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Related Concept Videos

Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.
Disturbances in Heart Rhythm01:29

Disturbances in Heart Rhythm

Arrhythmia or dysrhythmia refers to an abnormal heart rhythm caused by a defect in the heart's conduction system. It can cause the heart to beat irregularly, too quickly, or too slowly, leading to symptoms like chest pain, shortness of breath, and fainting. Factors such as stress, caffeine, alcohol, nicotine, cocaine, certain drugs, congenital defects, diseases, and electrolyte abnormalities can trigger arrhythmias.
Arrhythmias are categorized by their speed, rhythm, and origin. A slow heart...
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...
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...
Disorders of Hemostasis01:24

Disorders of Hemostasis

Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
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...

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Related Experiment Video

Updated: Jun 3, 2026

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

Platelets and cardiac arrhythmia.

Jonas S S G de Jong1, Lukas R C Dekker

  • 1Department of Cardiology, Academic Medical Center Amsterdam, Netherlands. jssgdejong@drj.nl

Frontiers in Physiology
|March 23, 2011
PubMed
Summary
This summary is machine-generated.

Platelets release substances during clot formation that can cause cardiac arrhythmias. Antiplatelet therapy may prevent sudden cardiac death by inhibiting these pro-arrhythmic platelet products.

Keywords:
arrhythmiascardiacplateletssudden deathventricular fibrillation

More Related Videos

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
09:38

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

Related Experiment Videos

Last Updated: Jun 3, 2026

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

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
09:38

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

Area of Science:

  • Cardiology
  • Biochemistry
  • Pharmacology

Background:

  • Sudden cardiac death (SCD) is a leading cause of mortality, primarily due to myocardial ischemia from coronary thrombosis.
  • Platelets play a critical role in SCD, not only through clot formation but also by releasing pro-arrhythmic substances.

Purpose of the Study:

  • To review substances released by platelets during clot formation and their arrhythmic properties.
  • To explore the mechanisms by which platelet products induce cardiac arrhythmias.
  • To discuss the anti-arrhythmic effects of antiplatelet therapy during ischemia.

Main Methods:

  • Review of scientific literature on platelet granule contents and their physiological effects.
  • Analysis of the mechanisms of action of platelet-derived substances on cardiac electrophysiology.
  • Evaluation of evidence for anti-arrhythmic effects of antiplatelet therapy.

Main Results:

  • Platelet dense core granules release serotonin, histamine, purines, and ions that can induce coronary constriction, calcium overload, and after-depolarizations.
  • Alpha-granules release thromboxanes and other arachidonic acid products affecting cardiac ion channels, and proteins that may interact with cardiomyocytes.
  • Lysosomal products have minimal arrhythmic effects; however, platelet products can increase coronary permeability, enhancing cardiomyocyte interaction.

Conclusions:

  • Platelet-derived substances, particularly from dense granules, are significant contributors to cardiac arrhythmias during ischemia.
  • Antiplatelet therapy improves survival post-myocardial infarction not only by preventing thrombosis but also by mitigating ischemia-induced arrhythmias.
  • Targeting platelet activation products offers a potential strategy for managing SCD.