Abnormality of alpha-adrenergic vascular response in patients with neurally mediated syncope.

Although diagnosis of neurally mediated syncope (NMS) using the head-up tilt (HUT) test has been established, the precise etiologic mechanism of NMS is still obscure. Previously, we reported the contribution of impaired alpha-adrenergic vascular response to syncope in patients with various arrhythmias. This study evaluates alpha-adrenergic vascular response in 21 NMS patients with syncope and a positive HUT test (80 degrees, 30 minutes, and low-dose isoproterenol, NMS group, mean age 31 +/- 14 years) and 21 control subjects (C group, 33 +/- 14 years) who had no evidence of syncope and no structural heart disease. After 30 minutes in a recumbent position, pharmacologic total autonomic blockade was attained using atropine and propranolol. Thereafter, increased systolic blood pressure with 0.4 microg/kg/min phenylephrine (designated as deltaBPphenyl) and decreased systolic blood pressure with 0.5 microg/kg/30 seconds of phentolamine (designated as deltaBPphent) were measured as indexes of alpha-adrenergic vascular sensitivity and activity, respectively. DeltaBPphenyl in the NMS group (70.0 +/- 37) was significantly less than that in C group (107 +/- 38, p <0.005). DeltaBPphent was significantly greater in the NMS group than in the C group (33.5 +/- 10 vs 21.0 +/- 14, p <0.005). Thus, decreased alpha-adrenergic vascular sensitivity and elevated alpha-adrenergic vascular tone were observed in patients with NMS. Although it is not known whether the mechanism causing NMS can be attributed to this abnormal alpha-adrenergic vascular response, the abnormality could at least contribute to augmenting the symptoms of NMS.