Abstract
The cardiovascular autonomous neural system represents an integrative fiber network that regulates cardiovascular hemodynamic and electrophysiological processes. During normal physiology, the autonomic nervous system represents a short latency responder that quickly compensates for temporary changes of cardiac function (eg, pumping force, blood pressure, and heart rate). However, when compensation becomes permanent during cardiovascular disease, specifically sympathetic activation catalyzes a further deterioration of the disease process. Besides functional effects on heart rate, inotropy, vasomotion, and cardiac electrophysiology, the sympathetic/parasympathetic nervous systems exert profound pro-/anti-inflammatory effects. There are circumstances in which the parasympathetic branch may play a dominant negative role: during neurocardiogenic syncope, an exaggerated parasympathetic tone acts as a final common pathway resulting in bradycardia and/ or vasodilatation. Likewise, in some forms of paroxysmal atrial fibrillation, predominance of vagally mediated shortening of refractoriness has been suggested to be a driver for the occurrence of AF paroxysms. Also, activation of intrinsic cardiac nerves prior to the onset of atrial fibrillation has been observed, possibly contributing to the development of AF, as may abnormal parasympathetic nerve outgrowth. Since the neural autonomic network is a hardware-based system compared to the neurohumoral system, strategies have been developed to eliminate pathologically increased sympathetic or parasympathetic tone via surgical or catheter ablation techniques of neuronal structures: left cardiac sympathetic denervation effectively reduces cardiac sympathetic tone and arrhythmia burden in patients with long QT syndrome. Likewise, transvascular renal sympathetic denervation can be applied to decrease systemic sympathetic tone and blood pressure in patients with resistant arterial hypertension. Selective ablation of intracardiac atrial parasympathetic plexus would be intriguing since it might increase atrial refractory periods without negatively affecting
Published Version
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