SPECTRAL CHARACTERISTICS OF HEART-RATE AND BLOOD-PRESSURE VARIABILITYIN PRIMARY ALDOSTERONISM

Citation
F. Veglio et al., SPECTRAL CHARACTERISTICS OF HEART-RATE AND BLOOD-PRESSURE VARIABILITYIN PRIMARY ALDOSTERONISM, American journal of hypertension, 8(5), 1995, pp. 479-486
Citations number
NO
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
08957061
Volume
8
Issue
5
Year of publication
1995
Part
1
Pages
479 - 486
Database
ISI
SICI code
0895-7061(1995)8:5<479:SCOHAB>2.0.ZU;2-Y
Abstract
A disturbance of the autonomic cardiovascular function has been postul ated in primary aldosteronism as a possible mechanism for hypertension . Using the method of spectral analysis of heart rate and blood pressu re variability, the aim of this study was to assess sympathovagal inte ractions modulating cardiovascular function and baroreflex control in patients with primary aldosteronism. Seventeen patients (7 with adenom as and 10 with idiopathic hyperaldosteronism) and a control group of 1 1 essential hypertensives (EH) and 10 normotensive subjects were studi ed. Continuous finger blood pressure was measured using a Finapres dev ice and heart rate was measured using an electrocardiographic monitor. The studies were conducted in each patient for 20 min in the supine p osition and 10 min during a passive head-up tilt to 60 degrees. The lo w frequency and the low frequency-to-high frequency ratio of systolic and diastolic blood pressures were significantly higher both in primar y aldosteronism and in EH patients compared with normotensives (P < .0 1). Impaired response to tilt was found in the heart rate and blood pr essure variability in primary aldosteronism and EH patients; the incre ase in low frequency was smaller than in normotensives. Baroreflex gai n (assessed by or index) was less in primary aldosteronism and EH pati ents as compared with normotensives. These findings may suggest that v olume expansion or sympathetically mediated central translocation of t he blood volume, or both, could stimulate the cardiopulmonary receptor s and impair the baroreflex gain. Our findings suggest that an enhance d peripheral vascular responsiveness to a normal sympathetic outflow m ay be involved in the pathogenesis of hypertension in primary aldoster onism.