meticulously was noted. ARI was analyzed from unipolar electrograms of each electrode using iScaldyn (University of Utah, Salt Lake City, Utah, USA) (47,54,55). Briefly, activation time was defined from the origin to the minimum dV/dt of the activation wavefront of the unipolar electrogram, and recovery time was defined as the start of activation to the maximum dV/dt of repolarization wavefront.…”

Translational neurocardiology: preclinical models and cardioneural integrative aspects

“…; Yamakawa et al . ). Taken together, these data support the thesis that the intrinsic cardiac nervous system, as a collective, acts to coordinate regional cardiac electrical and mechanical function (Armour, ; Kember et al .…”

Role of abnormal repolarization in the mechanism of cardiac arrhythmia

“…In both cases, autonomic stimulation reverses the direction of the repolarization gradient. Non‐uniform APD shortening in apical vs. basal regions has been observed following the infusion of adrenergic agonist in human patients, and upon stellate ganglia stimulation, or vagal stimulation in anaesthetized, open‐chest pigs. These findings are likely accounted for by the non‐uniform distribution of autonomic innervation and/or adrenergic and muscarinic receptors throughout the apico‐basal axis.…”