Mineralocorticoid receptor antagonism in acutely decompensated chronic heart failure

Ferreira, João Pedro; Santos, Mário; Almeida, Sofia; Marques, Irene; Bettencourt, Paulo; Carvalho, Henrique

doi:10.1016/j.ejim.2013.08.711

Cited by 77 publications

(50 citation statements)

References 36 publications

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“…Spironolactone improved diastolic cardiac function in patients with heart failure with preserved ejection fraction [75]. Further, high doses of spironolactone in acutely decompensated chronic heart failure were shown to be safe relative to serum potassium levels and to exert a positive impact on the resolution of congestion [76].…”

Section: Mr and Diabetic Complications In Humansmentioning

confidence: 98%

Aldosterone and the Mineralocorticoid Receptor: Risk Factors for Cardiometabolic Disorders

Garg

Adler

2015

Curr Hypertens Rep

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Preclinical studies have convincingly demonstrated a role for the mineralocorticoid receptor (MR) in adipose tissue physiology. These studies show that increased MR activation causes adipocyte dysfunction leading to decreased production of insulin-sensitizing products and increased production of inflammatory factors, creating an environment conducive to metabolic and cardiovascular disease. Accumulating data also suggest that MR activation may be an important link between obesity and metabolic syndrome. Moreover, MR activation may mediate the pathogenic consequences of metabolic syndrome. Recent attempts at reversing cardiometabolic damage in patients with type 2 diabetes using MR antagonists have shown promising results. MR antagonists are already used to treat heart failure where their use decreases mortality and morbidity over and above the use of traditional therapies alone. However, more data are needed to establish the benefits of MR antagonists in diabetes, obesity, and metabolic syndrome.

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Section: Mr and Diabetic Complications In Humansmentioning

confidence: 98%

Aldosterone and the Mineralocorticoid Receptor: Risk Factors for Cardiometabolic Disorders

Garg

Adler

2015

Curr Hypertens Rep

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“…The information derived from a simple measure of DE can help clinicians in difficult therapeutic decisions, such as escalating diuretics and/or selecting other classes of diuretics (such as mineralocorticoid receptor antagonists [27,28]), in-hospital department allocation (e.g., low monitoring vs. intensive monitoring ward), personalized follow-up, management expectations about disease prognosis, clinical record registries to inform future care providers (e.g., patient required high-intensity diuretic strategy or high-dose spironolactone or ultrafiltration to obtain the fluid loss goal), and it can also provide a potential endpoint for clinical trials [29,30]. …”

Section: Discussionmentioning

confidence: 99%

Lack of Diuretic Efficiency (but Not Low Diuresis) Early in An Acutely Decompensated Heart Failure Episode Is Associated with Increased 180-Day Mortality

Ferreira

Girerd

Ricardo³

et al. 2017

Cardiorenal Med

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Introduction: The assessment of the amount of urine produced by the dose of administered diuretic has been proposed as the main signal of interest in diuretic responsiveness - diuretic efficiency (DE). The main aim of our study is to determine if a low DE is associated with 180-day all-cause mortality (ACM). Methods: During a 3-year period, we retrospectively studied patients with acutely decompensated heart failure (ADHF) and respiratory insufficiency admitted to the emergency room of a tertiary university hospital in Porto, Portugal. A total of 170 patients (age 76.2 ± 10.3 years) were included. The outcome of ACM occurred in 43 (25.3%) patients during the 180-day follow-up period. DE was evaluated for a maximum of 3 h after emergency room admission. The lowest DE was defined as ≤140 mL of diuresis per 40 mg of furosemide equivalents. Results: No significant differences in age, comorbidities, baseline HF symptoms, or disease-modifying medication were found between the lowest and highest DE groups. The lowest DE group had higher blood urea and lower estimated glomerular filtration rate (eGFR) levels (41.3 ± 24.5 vs. 56.7 ± 23.2 mL/min/1.73 m², p < 0.001). The patients with the lowest DE had significantly higher rates of ACM during the 180-day follow-up, even after adjustment for other clinically relevant variables: hazard ratio (HR) [95% CI] = 2.31 [1.16-4.58], p = 0.016. The lowest diuresis (≤300 mL) and the highest intravenous furosemide dose (>80 mg) alone were not significantly associated with the outcome. After adjustment for N-terminal prohormone of brain natriuretic peptide, the association between the lowest DE and the outcome lost strength (HR [95% CI] = 1.53 [0.75-3.13], p = 0.240). Conclusion: A low DE (≤140 mL/40 mg of furosemide) in the first 3 h after an ADHF episode was associated with increased mid-term mortality rates.

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“…Regarding this matter, high dose spironolactone as add-on therapy in the acutely decompensated heart failure (ADHF) setting has been demonstrated to be safe and likely to provide greater symptomatic relief translated into a more pronounced decrease in natriuretic peptides [12].…”

Section: Introductionmentioning

confidence: 99%

High-dose spironolactone changes renin and aldosterone levels in acutely decompensated heart failure

Ferreira¹,

Santos²,

Almeida³

et al. 2014

Cor Vasa

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c o r e t v a s a 5 6 ( 2 0 1 4 ) e 4 6 3 -e 4 7 0 antagonism Renin Aldosterone Acute heart failure a b s t r a c t Background: In acutely decompensated heart failure (ADHF) patients with higher aldosterone levels correlate with worse postdischarge outcomes, suggesting that further modulation of the mineralocorticoid system during or immediately after hospitalization might favorably improve outcomes. Methods and results: This was an observational, retrospective secondary analysis of a study including 100 patients with ADHF. In that study 50 patients were submitted to spironolactone treatment (50-100 mg/day). A higher proportion of patients with renin levels above 16.5 pg/mL and aldosterone levels above 100 ng/dL were observed in subjects submitted to spironolactone treatment (44.7% vs. 66.7% and 56% vs. 64.7%, respectively, both p < 0.05). In the group of patients submitted to spironolactone treatment the proportion of patients with renin and aldosterone levels above the cutoff had a significant increase from baseline to day 3 (24-32% and 16-44%, respectively, both p < 0.05). Log renin and aldosterone were higher in patients with renin and aldosterone levels above the cutoff point (both p < 0.05). Conclusions: High-dose spironolactone added to standard ADHF therapy induces an additional increase in renin and aldosterone levels. Whether higher levels of renin and aldosterone due to the reactive response to full MRA still have prognostic value requires further investigation.

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Mineralocorticoid receptor antagonism in acutely decompensated chronic heart failure

Cited by 77 publications

References 36 publications

Aldosterone and the Mineralocorticoid Receptor: Risk Factors for Cardiometabolic Disorders

Aldosterone and the Mineralocorticoid Receptor: Risk Factors for Cardiometabolic Disorders

Lack of Diuretic Efficiency (but Not Low Diuresis) Early in An Acutely Decompensated Heart Failure Episode Is Associated with Increased 180-Day Mortality

High-dose spironolactone changes renin and aldosterone levels in acutely decompensated heart failure

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