Clinical improvement in patients with orthostatic intolerance after treatment with bisoprolol and fludrocortisone

Citation
J. Freitas et al., Clinical improvement in patients with orthostatic intolerance after treatment with bisoprolol and fludrocortisone, CLIN AUTON, 10(5), 2000, pp. 293-299
Citations number
28
Categorie Soggetti
Neurology
Journal title
CLINICAL AUTONOMIC RESEARCH
ISSN journal
09599851 → ACNP
Volume
10
Issue
5
Year of publication
2000
Pages
293 - 299
Database
ISI
SICI code
0959-9851(200010)10:5<293:CIIPWO>2.0.ZU;2-J
Abstract
Orthostatic intolerance is the development of disabling symptoms upon assum ing an upright posture that are relieved partially by resuming the supine p osition. Postural tachycardia syndrome (POTS) is an orthostatic intolerance syndrome characterized by palpitations because of excessive orthostatic si nus tachycardia, lightheadedness, tremor, and near-syncope. Patients usuall y undergo extensive medical, cardiac, endocrine, neurologic, and psychiatri c evaluation, which usually fails to identify a specific abnormality. The a uthors investigated the autonomic and hemodynamic profile of patients with POTS and the effectiveness of bisoprolol and fludrocortisone. The authors e valuated II female patients with POTS before and after medical treatment wi th a cardioselective bisoprolol P-blocker or fludrocortisone, or both, and II age-matched control patients. Variability of heart rate and systolic blo od pressure was assessed by fast Fourier transform, and spontaneons barorec eptor gain was assessed by use of the temporal sequences slope and a index. Modelflow was used to quantify hemodynamics. Symptoms in all patients impr oved greatly after medication. The autonomic and hemodynamic impairment obs erved in patients with POTS, particularly after orthostatic stress, is trea ted effectively with bisoprolol or fludrocortisone or both. These results n eed further confirmation in a controlled double-blind study. Proper medical treatment improves dramatically the clinical and autonomic-hemodynamic dis turbances observed in patients with POTS. The data support the hypothesis t hat POTS is the result of a hyperadrenergic activation or hypovolemia durin g orthostasis.