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Objective: Syncope is a transient loss of consciousness resulting from cerebral hypoperfusion. Vasovagal syncope (VVS) is a form of orthostatic intolerance (OI). Its clinical signs such as dizziness and hypotension may mimic symptoms of adrenal insufficiency. The objective of this study was to evaluate the adrenal gland function in patients with vasovagal syncope after stimulation with synthetic adrenocorticotropic hormone (ACTH)., Design: Case-control study on patients with VVS and healthy controls., Methods: The study involved 42 participants, including 27 patients diagnosed with VVS using the head-up tilt test and 15 healthy individuals with no history of syncope or any orthostatic symptoms. Serum cortisol and aldosterone concentrations were measured under basal conditions and at 30 and 60 min after intramuscular ACTH stimulation., Results: Patients with VVS had significantly higher cortisol levels at baseline (441 ± 143 vs. 331 ± 84.7 nmol/L, p = 0.01), at 30 min (802 ± 143 vs. 686 ± 105 nmol/L, p = 0.01) and at 60 min (931 ± 141 nmol/L vs. 793 ± 147 nmol/L, p = 0.001) after ACTH administration (Synacthen 250 μg). Plasma aldosterone increased after ACTH stimulation, but did not show significant differences among groups. Furthermore, there was also no significant correlation between cortisol levels and blood pressure or heart rate., Conclusion: Patients diagnosed with VVS have higher cortisol levels both at baseline and after ACTH stimulation. This finding indicates that individuals with VVS have higher adrenocortical activity potentially as a response to the orthostatic stress induced by syncope, which acts as a stressful stimulus on the autonomic nervous system., Competing Interests: Declaration of competing interest None., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background and Aim: Vasovagal syncope (VVS) in children and adolescents is a common disorder. There may be an internal relationship between creatine kinase (CK) and its isoenzymes (CKMB) and syncope. The aim of this study was to evaluate the changes of CK and CKMB in children and adolescents with VVS., Methods and Results: The VVS group included 218 patients (93 male and 125 female). The control group included 129 healthy children (78 male and 51 female). Serum CK and CKMB levels were estimated. We founded ①Serum CK and CK-MB levels decreased in VVS group than that in control group (P < 0.05). ②The CK levels of female were significantly lower than those of male in VVS group (P < 0.05). ③Serum level of CK-MB were in negative correlation with age, height, weight, BMI whereas in positively correlation with HR. ④CK was effected by CK-MB (β = 0.147, P = 0.037) while CK-MB was independently influenced by age (β = -0.203, P = 0.002) and DBP (β = 0.171, P = 0.011). ⑤Both CK and CK-MB significantly influenced on VVS occurrence after adjusting for the effects of gender, age, height, weight, BMI and HR., Conclusion: The serum CK and CKMB levels decrease in children and adolescents with VVS. CK and CK-MB are the independent protective factors with VVS., Competing Interests: Declaration of Competing Interest The authors declare that they have no competing interest., (Copyright © 2020 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.)

Background and Purpose: Vasovagal syncope (VVS) is linked to more than one pathophysiologic mechanisms. Copeptin, an emerging cardiovascular marker, is a surrogate for arginine-vasopressin, which increases following VVS. We aimed to assess the dynamic pattern of copeptin levels in typical VVS, categorized by the degree of vasoconstriction during orthostasis, and healthy controls., Methods: The following groups were studied: Group A (n=21), with adequate limb vasoconstriction during the first min. of tilt, assessed by limb plethysmography (at least 30% flow reduction); Group B (n=15), showing impaired vasoconstriction during orthostasis (<10% reduction); Group C (n=18), history of VVS and negative tilt test result; Group D (n=18), healthy controls. Copeptin plasma levels were assessed before and 5min following tilt test positivity or termination., Results: Baseline copeptin values were similar in all groups (8.3±6.4 in Group A, 5.7±2.3pmol/l in B, 6.0±1.9 in C, and 6.9±2.6 in D, p: 0.41). Significant increases in copeptin during tilt were observed in all Groups of VVS patients (A, B, C), including those with negative tilt (Group C: from 6.0±1.9 to 27.7±12.6pmol/l, p: 0.001), but not in controls. Following tilt termination, a greater increase was observed in copeptin values in Group B vs all other Groups A, C, and D (111.6±63.5 vs 29.5±51.3, 27.7±12.6, and 8.3±2.9, respectively)., Conclusions: Copeptin increases following tilt not only in VVS with a positive response, but also in typical history patients with a negative test. Increased copeptin levels following orthostasis may be useful for diagnosing VVS., (Copyright © 2017. Published by Elsevier B.V.)

