Rapid reversal of left ventricular hypertrophy and intracardiac volume overload in patients with resistant hypertension and hyperaldosteronism: A prospective clinical study

Gaddam, Krishna, Corros, Cecilia, Pimenta, Eduardo, Ahmed, Mustafa, Denney, Thomas, Aban, Inmaculada, Inusah, Seidu, Gupta, Himanshu, Lloyd, Steven G., Oparil, Suzanne, Husain, Ahsan, Dell'Italia, Louis J. and Calhoun, David A. (2010) Rapid reversal of left ventricular hypertrophy and intracardiac volume overload in patients with resistant hypertension and hyperaldosteronism: A prospective clinical study. Hypertension, 55 5: 1137-1142. doi:10.1161/HYPERTENSIONAHA.109.141531


Author Gaddam, Krishna
Corros, Cecilia
Pimenta, Eduardo
Ahmed, Mustafa
Denney, Thomas
Aban, Inmaculada
Inusah, Seidu
Gupta, Himanshu
Lloyd, Steven G.
Oparil, Suzanne
Husain, Ahsan
Dell'Italia, Louis J.
Calhoun, David A.
Title Rapid reversal of left ventricular hypertrophy and intracardiac volume overload in patients with resistant hypertension and hyperaldosteronism: A prospective clinical study
Journal name Hypertension   Check publisher's open access policy
ISSN 0194-911X
1524-4563
0073-425X
Publication date 2010-05-01
Sub-type Article (original research)
DOI 10.1161/HYPERTENSIONAHA.109.141531
Volume 55
Issue 5
Start page 1137
End page 1142
Total pages 6
Editor John E. Hall
Place of publication Baltimore, MD, U.S.A.
Publisher Lippincott Williams & Wilkins for the American Heart Association
Language eng
Formatted abstract
We have shown previously that patients with resistant hypertension and hyperaldosteronism have increased brain natriuretic peptide suggestive of increased intravascular volume. In the present study, we tested the hypothesis that hyperaldosteronism contributes to cardiac volume overload. Thirty-seven resistant hypertensive patients with hyperaldosteronism (urinary aldosterone ≥12 µg/24 hours and plasma renin activity ≤1.0 ng/mL per hour) and 71 patients with normal aldosterone status were studied. Both groups had similar blood pressure and left ventricular mass, whereas left and right ventricular end-diastolic volumes measured by cardiac MRI were greater in high versus normal aldosterone subjects (P<0.05). Spironolactone treatment (19 patients in the high aldosterone group and 15 patients from the normal aldosterone group participated in the follow-up) resulted in a significant decrease in clinic systolic blood pressure, right and left ventricular end diastolic volumes, left atrial volume, left ventricular mass, and brain natriuretic peptide at 3 and 6 months of follow-up in patients with high aldosterone, whereas in those with normal aldosterone status, spironolactone decreased blood pressure and left ventricular mass without changes in ventricular or atrial volumes or plasma brain natriuretic peptide. Hyperaldosteronism causes intracardiac volume overload in patients with resistant hypertension in spite of conventional thiazide diuretic use. Mineralocorticoid receptor blockade induces rapid regression of left ventricular hypertrophy irrespective of aldosterone status. In subjects with high aldosterone, mineralocorticoid receptor blockade induces a prominent diuretic effect compared with a greater vasodilatory effect in subjects with normal aldosterone status.
Copyright © 2010 American Heart Association. All rights reserved.
Keyword Resistant hypertension
Hyperaldosteronism
Cardiac volume
Cardiac hypertrophy
Chronic episodic hypoxia
Primary aldosteronism
Cardiac fibrosis
Blood-pressure
Renin-activity
Prevalence
Plasma
Heart
Chlorothiazide
Association
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: UQ Centre for Clinical Research Publications
Official 2011 Collection
 
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Created: Sun, 02 May 2010, 10:07:03 EST