Ventricular Activation Recovery Interval Research Articles

Antiarrhythmic Mechanisms of Epidural Blockade After Myocardial Infarction.

Thoracic epidural anesthesia (TEA) has been shown to reduce the burden of ventricular tachycardia in small case series of patients with refractory ventricular tachyarrhythmias and cardiomyopathy. However, its electrophysiological and autonomic effects in diseased hearts remain unclear, and its use after myocardial infarction is limited by concerns for potential right ventricular dysfunction. Myocardial infarction was created in Yorkshire pigs (N=22) by left anterior descending coronary artery occlusion. Approximately, six weeks after myocardial infarction, an epidural catheter was placed at the C7-T1 vertebral level for injection of 2% lidocaine. Right and left ventricular hemodynamics were recorded using Millar pressure-conductance catheters, and ventricular activation recovery intervals (ARIs), a surrogate of action potential durations, by a 56-electrode sock and 64-electrode basket catheter. Hemodynamics and ARIs, baroreflex sensitivity and intrinsic cardiac neural activity, and ventricular effective refractory periods and slope of restitution (Smax) were assessed before and after TEA. Ventricular tachyarrhythmia inducibility was assessed by programmed electrical stimulation. TEA reduced inducibility of ventricular tachyarrhythmias by 70%. TEA did not affect right ventricular-systolic pressure or contractility, although left ventricular-systolic pressure and contractility decreased modestly. Global and regional ventricular ARIs increased, including in scar and border zone regions post-TEA. TEA reduced ARI dispersion specifically in border zone regions. Ventricular effective refractory periods prolonged significantly at critical sites of arrhythmogenesis, and Smax was reduced. Interestingly, TEA significantly improved cardiac vagal function, as measured by both baroreflex sensitivity and intrinsic cardiac neural activity. TEA does not compromise right ventricular function in infarcted hearts. Its antiarrhythmic mechanisms are mediated by increases in ventricular effective refractory period and ARIs, decreases in Smax, and reductions in border zone electrophysiological heterogeneities. TEA improves parasympathetic function, which may independently underlie some of its observed antiarrhythmic mechanisms. This study provides novel insights into the antiarrhythmic mechanisms of TEA while highlighting its applicability to the clinical setting.

Vagal nerve stimulation activates vagal afferent fibers that reduce cardiac efferent parasympathetic effects.

Vagal nerve stimulation (VNS) has been shown to have antiarrhythmic effects, but many of these benefits were demonstrated in the setting of vagal nerve decentralization. The purpose of this study was to evaluate the role of afferent fiber activation during VNS on efferent control of cardiac hemodynamic and electrophysiological parameters. In 37 pigs a 56-electrode sock was placed over the ventricles to record local activation recovery intervals (ARIs), a surrogate of action potential duration. In 12 of 37 animals atropine was given systemically. Right and left VNS were performed under six conditions: both vagal trunks intact (n = 25), ipsilateral right (n = 11), ipsilateral left (n = 14), contralateral right (n = 7), contralateral left (n = 10), and bilateral (n = 25) vagal nerve transection (VNTx). Unilateral VNTx significantly affected heart rate, PR interval, Tau, and global ARIs. Right VNS after ipsilateral VNTx had augmented effects on hemodynamic parameters and increase in ARI, while subsequent bilateral VNTx did not significantly modify this effect (%change in ARI in intact condition 2.2 ± 0.9% vs. ipsilateral VNTx 5.3 ± 1.7% and bilateral VNTx 5.3 ± 0.8%, P < 0.05). Left VNS after left VNTx tended to increase its effects on hemodynamics and ARI response (P = 0.07), but only after bilateral VNTx did these changes reach significance (intact 1.1 ± 0.5% vs. ipsilateral VNTx 3.6 ± 0.7% and bilateral VNTx 6.6 ± 1.6%, P < 0.05 vs. intact). Contralateral VNTx did not modify VNS response. The effect of atropine on ventricular ARI was similar to bilateral VNTx. We found that VNS activates afferent fibers in the ipsilateral vagal nerve, which reflexively inhibit cardiac parasympathetic efferent electrophysiological and hemodynamic effects.

Abstract 18030: Electrophysiological Effects of Efferent and Afferent Right and Left Vagal Nerve Stimulation on Regional Ventricular Myocardial Repolarization

BACKGROUND: Vagal nerve stimulation (VNS) is thought to be cardioprotective and decreases ventricular arrhythmias. Regional ventricular electrophysiological differences of left and right and afferent vs. efferent VNS are unclear. The purpose of this study was to evaluate effects of right vs. left and afferent vs. efferent VNS on ventricular repolarization. METHODS: In 8 pigs, the heart, bilateral cervical vagus nerves, and stellate ganglia were exposed. A 56 electrode sock was placed on the ventricles and used to record activation recovery interval (ARI), a marker of action potential duration. ARIs were obtained at baseline and during intact left and right VNS. Further, ARIs were analyzed with afferent (proximal end) or efferent (distal end) VNS under 3 conditions: 1) contralateral vagus intact 2) bilateral vagal transection and 3) bilateral vagal nerve transection plus stellectomy. A Millar conductance catheter was used to record hemodynamics. RESULTS: Intact and efferent left and right VNS decreased heart rate, blood pressure, and dp/dt, P&lt;0.05 for all parameters. Intact and efferent VNS increased ARI by 49±20 ms (right intact), 45±16 ms (left intact), 46±15 ms (right efferent), and 36±8 ms (left efferent), P&lt;0.05 for all conditions vs. baseline. No significant regional differences in ARI were found with efferent VNS. Transection of the contralateral vagus nerve did not alter the effects of ipsilateral efferent VNS (403±36 ms vs. 396±31 ms, P=NS). Afferent VNS had no significant influence on ventricular ARI, with contralateral vagus nerve intact (from 365±27 ms to 373±28 ms, P=NS) or transected (from 354±25 ms to 346±27 ms, P=NS). Stellectomy reduced the impact of efferent VNS (412±26 ms pre vs. 382±25 ms post stellectomy, P&lt;0.05). CONCLUSIONS: Unlike left and right sympathetic innervation, epicardial vagal innervation is uniform without significant regional differences. Effects of efferent VNS are diminished by sympathectomy. Afferent VNS had no impact on ARI.