Neurally mediated syncope: pathogenesis, diagnosis, and treatment.

Neurally mediated syncope is the most frequent cause of syncope in patients who do not have structural heart disease. Neurally mediated syncope is believed to be a reflex triggered by excessive afferent discharge from mechanoreceptors located in the arterial tree or viscera, particularly the left ventricle of the heart. In response to these signals, a CNS-mediated sudden rise in parasympathetic efferent activity occurs, causing relative or absolute bradycardia and sympathoinhibition with arterial vasodilation and hypotension. Although our understanding of the pathophysiology of this syndrome is still incomplete, it is well established that sympathetic nerve activity and norepinephrine release fall inappropriately during neurally mediated syncope, whereas appropriate increases in plasma concentrations of epinephrine, angiotensin II, vasopressin, and endothelin-1 occur. Recent studies from our laboratory suggest that synthesis of the vasodilator nitric oxide increases during neurally mediated syncope. This suggests that nitric oxide-mediated arterial vasodilation could contribute to the profound hypotension characteristic of this syndrome. The diagnosis of neurally mediated syncope can be made with acceptable levels of specificity and sensitivity by the upright tilt test. Explaining the mechanisms responsible for arterial vasodilation in neurally mediated syncope may lead to effective treatment.