Is It Safe to Initiate/Optimize the Medication of HFrEF Patients During Hospitalization for Acute Decompensation? DOI Open Access
Ruxandra Christodorescu, Daniel Miron Brie,

Alina Diduța Brie

et al.

Journal of Clinical Medicine, Journal Year: 2025, Volume and Issue: 14(8), P. 2664 - 2664

Published: April 13, 2025

Background: Current guidelines emphasize the importance of initiating or optimizing four pillars heart failure with reduced ejection fraction (HFrEF) therapy—beta-blockers (BB), mineralocorticoid receptor antagonists (MRA), angiotensin receptor–neprilysin inhibitors (ARNI), and sodium–glucose cotransporter-2 (SGLT2i)—during hospitalization for acute decompensation. This study compares clinical characteristics outcomes in HFrEF patients hospitalized decompensated based on whether they were newly initiated already receiving at least one these pillars. Methods: prospective observational included 203 Patients divided into two groups: Group A (n = 126), not any prior to admission, B 77), one. Clinical biological parameters evaluated during hospitalization, including changes weight, blood pressure, rate, renal function (serum creatinine), electrolyte levels (sodium, potassium), 30-day mortality. Statistical analyses non-parametric Mann–Whitney test Chi-squared test. Results: Baseline (age, gender, LVEF, NT-proBNP) similar between groups. No significant difference was observed mortality (Group A: 7.14%, B: 5.55%, p 0.74). Both groups experienced improvements systolic diastolic pressure rate (p < 0.05). While serum creatinine remained stable both groups, dynamics (Δcreatinine) significantly different 0.02), exhibiting a higher increase. The improvement more pronounced 0.057) compared B. demonstrated NYHA functional class 0.001). In B, use MRAs SGLT2 increased 0.01 0.001, respectively). Conclusions: initiation optimization therapy decompensation is feasible well-tolerated. Early intervention leads status, supporting guideline recommendations in-hospital therapy. Special consideration should be given when

Language: Английский

Impact of aldosterone deficiency on the development of diuretic resistance in mice DOI Creative Commons
Daniel Essigke,

M. Zaher Kalo,

Andrea Janessa

et al.

Pflügers Archiv - European Journal of Physiology, Journal Year: 2025, Volume and Issue: unknown

Published: April 12, 2025

The effect of diuretics can be limited by stimulation counter-regulatory mechanisms, eventually leading to diuretic resistance. It is thought that the mineralocorticoid aldosterone might contribute development To test this, we challenged genetically modified mice with or without a deletion gene coding for synthase (AS) furosemide, hydrochlorothiazide (HCT) and triamterene. Urinary excretion was studied in metabolic cages; kidneys were expression sodium transporters. In both genotypes, 4-day treatment HCT via drinking water (400 mg/l) induced similar natriuresis modest loss body weight < 10%. contrast, furosemide (125 triamterene (200 stimulated significantly higher AS-/- addition, caused massive hyperkalemia > 9 mM acidosis (pH 7.0). AS+/+ mice, plasma concentration tended increase under administration, while robust ~ sixfold increase. kidney, apical targeting proteolytic activation epithelial channel ENaC treatment, an diminished mice. conclusion, essentially involved resistance blockade lesser extent furosemide. independent aldosterone.

Language: Английский

Citations

0
Is It Safe to Initiate/Optimize the Medication of HFrEF Patients During Hospitalization for Acute Decompensation? DOI Open Access
Ruxandra Christodorescu, Daniel Miron Brie,

Alina Diduța Brie

et al.

Journal of Clinical Medicine, Journal Year: 2025, Volume and Issue: 14(8), P. 2664 - 2664

Published: April 13, 2025

Background: Current guidelines emphasize the importance of initiating or optimizing four pillars heart failure with reduced ejection fraction (HFrEF) therapy—beta-blockers (BB), mineralocorticoid receptor antagonists (MRA), angiotensin receptor–neprilysin inhibitors (ARNI), and sodium–glucose cotransporter-2 (SGLT2i)—during hospitalization for acute decompensation. This study compares clinical characteristics outcomes in HFrEF patients hospitalized decompensated based on whether they were newly initiated already receiving at least one these pillars. Methods: prospective observational included 203 Patients divided into two groups: Group A (n = 126), not any prior to admission, B 77), one. Clinical biological parameters evaluated during hospitalization, including changes weight, blood pressure, rate, renal function (serum creatinine), electrolyte levels (sodium, potassium), 30-day mortality. Statistical analyses non-parametric Mann–Whitney test Chi-squared test. Results: Baseline (age, gender, LVEF, NT-proBNP) similar between groups. No significant difference was observed mortality (Group A: 7.14%, B: 5.55%, p 0.74). Both groups experienced improvements systolic diastolic pressure rate (p < 0.05). While serum creatinine remained stable both groups, dynamics (Δcreatinine) significantly different 0.02), exhibiting a higher increase. The improvement more pronounced 0.057) compared B. demonstrated NYHA functional class 0.001). In B, use MRAs SGLT2 increased 0.01 0.001, respectively). Conclusions: initiation optimization therapy decompensation is feasible well-tolerated. Early intervention leads status, supporting guideline recommendations in-hospital therapy. Special consideration should be given when

Language: Английский

Citations

0