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Provocative Stimuli (provocative + stimulus)
Selected AbstractsAbnormal cardiovascular responses to carotid sinus massage also occur in vasovagal syncope , implications for diagnosis and treatmentEUROPEAN JOURNAL OF NEUROLOGY, Issue 8 2010A. M. Humm Background and purpose:, Carotid sinus massage (CSM) is commonly used to identify carotid sinus hypersensitivity (CSH) as a possible cause for syncope, especially in older patients. However, CSM itself could provoke classical vasovagal syncope (VVS) in pre disposed subjects. Methods:, Retrospective analysis of CSM, cardiovascular autonomic function tests (including tilt table testing) and medical history in 388 patients with recurrent syncope to identify and characterize patients in whom an abnormal response to CSM was more likely to reflect VVS than CSH. Results:, CSM was abnormal in 79 patients. In 53 patients (77.2 ± 8.7 years), CSH was the likely cause of syncope. VVS was the more likely diagnosis in 26 younger patients (59.7 ± 12.6 years) with longstanding syncope from youth, in whom fear or pain was as a trigger; 7/26 suffered from intense chronic or intermittent neck pain and one exacerbation of syncopal attacks followed a physical and emotional trauma to the neck. In VVS, 4/26 had spontaneous VVS during head-up tilt, another six after venepuncture (performed in 17/26). In 6/26, the abnormal response to CSM was delayed, occurring 62.8 ± 28.4 s after completion of CSM. The response to CSM was predominantly of the mixed type (20/26) and abnormal on both sides in 14/26. Conclusions:, An abnormal response to CSM may not indicate syncope caused by CSH and needs to be considered in the light of the patient's age, duration of syncopal episodes and detailed history of provocative stimuli. Differentiating CSH from VVS with an abnormal response to CSM has various implications from advice on driving to treatment strategies. [source] Exercise is Superior to Pacing for T Wave Alternans Measurement in Subjects with Chronic Coronary Artery Disease and Left Ventricular DysfunctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2002ERIC J. RASHBA M.D. Exercise vs Pacing for TWA Measurement.Introduction: T wave alternans (TWA) is a heart rate-dependent marker of vulnerability to ventricular arrhythmias. Atrial pacing and exercise both are used as provocative stimuli to elicit TWA. However, the prognostic value of the two testing methods has not been compared. The aim of this prospective study was to compare the prognostic value of TWA measured during bicycle exercise and atrial pacing in a large cohort of high-risk patients with ischemic heart disease and left ventricular dysfunction. Methods and Results: This was a prospective study of 251 patients with coronary artery disease and left ventricular dysfunction who were referred for electrophysiologic studies (EPS) for standard clinical indications. Patients underwent TWA testing using bicycle ergometry (exercise TWA, n = 144) and/or atrial pacing (pacing TWA, n = 178). The primary endpoint was the combined incidence of death, sustained ventricular arrhythmias, and appropriate implantable cardioverter defibrillator therapy. The predictive value of exercise and pacing TWA for EPS results and for endpoint events was determined. Exercise and pacing TWA both were significant predictors of EPS results (odds ratios 3.0 and 2.9 respectively, P < 0.02). Kaplan-Meier survival analysis of the primary endpoint revealed that exercise TWA was a significant predictor of events (hazard ratio 2.2, P = 0.03). In contrast, pacing TWA had no prognostic value for endpoint events (hazard ratio 1.1, P = 0.8). Conclusion: TWA should be measured during exercise when it is used for clinical risk stratification. EPS results may not be an adequate surrogate for spontaneous events when evaluating new risk stratification tests. [source] Impaired GH secretion to provocative stimuli in two families with hypocalciuric hypercalcaemiaCLINICAL ENDOCRINOLOGY, Issue 5 2003Elisabetta Cecconi Summary objective, To determine whether hypercalcemia per se might be responsible for an impairment in GH secretion. design, Prospective study. patients, Six subjects of two unrelated families with familial hypocalciuric