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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...
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...
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...
Antihypertensive Drugs: Types of β-Blockers01:28

Antihypertensive Drugs: Types of β-Blockers

β receptors are classified into three subclasses: β1, β2, and β3. β1 receptors are primarily located in the heart and kidneys. When they get activated, they increase heart rate, contractility, and renin release. This process enhances blood pressure and aids in stress management. In contrast, β2 receptors are situated mainly in the lungs, blood vessels, and skeletal muscles. Upon activation, they trigger smooth muscle relaxation, causing bronchodilation and vasodilation. This widens airways and...
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: 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...

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Beta-Blocker Discontinuation in Acute Heart Failure: A Systematic Review and Meta-Analysis.

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Related Experiment Videos

Beta-Blocker Discontinuation After Myocardial Infarction: A Systematic Review and Meta-Analysis.

Wade Thompson1, Nima Alaeiilkhchi1, Lisa M McCarthy2

  • 1Department of Anesthesiology, Pharmacology, and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, Canada.

JACC. Advances
|June 18, 2026
PubMed
Summary
This summary is machine-generated.

Discontinuing beta-blockers after myocardial infarction (MI) in patients with preserved ejection fraction may not increase mortality or MI risk. However, it might raise the risk of major adverse cardiovascular events (MACE), mainly due to hospitalizations.

Keywords:
beta-blockersdeprescribingmyocardial infarction

Related Experiment Videos

Area of Science:

  • Cardiology
  • Clinical Trials
  • Evidence-Based Medicine

Background:

  • Beta-blocker use post-myocardial infarction (MI) is debated, particularly in patients with preserved left ventricular ejection fraction (LVEF).
  • Consideration for beta-blocker discontinuation is increasing in this patient population.

Purpose of the Study:

  • To systematically review and meta-analyze the effects of beta-blocker discontinuation versus continuation after MI.
  • To assess the impact on mortality and major adverse cardiovascular (CV) events.

Main Methods:

  • Systematic search of multiple databases (MEDLINE, Embase, Cochrane, Google Scholar, Epistemonikos) up to September 11, 2025.
  • Inclusion of randomized controlled trials and nonrandomized studies in adults (≥18 years).
  • Meta-analysis using inverse-variance random-effects model; certainty of evidence assessed by Grading of Recommendations, Assessment, Development, and Evaluation (GRADE).

Main Results:

  • Ten studies (1 RCT, 9 observational; N=121,114) met eligibility criteria; 8 focused on patients with LVEF >40% and/or no heart failure.
  • Beta-blocker discontinuation showed no significant increase in mortality risk (HR: 1.11; low certainty evidence).
  • Discontinuation may increase MACE risk (HR: 1.12; low certainty), driven by CV hospitalizations, but not MI risk (HR: 1.39; low certainty).

Conclusions:

  • In post-MI patients with LVEF >40% and no heart failure, beta-blocker discontinuation may not elevate mortality or MI risk.
  • A potential increase in MACE, primarily due to cardiovascular hospitalizations, is associated with beta-blocker discontinuation.
  • Low certainty of evidence highlights the need for cautious interpretation of these findings.