Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Adrenergic Antagonists: Chemistry and Classification of β-Receptor Blockers01:25

Adrenergic Antagonists: Chemistry and Classification of β-Receptor Blockers

β-adrenergic antagonists, or β-blockers, modulate the sympathetic nervous system by targeting β-adrenoceptors and inhibiting catecholamine-mediated sympathetic responses. β-blockers differ in their adrenoceptor subtype affinity, lipophilicity, and α-blocking capabilities. The history of β-blocker development began with the prototype, dichloroisoprenaline, which exhibited partial agonist activity. As a result, propranolol was developed as a pure antagonist but nonselective agent, paving the way...
Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers01:27

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers

β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in bronchial smooth...
Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

Adrenergic Antagonists: ɑ and β-Receptor Blockers

Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is clinically...
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 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 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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Epoprostenol increased mortality in patients with severe CHF.

Evidence-based cardiovascular medicine·2005
Same author

Uptake of self-management strategies in a heart failure management programme.

European journal of heart failure·2003
Same author

Factors influencing the length of hospital stay of patients with heart failure.

European journal of heart failure·2003
Same author

Matching the standards of clinical trial evidence with application in practice.

International journal of clinical practice·2003
Same author

Optimization of ACE inhibitor therapy in heart failure.

European heart journal·2002
Same author

The effects of intensive glycaemic control on body composition in patients with type 2 diabetes.

Diabetes, obesity & metabolism·2002

Related Experiment Video

Updated: Jun 23, 2026

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
12:45

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

Beta-blockers in heart failure. Future directions

N Sharpe1

  • 1Department of Medicine, University of Auckland School of Medicine, New Zealand.

European Heart Journal
|April 1, 1996
PubMed
Summary
This summary is machine-generated.

Beta-blockers offer potential for heart failure mortality reduction, especially in ischemic heart disease. Large trials are needed to confirm a 15-20% mortality benefit and establish beta-blockade as a key heart failure therapy.

More Related Videos

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice
05:08

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Published on: October 3, 2019

Cardiac Loading using Passive Left Atrial Pressurization and Passive Afterload for Graft Assessment
08:49

Cardiac Loading using Passive Left Atrial Pressurization and Passive Afterload for Graft Assessment

Published on: August 2, 2024

Related Experiment Videos

Last Updated: Jun 23, 2026

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
12:45

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

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice
05:08

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Published on: October 3, 2019

Cardiac Loading using Passive Left Atrial Pressurization and Passive Afterload for Graft Assessment
08:49

Cardiac Loading using Passive Left Atrial Pressurization and Passive Afterload for Graft Assessment

Published on: August 2, 2024

Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Heart failure mortality remains high despite treatments like ACE inhibitors.
  • Neurohormonal activation predicts mortality in heart failure.
  • Beta-blockade is established for heart failure, with benefits seen post-myocardial infarction.

Purpose of the Study:

  • To evaluate the efficacy and tolerability of beta-blocker treatment in patients with heart failure of ischemic etiology.
  • To assess the overall mortality benefit of beta-blockade in heart failure based on existing trials.
  • To determine the need for large-scale trials to confirm mortality reduction in heart failure.

Main Methods:

  • The Australia and New Zealand carvedilol heart failure study randomized 415 patients to carvedilol or placebo.
  • Meta-analysis of all available randomized clinical trials of beta-blockade in heart failure (>1600 patients).

Main Results:

  • Carvedilol showed excellent tolerability and improved ventricular function in ischemic heart failure after 6 months.
  • An overview of trials suggests approximately 20% mortality risk reduction with beta-blockade, but with wide confidence intervals.
  • Current evidence necessitates large-scale trials to reliably detect a 15-20% mortality reduction.

Conclusions:

  • Beta-blockade demonstrates therapeutic potential in heart failure, particularly in ischemic subtypes.
  • Further large-scale, adequately powered mortality studies are crucial to solidify beta-blockade's role in heart failure management.
  • A definitive mortality study could establish beta-blockade as a cornerstone therapy for heart failure.