Related Experiment Video

Updated: May 26, 2025

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker
08:32

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker

Published on: December 18, 2014

22.8K

A randomized controlled trial of beta-blockers effects on cardiac anxiety

Philip Leissner1, Katarina Mars2, Sophia Humphries1

  • 1Department of Women's and Children's Health, Uppsala University, Uppsala, Sweden.

General Hospital Psychiatry
|February 21, 2025
PubMed

Insights

Beta-blockers did not significantly reduce cardiac anxiety (CA) in most patients after acute myocardial infarction (AMI). However, a potential benefit was observed in those with moderate baseline CA, warranting further investigation into this specific subgroup.

Area of Science:

  • Cardiology
  • Psychiatry
  • Clinical Trials

Background:

  • Cardiac anxiety (CA) is prevalent post-acute myocardial infarction (AMI) and linked to adverse outcomes.
  • Beta-blockers are standard post-AMI care with known anxiolytic effects in psychiatric populations.
  • The impact of beta-blockers on CA in post-AMI patients with preserved cardiac function remains under-investigated.

Purpose of the Study:

  • To evaluate the efficacy of beta-blockers in reducing cardiac anxiety (CA) among patients following an acute myocardial infarction (AMI).
  • To assess both short-term and long-term effects of beta-blocker treatment on CA.
  • To explore potential differential effects based on baseline CA levels.

Main Methods:

  • A parallel-group, open-label, registry-based randomized clinical trial involving 806 patients post-AMI.
  • Cardiac Anxiety Questionnaire (CAQ) assessments at hospitalization, 6-10 weeks, and 12-14 months.
  • Intention-to-treat (ITT) analysis using multiple linear regression, with stratified analyses by baseline CA severity.

Main Results:

  • No significant treatment effect of beta-blockers on overall CA was detected at either follow-up point.
  • Stratified analysis revealed a significant reduction in CA symptoms at the 12-14 month follow-up for patients with moderate baseline CA randomized to beta-blockers (β = -0.12, P = 0.016).

Conclusions:

  • Beta-blockers demonstrated no overall efficacy in reducing cardiac anxiety in post-AMI patients with preserved cardiac function.
  • The study suggests a potential differential effect, with moderate baseline CA patients showing improvement.
  • Limitations include the lack of data on beta-blocker adherence, necessitating cautious interpretation of findings.
Abstract

Keywords:
Cardiac anxietyMyocardial infarctionRandomized controlled trialbeta-blocker

More Related Videos

Reducing State Anxiety Using Working Memory Maintenance08:17

Reducing State Anxiety Using Working Memory Maintenance

Published on: July 19, 2017

7.5K
Cardiac Stress Test Induced by Dobutamine and Monitored by Cardiac Catheterization in Mice15:45

Cardiac Stress Test Induced by Dobutamine and Monitored by Cardiac Catheterization in Mice

Published on: February 10, 2013

18.1K

Related Concept Videos

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...
522
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,...
308
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...
563
Anxiolytic Drugs: Overview01:26

Anxiolytic Drugs: Overview

Anxiolytic drugs are vital in managing anxiety disorders by effectively alleviating symptoms such as excessive fear, tachycardia, and tremors. There are several classes of anxiolytic medications, each with unique mechanisms of action and potential side effects.
Primary Types of Anxiolytic Drugs
1. Benzodiazepines:
Benzodiazepines bind to the GABA-A receptor in the brain, enhancing GABA's interaction. This action reduces neurotransmission, effectively blocking anxiety-associated limbic...
212
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...
401
Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this,...
303