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Aldosterone Receptor Antagonism (aldosterone + receptor_antagonism)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Aldosterone Receptor Antagonism: Interface With Hyperkalemia in Heart Failure

CONGESTIVE HEART FAILURE, Issue 5 2004
Domenic A. Sica MD
Aldosterone receptor antagonism (ARA) is an increasingly well-accepted element of heart failure therapy. The experimental underpinnings for the use of ARA in heart failure are strong being linked to a variety of tissue-based cardiac effects characteristic of drugs in this class. However, the benefits of ARA therapy do not come without some risk since drugs in this class are potent inhibitors of renal potassium (K+) elimination. Thus, some increment in serum K+, up to and including the development of overt hyperkalemia (typically defined as a serum K+ value in excess of 6.0 mEq/L), is to be expected whenever they are used. Hyperkalemia attributable to ARA relates to several factors including ARA dose, patient predisposition to hyperkalemia, as in the case of renal failure, and dietary intake of K+. The risk of some change in serum K+ with ARA should not be a deterrent to use of drugs in this class but, rather should prompt careful surveillance for the onset of this potentially life-threatening electrolyte disturbance. The frequency of such scrutiny should be patient-specific and based on the constellation of risk factors for hyperkalemia. [source]

Sex-Specific Impact of Aldosterone Receptor Antagonism on Ventricular Remodeling and Gene Expression after Myocardial Infarction

CLINICAL AND TRANSLATIONAL SCIENCE, Issue 2 2009
Ph.D., Rosemeire M. Kanashiro-Takeuchi D.V.M.
Abstract Aldosterone receptor antagonism reduces mortality and improves post-myocardial infarction (Ml) remodeling. Because aldosterone and estrogen signaling pathways interact, we hypothesized that aldosterone blockade is sex-specific. Therefore, we investigated the mpact of eplerenone on left ventricular (LV) remodeling and gene expression of male infarcted rats versus female infarcted rats. Ml and Sham animals were randomized to receive eplerenone (100 mg/kg/day) or placebo 3 days post-surgery for 4 weeks and assessed by echocardiography. In the Ml placebo group, left ventricular end-diastolic dimension (LVEDD) increased from 7.3 ± 0.4 mm to 10.2 ± 1.0 mm (p < 0.05) and ejection fraction (EF) decreased from 82.3 + 4% to 45.5 + 11% (p < 0.05) in both sexes (p= NS between groups). Eplerenone attenuated LVEDD enlargement more effectively in females (8.8 ± 0.2 mm, p < 0.05 vs. placebo) than in males (9.7 ± 0.2 mm, p= NS vs. placebo) and improved EF in females (56.7 ± 3%, p < 0.05 vs. placebo) but not in males (50.6 + 3%, p= NS vs. placebo). Transcriptomic analysis using Rat_230,2.0 microarrays (Affymetrix) revealed that in females 19% of downregu-lated genes and 44% of upregulated genes post-MI were restored to normal by eplerenone. In contrast, eplerenone only restored 4% of overexpressed genes in males. Together, these data suggest that aldosterone blockade reduces Ml-induced cardiac remodeling and phenotypic alterations of gene expression preferentially in females than in males. The use of transcriptomic signatures to detect greater benefit of eplerenone in females has potential implications for personalized medicine. [source]

Aldosterone Receptor Antagonism: Interface With Hyperkalemia in Heart Failure

CONGESTIVE HEART FAILURE, Issue 5 2004
Domenic A. Sica MD
Aldosterone receptor antagonism (ARA) is an increasingly well-accepted element of heart failure therapy. The experimental underpinnings for the use of ARA in heart failure are strong being linked to a variety of tissue-based cardiac effects characteristic of drugs in this class. However, the benefits of ARA therapy do not come without some risk since drugs in this class are potent inhibitors of renal potassium (K+) elimination. Thus, some increment in serum K+, up to and including the development of overt hyperkalemia (typically defined as a serum K+ value in excess of 6.0 mEq/L), is to be expected whenever they are used. Hyperkalemia attributable to ARA relates to several factors including ARA dose, patient predisposition to hyperkalemia, as in the case of renal failure, and dietary intake of K+. The risk of some change in serum K+ with ARA should not be a deterrent to use of drugs in this class but, rather should prompt careful surveillance for the onset of this potentially life-threatening electrolyte disturbance. The frequency of such scrutiny should be patient-specific and based on the constellation of risk factors for hyperkalemia. [source]

