NEURALLY-MEDIATED SYNCOPE - PATHOGENESIS, DIAGNOSIS, AND TREATMENT

Neurally mediated syncope is the most frequent cause of syncope in pat ients who do not have structural heart disease. Neurally mediated sync ope is believed to be a reflex triggered by excessive afferent dischar ge from mechanoreceptors located in the arterial tree or viscera, part icularly the left ventricle of the heart. In response to these signals , a CNS-mediated sudden rise in parasympathetic efferent activity occu rs, causing relative or absolute bradycardia and sympathoinhibition wi th arterial vasodilation and hypotension. Although our understanding o f the pathophysiology of this syndrome is still incomplete, it is well established that sympathetic nerve activity and norepinephrine releas e fall inappropriately during neurally mediated syncope, whereas appro priate increases in plasma concentrations of epinephrine, angiotensin II, vasopressin, and endothelin-1 occur. Recent studies from our labor atory suggest that synthesis of the vasodilator nitric oxide increases during neurally mediated syncope. This suggests that nitric oxide-med iated arterial vasodilation could contribute to the profound hypotensi on characteristic of this syndrome. The diagnosis of neurally mediated syncope can be made with acceptable levels of specificity and sensiti vity by the upright tilt test. Explaining the mechanisms responsible f or arterial vasodilation in neurally mediated syncope may lead to effe ctive treatment.