title: Rapid reversal of left ventricular hypertrophy and intracardiac volume overload in patients with resistant hypertension and hyperaldosteronism: a prospective clinical study.
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 > 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.
authors.affiliation: Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA. kgaddam@ochsner.org
authors.forename: Krishna
authors.initials: K
authors.lastname: Gaddam
authors.forename: Cecilia
authors.initials: C
authors.lastname: Corros
authors.forename: Eduardo
authors.initials: E
authors.lastname: Pimenta
authors.forename: Mustafa
authors.initials: M
authors.lastname: Ahmed
authors.forename: Thomas
authors.initials: T
authors.lastname: Denney
authors.forename: Inmaculada
authors.initials: I
authors.lastname: Aban
authors.forename: Seidu
authors.initials: S
authors.lastname: Inusah
authors.forename: Himanshu
authors.initials: H
authors.lastname: Gupta
authors.forename: Steven G
authors.initials: SG
authors.lastname: Lloyd
authors.forename: Suzanne
authors.initials: S
authors.lastname: Oparil
authors.forename: Ahsan
authors.initials: A
authors.lastname: Husain
authors.forename: Louis J
authors.initials: LJ
authors.lastname: Dell'Italia
authors.forename: David A
authors.initials: DA
authors.lastname: Calhoun
mesh_terms: D017668:Age of Onset; D002306:Cardiac Volume; D003404:Creatinine / Q000097:blood; D003971:Diastole; D004232:Diuretics / Q000627:therapeutic use; D004562:Electrocardiography; D005260:Female; D006321:Heart / Q000503:physiopathology; D006325:Heart Atria / Q000033:anatomy & histology / Q000187:drug effects; D006339:Heart Rate; D006352:Heart Ventricles / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications*; D006973:Hypertension / Q000150:complications*; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000209:etiology* / Q000517:prevention & control*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012964:Sodium / Q000652:urine; D013148:Spironolactone / Q000627:therapeutic use*; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology; D013599:Systole
chemical_list: D004232:Diuretics; D013148:Spironolactone; D012964:Sodium; D003404:Creatinine