Tilt-induced responses of hemodynamics and plasma catecholamine in patients with neurocardiogenic syncope

This study was undertaken to clarify the mechanism of induction of neurocardiogenic syncope by evaluating tilt-induced responses of the hemodynamics and plasma catecholamine in patients with neurocardiogenic syncope. The pathophysiological mechanisms of neurocardiogenic syncope are thought to be associated with an inappropriate response of the autonomic nervous system. In the present study, the plasma concentrations of catecholamine were measured at rest and during head-up tilt (80°, 15 min) testing in 8 patients with neurocardiogenic syncope and in 8 control subjects. In the patients with neurocardiogenic syncope, the increase in plasma epinephrine (PE) with head-up tilt was larger, and the increase in plasma norepinephrine (PNE) was smaller than that in the control subjects, despite a decrease in blood pressure. These findings suggest that the paradox of head-up tilt-induced increased adrenomedullary activity and diminished neuronal sympathetic activation, indicated by the imbalance of the increases in PE and PNE, may be related to background vasodilation before sympathetic withdrawal. The larger increase in PE during orthostatic stress augments the ventricular mechanoreceptor response, leading to centrally mediated sympathetic withdrawal and finally syncope induction.