DIFFERENT HUMORAL RESPONSES DURING HEAD-UP TILT TESTING AMONG PATIENTS WITH NEUROCARDIOGENIC SYNCOPE

Neurocardiogenic dysfunction is believed to result from activation of ventricular mechanoreceptors. To asses other humoral and circulatory m echanisms activated during vasovogal syncope, epinephrine, norepinephr ine, renin, and aldosterone levels were measured during head-up tilt t esting. Twenty-three patients referred because of vasovagal syncope un derwent passive heed-up tilt testing (80 degrees). Blood samples were taken at baseline, after 30 minutes of supine rest and at syncope. Fiv e patients (four men, one woman; mean age 46 +/- 27 years) had cardioi nhibitory syncope. Seven patients (five men, two women; mean age 40 +/ - 12 years) had vasodepressor syncope. Eleven patients (eight men, thr ee women; mean age 55 +/- 21 years) had negative results of head-up ti lt tests. Among patients with cardioinhibitory Syncope, norepinephrine concentration rose significantly from baseline to syncope (0.44 +/- 0 .12 ng/ml versus 1.14 +/- 0.72 ng/ml; p < 0.05), whereas no significan t change was observed in epinephrine (0.08 +/- 0.03 ng/ml versus 2.74 +/- 2.85 ng/ml; p = not significant [NS]), renin (5.68 +/- 3.03 pg/ml versus 19.58 +/- 11.47 pg/ml; p = NS), or aldosterone concentration (6 6.60 +/- 16.10 ng/ml versus 109.00 +/- 44.70 ng/ml; p = NS). Patients with vasodepressor syncope had a significant rise in renin (9.03 +/- 4 .56 pg/ml versus 52.53 +/- 41.63 pg/ml; p < 0.05) and aldosterone conc entration (95.43 +/- 103.03 ng/ml versus 249.57 +/- 191.54 ng/ml; p < 0.05), whereas no change in level of epinephrine (0.12 +/- 0.12 ng/ml versus 0.28 +/- 0.33 ng/ml; p = NS) or norepinephrine (0.60 +/- 0.26 n g/ml versus 0.86 +/- 0.53 ng/ml; p = NS) was detected. Among patients with negative results of tilt tests, levels of renin (7.94 +/- 719 pg/ ml versus 27.71 +/- 18.50 pg/ml; p < 0.01) and aldosterone (64.64 +/- 28.33 ng/ml versus 160.91 +/- 79.58 ng/ml; p < 0.01) rose significantl y, whereas no change was seen in epinephrine (0.12 +/- 0.14 ng/ml vers us 0.23 +/- 0.31; p = NS) or norepinephrine concentration (0.54 +/- 0. 21 ng/ml versus 0.82 +/- 0.52; p = NS). Patients with cardioinhibitory syncope were characterized by a rise in norepinephrine level and blun ted activation of the renin-angiotensin-aldosterone axis at syncope. U nlike patients with cardioinhibitory syncope, the renin-angiotensin-al dosterone axis is activated in patients with vasodepressor syncope and patients with a negative result of head-up fit test without a statist ically significant increase in catecholamine levels. Patients with car dioinhibitory syncope have higher epinephrine levels at syncope compar ed with patients with a negative result of head-up tilt test and patie nts with vasodepressor syncope.