Document Detail

Rapid reversal of left ventricular hypertrophy and intracardiac volume overload in patients with resistant hypertension and hyperaldosteronism: a prospective clinical study.
MedLine Citation:
PMID:  20351345     Owner:  NLM     Status:  MEDLINE    
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 > or = 12 microg/24 hours and plasma renin activity < or = 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.
Krishna Gaddam; Cecilia Corros; Eduardo Pimenta; Mustafa Ahmed; Thomas Denney; Inmaculada Aban; Seidu Inusah; Himanshu Gupta; Steven G Lloyd; Suzanne Oparil; Ahsan Husain; Louis J Dell'Italia; David A Calhoun
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Publication Detail:
Type:  Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-03-29
Journal Detail:
Title:  Hypertension     Volume:  55     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-04-15     Completed Date:  2010-05-28     Revised Date:  2014-09-24    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1137-42     Citation Subset:  IM    
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MeSH Terms
Age of Onset
Cardiac Volume
Creatinine / blood
Diuretics / therapeutic use
Heart / physiopathology
Heart Atria / anatomy & histology,  drug effects
Heart Rate
Heart Ventricles / drug effects,  physiopathology
Hyperaldosteronism / complications*
Hypertension / complications*
Hypertrophy, Left Ventricular / drug therapy*,  etiology*,  prevention & control*
Magnetic Resonance Imaging
Middle Aged
Prospective Studies
Sodium / urine
Spironolactone / therapeutic use*
Stroke Volume / drug effects,  physiology
Grant Support
M01-RR00032/RR/NCRR NIH HHS; P50 HL077100/HL/NHLBI NIH HHS; P50 HL077100/HL/NHLBI NIH HHS; P50 HL077100-050002/HL/NHLBI NIH HHS; R01 HL075614/HL/NHLBI NIH HHS; R01 HL075614-06/HL/NHLBI NIH HHS; R01-HL79040/HL/NHLBI NIH HHS; T32 HL007457/HL/NHLBI NIH HHS; T32 HL007457/HL/NHLBI NIH HHS; T32 HL007457-29/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Diuretics; 27O7W4T232/Spironolactone; 9NEZ333N27/Sodium; AYI8EX34EU/Creatinine
Comment In:
Hypertension. 2010 Sep;56(3):e26; author reply e27   [PMID:  20696990 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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