Related Experiment Video

Updated: May 1, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

1.7K

Effect of β-blockers on platelet aggregation: a systematic review and meta-analysis

Tobias N Bonten1, Chiara E I Plaizier, Jaap-Jan D Snoep

  • 1Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands.

British Journal of Clinical Pharmacology
|April 16, 2014
PubMed

Insights

Beta-blockers significantly reduce platelet aggregation, a key factor in cardiovascular disease. Nonselective, lipophilic beta-blockers show a greater effect than selective, nonlipophilic ones.

Area of Science:

  • Cardiovascular pharmacology
  • Hemostasis and thrombosis

Background:

  • Platelets are crucial in cardiovascular disease (CVD) pathogenesis.
  • Beta-blockers are widely used for CVD prevention.
  • Beta-adrenergic receptors on platelets suggest a direct impact of beta-blockers on platelet function.

Purpose of the Study:

  • To systematically review and meta-analyze the effect of beta-blockers on platelet aggregation.
  • To clarify the magnitude of beta-blocker influence on platelet activity.

Main Methods:

  • Systematic search of MEDLINE and EMBASE databases up to April 2014.
  • Independent data extraction and risk of bias assessment by two reviewers.
  • Random-effects meta-analysis of standardized mean differences in platelet aggregation.

Main Results:

  • Beta-blockers significantly decreased platelet aggregation (SMD -0.54, P < 0.0001).
  • This represents a 13% reduction in platelet aggregation.
  • Nonselective lipophilic beta-blockers demonstrated a more pronounced reduction compared to selective nonlipophilic agents.

Conclusions:

  • Clinically utilized beta-blockers effectively reduce platelet aggregation.
  • The anti-aggregatory effect is more potent with nonselective lipophilic beta-blockers.
  • These findings may elucidate differential efficacy of beta-blockers in CVD prevention.
Abstract

Keywords:
meta-analysisplatelet aggregationβ-blockers

More Related Videos

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation09:13

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation

Published on: April 6, 2017

11.3K
Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells10:10

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells

Published on: October 27, 2009

21.5K

Related Concept Videos

Adrenergic Antagonists: Pharmacological Actions of &#946;-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...
1.8K
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
1.6K
Antihypertensive Drugs: Types of &#946;-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...
2.0K
Adrenergic Antagonists: Chemistry and Classification of &#946;-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...
1.7K
Heart Failure Drugs: &#946;-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,...
2.7K
Antihypertensive Drugs: Action of &#946;1 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,...
2.2K