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Related Concept Videos

Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

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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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Heart Failure II: Pathophysiology01:29

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Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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Heart Failure Drugs: Diuretics01:22

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Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
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Heart Failure Drugs: Inotropic Agents01:26

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Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
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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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β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
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Articles linked to this work by shared authors, journal, and citation graph.

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Finerenone and Blood Pressure in Heart Failure With Mildly Reduced or Preserved Ejection Fraction: The FINEARTS-HF Randomized Clinical Trial.

JAMA cardiology·2026
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AHA/ACC/ESC/WHF Expert Consensus Document: Second Universal Definition of Heart Failure (2026).

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Health Status in Heart Failure With Preserved Ejection Fraction in Asia: Insights From Global Trials.

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AHA/ACC/ESC/WHF Expert Consensus Document: Second Universal Definition of Heart Failure (2026).

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Related Experiment Video

Updated: Mar 19, 2026

A Surgical Model of Heart Failure with Preserved Ejection Fraction in Tibetan Minipigs
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Spironolactone for heart failure with preserved ejection fraction.

Bertram Pitt1, Marc A Pfeffer, Susan F Assmann

  • 1From the University of Michigan School of Medicine, Ann Arbor (B.P.); the Cardiovascular Division, Brigham and Women's Hospital, Boston (M.A.P., B.C., A.S.D., E.F.L., S.D.S.); New England Research Institutes, Watertown, MA (S.F.A., B.H., C.T.K., S.M.M.); National Heart, Lung, and Blood Institute, Bethesda, MD (R.B., J.L.F., S.Y.); Veterans Affairs Medical Center and University of Minnesota, Minneapolis (I.S.A.); Hospital de Clinicas de Porto Alegre, Porto Alegre, Brazil (N.C.); Estudios Clinicos Latinoamerica, Rosario, Argentina (R.D.); Pirogov Russian National Research Medical University, Moscow (I.G.); New York Methodist Hospital, Brooklyn (J.F.H.); Montreal Heart Institute, Montreal (E.O.); University of Washington Medical Center, Seattle (J.L.P.); Diagnostic Services Clinic, Tbilisi, Georgia (T.S.); Northwestern University, Chicago (S.J.S.); and the University of Wisconsin, Madison (N.K.S.).

The New England Journal of Medicine
|April 11, 2014
PubMed
Summary

Spironolactone did not significantly reduce major adverse events in patients with heart failure and preserved ejection fraction. However, it did lower heart failure hospitalizations but increased hyperkalemia risk.

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Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Mineralocorticoid-receptor antagonists are beneficial for heart failure with reduced ejection fraction.
  • The efficacy of spironolactone in heart failure with preserved ejection fraction (HFpEF) was previously unevaluated.

Purpose of the Study:

  • To assess the effects of spironolactone on clinical outcomes in patients with HFpEF.

Main Methods:

  • A randomized, double-blind trial involving 3445 patients with HFpEF (left ventricular ejection fraction >= 45%).
  • Patients received either spironolactone (15-45 mg daily) or placebo.
  • The primary outcome was a composite of cardiovascular death, aborted cardiac arrest, or heart failure hospitalization.

Main Results:

  • Spironolactone did not significantly reduce the primary composite outcome (18.6% vs. 20.4%, P=0.14).
  • A significant reduction was observed in hospitalizations for heart failure (12.0% vs. 14.2%, P=0.04).
  • Spironolactone increased the risk of hyperkalemia (18.7% vs. 9.1%) and serum creatinine levels without increasing serious adverse events.

Conclusions:

  • Spironolactone did not significantly improve the primary composite outcome in patients with HFpEF.
  • Spironolactone may reduce heart failure hospitalizations but carries an increased risk of hyperkalemia.