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Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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Heart Failure V: Medical Management01:30

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Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
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Renal Failure: Dose Adjustments01:11

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In patients with renal impairment, drugs undergo significant changes in their pharmacokinetics, which require dosage adjustments to ensure safe and effective therapy.
Reduced renal clearance and elimination rate are common outcomes of renal impairment. These alterations lead to a prolonged elimination half-life and an altered apparent volume of distribution for drugs. As a result, dosage adjustments are typically necessary to maintain optimal drug levels in the body.
However, dosage adjustments...
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Heart Failure VI: Adjunct Therapies01:22

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Additional therapies for treating patients with heart failure (HF) may include procedural interventions, supplemental oxygen, the management of sleep disorders, and nutritional therapy.Procedural InterventionsImplantable Cardioverter-Defibrillator: For patients at risk of life-threatening arrhythmias due to severe left ventricular dysfunction, an Implantable Cardioverter-Defibrillator (ICD) can detect and terminate these arrhythmias, preventing sudden cardiac death and improving survival rates.
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Glomerular Filtration Rate and its Regulation01:28

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The Glomerular Filtration Rate (GFR) is a measure of kidney function, reflecting the volume of filtrate formed per minute in the kidneys. On average, GFR is approximately 125 mL/min in males and 105 mL/min in females. Maintaining a relatively constant GFR is essential for the kidneys to effectively regulate body fluid homeostasis and maintain extracellular stability.
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Updated: Oct 15, 2025

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FGF-23 (Fibroblast Growth Factor-23) and Cardiorenal Interactions.

Juan B Ivey-Miranda1,2, Brendan Stewart1, Zachary L Cox3

  • 1Department of Internal Medicine, Section of Cardiovascular Medicine (J.B.I.-M., B.S., C.M., O.G., G.M., J.M.-V., D.M., V.S.R., J.M.T.), Yale University School of Medicine, New Haven, CT.

Circulation. Heart Failure
|October 25, 2021
PubMed
Summary
This summary is machine-generated.

Fibroblast growth factor-23 (FGF-23) is not significantly linked to cardiorenal dysfunction in heart failure patients. This study suggests FGF-23 is unlikely to be a primary cause of these complex interactions in humans.

Keywords:
chloridediureticheart failuremodels, animaloutpatient

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Area of Science:

  • Cardiorenal medicine
  • Endocrinology
  • Heart failure research

Background:

  • Animal models suggest FGF-23 contributes to cardiorenal dysfunction.
  • Human studies are needed to confirm FGF-23's role in heart failure.
  • Adverse cardiorenal interactions include sodium avidity, diuretic resistance, and neurohormonal activation.

Purpose of the Study:

  • To investigate the association between FGF-23 and cardiorenal dysfunction in human heart failure patients.
  • To determine if FGF-23 is an independent predictor of cardiorenal parameters.
  • To evaluate FGF-23's role in sodium avidity, diuretic resistance, and neurohormonal activation.

Main Methods:

  • 199 heart failure outpatients undergoing diuretic treatment were enrolled.
  • Blood and urine samples were collected before and after diuretic administration.
  • FGF-23 levels were measured and correlated with cardiorenal parameters.

Main Results:

  • FGF-23 correlated with heart failure severity markers (diuretic dose, NT-proBNP, eGFR, chloride, albumin).
  • No significant association was found between FGF-23 and sodium avidity, diuretic resistance, or neurohormonal activation.
  • FGF-23 was not independently associated with mortality in heart failure patients.

Conclusions:

  • FGF-23 does not appear to be a significant factor in cardiorenal dysfunction in heart failure.
  • The study suggests FGF-23 is unlikely to be a primary driver of cardiorenal interactions in humans.
  • Further research may explore potential minor roles or specific subgroups.