Objectives: To assess whether head-up tilt-induced hyperventilation is seen more often in patients with chronic fatigue syndrome (CFS), fibromyalgia, dizziness, or neurally mediated syncope (NMS) as compared to healthy subjects or those with familial Mediterranean fever (FMF)., Patients and Methods: A total of 585 patients were assessed with a 10-minute supine, 30-minute head-up tilt test combined with capnography. Experimental groups included CFS (n = 90), non-CFS fatigue (n = 50), fibromyalgia (n = 70), nonspecific dizziness (n = 75), and NMS (n =160); control groups were FMF (n = 90) and healthy (n = 50). Hypocapnia, the objective measure of hyperventilation, was diagnosed when end-tidal pressure of CO2 (PETCO2) less than 30 mm Hg was recorded consecutively for 10 minutes or longer. When tilting was discontinued because of syncope, one PETCO2 measurement of 25 or less was accepted as hyperventilation., Results: Hypocapnia was diagnosed on tilt test in 9% to 27% of patients with fibromyalgia, CFS, dizziness, and NMS versus 0% to 2% of control subjects. Three patterns of hypocapnia were recognized: supine hypocapnia (n = 14), sustained hypocapnia on tilt (n = 76), and mixed hypotensive-hypocapnic events (n = 80). Hypocapnia associated with postural tachycardia syndrome (POTS) occurred in 8 of 41 patients., Conclusions: Hyperventilation appears to be the major abnormal response to postural challenge in sustained hypocapnia but possibly merely an epiphenomenon in hypotensive-hypocapnic events. Our study does not support an essential role for hypocapnia in NMS or in postural symptoms associated with POTS. Because unrecognized hypocapnia is common in CFS, fibromyalgia, and nonspecific dizziness, capnography should be a part of the evaluation of patients with such conditions.

Loss of consciousness and falling are the key features of syncope. Common accompaniments include tonic and myoclonic muscle activity, eye deviations, automatisms, vocalizations and hallucinations that may render the distinction from epileptic seizures difficult. The frequently increased levels of serum prolactin (SPRL) were observed immediately after generalized and complex partial seizures. Presumably, the hormone release is caused by the propagation of epileptic activity, usually from the temporal lobe to the hypothalamic pituitary axis. Numerous reports have demonstrated that the post-ictal SPRL level may be used to differentiate between epileptic and syncopal, non-epileptic attacks. In order to confirm the hypothesis, the SPRL levels were measured in patients with complex partial seizures (CPS) and patients with vaso-vagal syncopal attacks (VVS). The SPRL levels were prospectively measured for each patient as soon as possible after the event (within 1 hour), then 1 hour after the first determination and finally blood was sampled 24 hours later. During the study period (18 months), 18 patients with CPS and 15 patients with VVS were investigated in total. The mean values of SPRL levels in both groups were increased immediately after the event (CPS group: 1142 +/- 305 mIU/l; VVS group: 874 +/- 208 mIU/l). The elevated SPRL levels were found in 14 (78%) patients immediately after CPS and in 9 (60%) patients immediately after VVS. After examining the results of the present study we conclude that the elevated serum prolactin level after an epileptic attack is of no significant value in differential diagnosis between epileptic and vaso-vagal syncopal attacks., (Copyright 1999 BEA Trading Ltd.)

The pathogenesis of neurocardiogenic syncope is not completely understood. To examine the possible role of biogenic amines in patients with neurocardiogenic syncope, 18 consecutive patients (age 30 +/- 13 years, 15 males, 3 females) of unexplained syncope were subjected to Head-Up Tilt Testing (HUTT). Blood was sampled by an indwelling cannula at baseline, end of tilt test (or at syncope) and 1 min after returning to the supine position. Biogenic amines, epinephrine (E), norepinephrine (NE), serotonin (5-HT) and their metabolites, homovanillic acid (HVA) and 5-hydroxy indole acetic acid (5-HIAA), were measured in the serum after serial organic phase extraction by high-performance liquid chromatography (HPLC) using ultraviolet detection at a wavelength of 280 nm. Twelve patients were found to be HUTT negative while 6 patients were HUTT positive. Baseline E, NE and 5-HT levels were significantly greater in the HUTT positive patients [E 510 +/- 154 versus 302 +/- 96 pg/ml (p < 0.01), NE 253 +/- 99 versus 159 +/- 62 pg/ml (p < 0.05), 5-HT 174 +/- 32 versus 118 +/- 22 pg/ml (p < 0.01)]. E and HVA levels at the end of the test were significantly higher in HUTT positive patients [E 788 +/- 268 versus 465 +/- 119 pg/ml (p < 0.01), HVA 308 +/- 91 versus 112 +/- 12 pg/ml (p < 0.001)]. A significantly greater rise of E from the baseline was observed in HUTT positive patients (510 +/- 154 versus 112 +/- 12 pg/ml (p < 0.01)]. The increase in the levels of E and HVA both at baseline and after the tilt test, without a corresponding rise in NE levels indicates enhanced activity of the adrenomedullary axis which is not paralleled by NE release from sympathetic nerve endings in patients of neurocardiogenic syncope.