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Related Concept Videos

Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

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, vasodilation, and...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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...
Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

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...
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

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...
Heart Failure VI: Adjunct Therapies01:22

Heart Failure VI: Adjunct Therapies

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.
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

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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Related Experiment Video

Updated: May 9, 2026

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
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Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

Published on: December 11, 2017

Early NT-proBNP decrease with ivabradine in ambulatory patients with systolic heart failure.

Luis Sargento1, Milan Satendra, Susana Longo

  • 1Heart Failure Unit, Pulido Valente Hospital, Lisbon North Hospital Centre, Lisbon, Portugal.

Clinical Cardiology
|August 10, 2013
PubMed
Summary
This summary is machine-generated.

Short-term ivabradine treatment significantly reduced N-terminal pro-brain natriuretic peptide (NT-proBNP) levels in systolic heart failure patients. This reduction in NT-proBNP closely correlated with the degree of heart rate reduction achieved.

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Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
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Published on: December 11, 2017

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Published on: July 24, 2012

Area of Science:

  • Cardiology
  • Pharmacology
  • Biomarkers

Background:

  • Heart rate reduction is a key therapy for systolic heart failure (HF).
  • N-terminal pro-brain natriuretic peptide (NT-proBNP) is a prognostic marker in HF.

Purpose of the Study:

  • To evaluate the short-term effect of ivabradine-induced heart rate reduction on NT-proBNP levels in outpatients with systolic HF.
  • To explore the association between heart rate decrease and NT-proBNP values.

Main Methods:

  • 25 outpatients with systolic HF, ejection fraction <40%, and HR >70 bpm were included.
  • Patients received optimized medical therapy and were treated with ivabradine for 3 months after a 1-month stability period.
  • NT-proBNP levels and heart rate were monitored throughout the study.

Main Results:

  • Ivabradine significantly decreased NT-proBNP by 44.5% (median decrease of 964 pg/mL, P = 0.002).
  • Baseline heart rate correlated with baseline NT-proBNP (rs = 0.411, P = 0.041).
  • Heart rate reduction correlated with NT-proBNP reduction (absolute: rs = 0.442, P = 0.027; percent: rs = 0.395, P = 0.05).

Conclusions:

  • Short-term ivabradine treatment effectively reduces NT-proBNP in systolic HF patients.
  • The degree of NT-proBNP reduction is closely linked to the extent of heart rate reduction achieved with ivabradine.