hypercalcaemia (FHH), an autosomal dominant disorder due to inactivating mutations in the calcium receptor gene, leading to an increase in serum calcium levels and inappropriately normal serum PTH concentrations. Forty normal subjects, matched for sex and age served as controls. measurements, Serum GH concentrations were measured after GHRH-Arginine (GHRH-Arg) stimulation test; serum IGF-I, ACTH, cortisol, FT4, FT3, TSH, PRL, LH, FSH levels were measured under basal conditions. results, All subjects (two male, four female, age range 24,74 years) had increased serum ionized calcium levels (range 1·36,1·56 mmol/l) and five of six patients had normal PTH levels (range for all patients was 14,68 ng/l). Basal serum GH concentrations ranged from 0·1 to 7·0 µg/l. Mean serum GH secretory peak after GHRH-Arg stimulation test was reduced in five subjects (mean 9·3 ± 3·6 µg/l, P < 0·006 vs. Controls, mean 67·0 ± 44·0 µg/l, cut-off, 16·0 µg/l) and normal in one subject (38·7 µg/l). However, serum IGF-I levels were reduced only in two patients (29 and 57 µg/l) and normal in four subjects (range 127,208 µg/l). The basal secretion of the other anterior pituitary hormones was within their normal ranges. conclusions, The results of the present study support the concept that elevated serum calcium levels impair GH secretion. However, the clinical relevance of GH deficiency in FHH remains to be elucidated. [source] Endocrine responses to ghrelin in adult patients with isolated childhood-onset growth hormone deficiencyCLINICAL ENDOCRINOLOGY, Issue 6 2002Gianluca Aimaretti Summary objective Ghrelin, a 28 amino acid acylated peptide, is a natural ligand of the GH secretagogues (GHS) receptor (GHS-R), which is specific for synthetic GHS. Similar to synthetic GHS, ghrelin strongly stimulates GH secretion but also displays significant stimulatory effects on lactotroph and corticotroph secretion. It has been hypothesized that isolated GH deficiency (GHD) could reflect hypothalamic impairment that would theoretically involve defect in ghrelin activity. patients In the present study, we verified the effects of ghrelin (1 µg/kg i.v.) on GH, PRL, ACTH and cortisol levels in adult patients with isolated severe GHD [five males and one female, age (mean ± SEM) 24·7 ± 2·6 years, BMI 25·7 ± 2·7 kg/m2]. In all patients, the GH response to insulin-induced hypoglycaemia (ITT, 0·1 IU regular insulin i.v.) and GH releasing hormone (GHRH) (1 µg/kg i.v.) + arginine (ARG, 0·5 g/kg i.v.) was also studied. The hormonal responses in GHD were compared with those in age-matched normal subjects (NS, seven males, age 28·6 ± 2·9 years, BMI 22·1 ± 0·8 kg/m2). results IGF-I levels in GHD were markedly lower than in NS (69·8 ± 11·3 vs. 167·9 ± 19·2 µg/l, P < 0·003). Ghrelin administration induced significant increase in GH, PRL, ACTH and cortisol levels in all GHD. In GHD, the GH response to ghrelin was higher (P < 0·05) than that to GHRH + ARG, which, in turn, was higher (P < 0·05) than that to ITT (9·2 ± 4·1 vs. 5·3 ± 1·7 vs. 1·4 ± 0·4 µg/l). These GH (1 µg/l = 2 mU/l) responses in GHD were markedly lower (P < 0·0001) than those in NS (ghrelin vs. GHRH + ARG vs. ITT 92·1 ± 16·7 vs. 65·3 ± 8·9 vs. 17·7 ± 3·5 µg/l). In GHD, the highest individual peak GH response to ghrelin was markedly lower than the lowest peak GH response in NS (28·5 vs. 42·9 µg/l). GHD and NS showed overlapping PRL (1 µg/l = 32 mU/l) (10·0 ± 1·4 vs. 14·9 ± 2·2 µg/l), ACTH (22·3 ± 5·3 vs. 18·7 ± 4·6 pmol/l) and cortisol responses (598·1 ± 52·4 vs. 486·9 ± 38·9 nmol/l). conclusions This study shows that ghrelin is one of the most powerful provocative stimuli of GH secretion, even in those patients with isolated severe GHD. In this condition, however, the somatotroph response is markedly reduced while the lactotroph and corticotroph responsiveness to ghrelin is fully preserved, indicating that this endocrine activity is fully independent of mechanisms underlying the GH-releasing effect. These results do not support the hypothesis that ghrelin deficiency is a major cause of isolated GH deficiency but suggest that ghrelin might represent a reliable provocative test to evaluate the maximal GH secretory capacity provided that appropriate cut-off limits are assumed. [source] | ||||||||||