Biochemical changes involved in the mechanism of vasovagal syncope

Vasovagal syncope elicits one of the most powerful transient vasodilatory responses in humans. Many studies have shown an altered neurohumoral response to tilting in patients with vasovagal syncope. Vasopressin (VP) has been of particular interest, but its exact role remains unclarified, whereas the possible role of the potent vasoactive end products of arachidonic acid metabolism has not yet been addressed. We determined the changes in plasma levels of VP, thromboxane (TXA2), and prostacyclin (PGI2) in 34 syncopal patients undergoing a standardized head-up tilt-table testing protocol and compared these changes between patients with positive and negative test results. Blood samples were collected at baseline, 15 minutes in the head-up position, and at the termination of the tilt test (the induction of syncope or the completion of a negative test). Sixteen patients had a positive test result, whereas 18 completed the test without developing any syncopal symptoms. In the tilt-positive group, VP levels presented a 20-fold increase at the time of syncope when compared with baseline levels (p = 0.0000), without any increase at earlier stages. No change was detected at any stage in the tilt-negative patients. We did not find any difference in the levels of PGI2 at any stage in any group of patients or between the 2 groups. TXA2 levels increased significantly at 15 minutes in the upright position in both tilt-positive and tilt-negative patients. No further increase was noticed at the time of syncope in the tilt-positive group, whereas in patients with a negative test result, there was a tendency to decline at the time of the test's completion. It is concluded that although VP is markedly increased during tilt-induced vasovagal syncope, vasoactive amines such as TXA2 and PGI2 play a minor role in the vasodilatory component of the response.