Aldosterone receptor antagonism and heart failure: insights from an outpatient clinic

JOURNAL OF CLINICAL PHARMACY & THERAPEUTICS, Issue 4 2008
R. Mariotti
Summary Objective:, In randomized clinical trials, aldosterone antagonists have been shown to reduce mortality and morbidity in heart failure (HF). The aim of the present study was to examine the risk-benefit profile of aldosterone antagonists in routine clinical practice. Methods:, A retrospective analysis, extending over a 1-year period, of the clinical, instrumental and laboratory data of 264 HF outpatients was performed. All patients were on a ,-blocker and an ACE-inhibitor (or angiotensin-II receptor-blocker) and 151 were taking an aldosterone antagonist. Results:, At baseline, subjects treated with aldosterone antagonists had a higher NYHA class, a larger left-ventricular end-diastolic volume, a worse ejection fraction and a higher systolic pulmonary arterial pressure (sPAP). During follow-up, a greater reduction in sPAP and a tendency towards improved systolic and diastolic function were observed in subjects treated with aldosterone antagonists. Moreover, clinical and laboratory parameters did not deteriorate in patients taking aldosterone antagonists. Mortality rates were similar in the two groups (8·6% vs. 8·8%, P = NS). Conclusions:, The use of aldosterone antagonists in HF is associated with an improvement in cardiac function and is well tolerated. In the present study, patients administered these agents had a comparable clinical outcome to that of the control group, despite important differences in baseline risk. [source]

Sex-Specific Impact of Aldosterone Receptor Antagonism on Ventricular Remodeling and Gene Expression after Myocardial Infarction

CLINICAL AND TRANSLATIONAL SCIENCE, Issue 2 2009
Ph.D., Rosemeire M. Kanashiro-Takeuchi D.V.M.
Abstract Aldosterone receptor antagonism reduces mortality and improves post-myocardial infarction (Ml) remodeling. Because aldosterone and estrogen signaling pathways interact, we hypothesized that aldosterone blockade is sex-specific. Therefore, we investigated the mpact of eplerenone on left ventricular (LV) remodeling and gene expression of male infarcted rats versus female infarcted rats. Ml and Sham animals were randomized to receive eplerenone (100 mg/kg/day) or placebo 3 days post-surgery for 4 weeks and assessed by echocardiography. In the Ml placebo group, left ventricular end-diastolic dimension (LVEDD) increased from 7.3 ± 0.4 mm to 10.2 ± 1.0 mm (p < 0.05) and ejection fraction (EF) decreased from 82.3 + 4% to 45.5 + 11% (p < 0.05) in both sexes (p= NS between groups). Eplerenone attenuated LVEDD enlargement more effectively in females (8.8 ± 0.2 mm, p < 0.05 vs. placebo) than in males (9.7 ± 0.2 mm, p= NS vs. placebo) and improved EF in females (56.7 ± 3%, p < 0.05 vs. placebo) but not in males (50.6 + 3%, p= NS vs. placebo). Transcriptomic analysis using Rat_230,2.0 microarrays (Affymetrix) revealed that in females 19% of downregu-lated genes and 44% of upregulated genes post-MI were restored to normal by eplerenone. In contrast, eplerenone only restored 4% of overexpressed genes in males. Together, these data suggest that aldosterone blockade reduces Ml-induced cardiac remodeling and phenotypic alterations of gene expression preferentially in females than in males. The use of transcriptomic signatures to detect greater benefit of eplerenone in females has potential implications for personalized medicine. [source]