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

Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
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...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Structure and Function of Platelets01:18

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias01:25

ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias

Arrhythmia is a condition characterized by an irregular heart rhythm, with ECG changes that differ based on its origin and nature. The types of arrhythmias discussed below include atrial, junctional, and ventricular arrhythmias.Atrial ArrhythmiasPremature Atrial Complexes (PACs): PACs are early atrial beats caused by stress, caffeine, alcohol, electrolyte imbalances, hypoxia, hyperthyroidism, or certain medications (e.g., bronchodilators and decongestants). The ECG shows early P waves with an...

You might also read

Related Articles

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

Sort by
Same author

Type 2 Diabetes: Platelets and Long-Term Metabolic Control as Estimated from Glycosylated Haemoglobin (HbA1c).

Hamostaseologie·2026
Same author

The impact of ethical implications intertwined with tuberculosis household contact investigation: a qualitative study.

medRxiv : the preprint server for health sciences·2024
Same author

Observation of Cabibbo-Suppressed Two-Body Hadronic Decays and Precision Mass Measurement of the Ω_{c}^{0} Baryon.

Physical review letters·2024
Same author

Type 2 Diabetes: Platelets and Long-Term Metabolic Control as Estimated from Glycosylated Haemoglobin (HbA1c).

Hamostaseologie·2024
Same author

Measurement of CP Violation in B^{0}→ψ(→ℓ^{+}ℓ^{-})K_{S}^{0}(→π^{+}π^{-}) Decays.

Physical review letters·2024
Same author

Observation of New Baryons in the Ξ_{b}^{-}π^{+}π^{-} and Ξ_{b}^{0}π^{+}π^{-} Systems.

Physical review letters·2023

Related Experiment Video

Updated: Jun 15, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Atrial fibrillation and platelet reactivity.

M Milovanovic1, E Fransson1, C Hallert1

  • 1Department of Internal Medicine, the Vrinnevi Hospital, Norrköping, Sweden.

International Journal of Cardiology
|March 19, 2010
PubMed
Summary

Atrial fibrillation (AF) patients showed altered platelet reactivity post-cardioversion. Those remaining in sinus rhythm (SR) had lower reactivity, while those reverting to AF exhibited higher reactivity after 26 months.

More Related Videos

Analyzing Platelet Subpopulations by Multi-color Flow Cytometry
08:04

Analyzing Platelet Subpopulations by Multi-color Flow Cytometry

Published on: June 10, 2025

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

Related Experiment Videos

Last Updated: Jun 15, 2026

Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Analyzing Platelet Subpopulations by Multi-color Flow Cytometry
08:04

Analyzing Platelet Subpopulations by Multi-color Flow Cytometry

Published on: June 10, 2025

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Clinical Research

Background:

  • The relationship between atrial fibrillation (AF) and platelet reactivity remains under-explored.
  • Investigating platelet function in AF patients is crucial for understanding thrombotic risk.

Purpose of the Study:

  • To assess the impact of electrical cardioversion (ECV) on platelet reactivity in patients with atrial fibrillation.
  • To compare platelet reactivity in patients who maintained sinus rhythm versus those who reverted to AF post-ECV.

Main Methods:

  • 33 AF patients underwent ECV; platelet reactivity was measured using flow cytometry with ADP and thrombin receptor activating peptide agonists.
  • Measurements were taken immediately before ECV and repeated after an average of 26 months.
  • Platelet surface-bound fibrinogen was determined as an indicator of platelet activation.

Main Results:

  • At 26 months, patients who reverted to AF (n=18) showed a trend towards lower platelet reactivity compared to baseline, significant with 1.7 μmol/L ADP.
  • Patients who maintained sinus rhythm (SR) (n=15) exhibited significantly lower platelet reactivity with all agonists at 26 months.
  • Crucially, patients with recurrent AF at follow-up had higher platelet reactivity than those in SR.

Conclusions:

  • Long-term sinus rhythm following cardioversion is associated with reduced platelet reactivity.
  • Recurrent atrial fibrillation after cardioversion is linked to increased platelet reactivity, suggesting a higher thrombotic risk.