AIMS: Vasovagal syncope appears related to transient changes in sympathetic neural outflow. Several studies have documented sympathetic inhibition at the time of syncope. However, data on the activity of the sympathetic nervous system a short time before the onset of syncope are controversial. The aim of the study was to examine sympathoadrenal activity by measuring levels of plasma catecholamines and plasma cAMP in patients with vasovagal syncope induced in the head-up tilt test (HUT). METHODS AND RESULTS: Sixty-one syncopal patients (age 35 +/- 15 years) underwent the passive HUT (60 degrees, 45 minutes). Blood samples for measurement of noradrenaline (NA), adrenaline (A) and dopamine (D) were obtained prior to tilt (0 minutes), at 5 minutes of tilt and at syncope or at the end of the HUT (45 minutes). Two samples were obtained for measurement of cAMP: at 0 minutes and at the end of the test. Plasma levels of NA, A and D were measured using high-performance liquid chromatography; plasma cAMP was measured using a radioimmunoassay technique. Thirty-three patients (15 men, age 35 +/- 16 years) developed vasovagal syncope during the test (HUT-positive); twenty-eight patients (15 men, age 34 +/- 14 years) completed the test without syncope (HUT-negative). No significant differences in NA, A and D were observed between the two groups at baseline or at 5 minutes of tilt. At the time of syncope, catecholamine levels in HUT-positive patients were higher than baseline levels (NA 428 vs. 209 pg/ml, A 90 vs. 55 pg/ml, D 297 vs. 142 pg/ml) and higher than in HUT-negative patients (NA 428 vs. 263 pg/ml, A 98 vs. 67 pg/ml, D 297 vs. 195 pg/ml). cAMP levels increased at syncope and were higher than in non-syncopal patients at the end of the HUT (607 +/- 460 vs. 328 +/- 297 nmol/ml). CONCLUSION: Vasovagal syncope induced by tilt testing is associated with increased levels of noradrenaline, adrenaline, dopamine and cAMP. These results suggest that sympathoadrenal activation antecedes development of vasovagal syncope and may play a role in its pathophysiology.
AIMS: Vasovagal syncope appears related to transient changes in sympathetic neural outflow. Several studies have documented sympathetic inhibition at the time of syncope. However, data on the activity of the sympathetic nervous system a short time before the onset of syncope are controversial. The aim of the study was to examine sympathoadrenal activity by measuring levels of plasma catecholamines and plasma cAMP in patients with vasovagal syncope induced in the head-up tilt test (HUT). METHODS AND RESULTS: Sixty-one syncopalpatients (age 35 +/- 15 years) underwent the passive HUT (60 degrees, 45 minutes). Blood samples for measurement of noradrenaline (NA), adrenaline (A) and dopamine (D) were obtained prior to tilt (0 minutes), at 5 minutes of tilt and at syncope or at the end of the HUT (45 minutes). Two samples were obtained for measurement of cAMP: at 0 minutes and at the end of the test. Plasma levels of NA, A and D were measured using high-performance liquid chromatography; plasma cAMP was measured using a radioimmunoassay technique. Thirty-three patients (15 men, age 35 +/- 16 years) developed vasovagal syncope during the test (HUT-positive); twenty-eight patients (15 men, age 34 +/- 14 years) completed the test without syncope (HUT-negative). No significant differences in NA, A and D were observed between the two groups at baseline or at 5 minutes of tilt. At the time of syncope, catecholamine levels in HUT-positive patients were higher than baseline levels (NA 428 vs. 209 pg/ml, A 90 vs. 55 pg/ml, D 297 vs. 142 pg/ml) and higher than in HUT-negative patients (NA 428 vs. 263 pg/ml, A 98 vs. 67 pg/ml, D 297 vs. 195 pg/ml). cAMP levels increased at syncope and were higher than in non-syncopalpatients at the end of the HUT (607 +/- 460 vs. 328 +/- 297 nmol/ml). CONCLUSION:Vasovagal syncope induced by tilt testing is associated with increased levels of noradrenaline, adrenaline, dopamine and cAMP. These results suggest that sympathoadrenal activation antecedes development of vasovagal syncope and may play a role in its pathophysiology.
Authors: Devin W McBride; Cesar Reis; Ethan Frank; Damon W Klebe; John H Zhang; Richard Applegate; Jiping Tang Journal: PLoS One Date: 2016-09-22 Impact factor: 3.240