Abstract
Objective: The purpose of this study is to investigate the effects of renal sympathetic nerve stimulation (RSN-S) and ablation (RSN-A) on atrial effective refractory period (ERP) and AF in normal canine heart. Atrial Fibrillation (AF) is a complex disease and one of the most frequent arrhythmias, especially in elderly patients. Multiple mechanisms are involved including interaction between the autonomic nervous system (ANS), electrophysiological properties of the atria, and vulnerability for AF. Cardiac overload increases the incidence of AF. In lone AF the triggers are in the pulmonary veins. AF caused by underlying disease has different mechanism. Atrial fibrillation (AF) is associated with activity of renin-angiotensin-aldosterone system (RAAS). Reduction in renal nor-adrenaline spillover could be achieved after renal sympathetic denervation (RSD). Methods: 1) Establish of atrial fibrillation model; 2) Ventricular rate analysis of AF; 3) Statistical analysis. Results: 1) The establishment of atrial fibrillation model; 2) Inducibility and duration of AF; 3) The changes of AERP dispersion. Conclusion: Left RSN-S shortened left atrial ERP, increased ERP dispersion, but did not change right atrial ERP. Bilateral RSN-A produced significant prolongation in both atrial ERP, but did not affect ERP dispersion. The on time of RD effect is at 4 hrs after RD procedure and the RD effect on AF will last for 20 hrs after RD procedure.
Highlights
Atrial fibrillation (AF) is one of the most frequent arrhythmias in adulthood, with its incidence increasing with age
Left RSN-S increased atrial ERP dispersion compared to BS (P < 0.05) (Figure 1(b))
Clinical observations show that enhanced parasympathetic tone contributes to some cases of paroxysmal AF, which were clinically referred to vagal AF
Summary
Atrial fibrillation (AF) is one of the most frequent arrhythmias in adulthood, with its incidence increasing with age. Atrial fibrillation is characterized by rapid and irregular activation of the atrium, and it is associated with increased morbidity and mortality. The kidney receives a dense innervation of sympathetic and sensory fibres and can be both a target of sympathetic activity and a source of signals that drive sympathetic tone [1]. The renal sympathetic nerves have been identified as a major contributor to the complex pathophysiology of hypertension and atrial fibrillation in both experimental models and in humans. Patients with essential hypertension generally have increased efferent sympathetic drive to the kidneys, as evidenced by elevated rates of renal norepinephrine spillover, defined as the amount of transmitter that escapes neuronal uptake and local metabolism and “spills over” into the circulation. Hypertension is characterized by an increased rate of sympathetic-nerve firing, possibly modulated by afferent signaling from renal sensory nerves
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