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Formation of the Platelet Plug01:22

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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...
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Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

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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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Clot Retraction and Fibrinolysis01:16

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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.
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Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

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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.
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Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

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Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
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Introduction to Hemostasis01:05

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Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
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Ferric Chloride-induced Murine Thrombosis Models
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Dual antithrombotic therapy dose-dependently alters hemostatic plug structure and function.

Christopher D Mansi1, Jenna R Severa1, Joseph N Wilhelm1

  • 1Department of Medicine, Cardeza Center for Hemostasis, Thrombosis, and Vascular Biology, Cardeza Foundation for Hematologic Research, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.

Journal of Thrombosis and Haemostasis : JTH
|December 24, 2023
PubMed
Summary

Dual antithrombotic therapy with antiplatelet and anticoagulant drugs increases bleeding risk. Combining these medications impairs hemostasis more than using either drug alone, highlighting the risks of dual antithrombotic treatment.

Keywords:
anticoagulantsfactor Xa inhibitorshemostasismultiphoton fluorescence microscopypurinergic P2Y12 receptor antagonist

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

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

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Area of Science:

  • Pharmacology
  • Hematology
  • Thrombosis Research

Background:

  • Antithrombotic medications, including anticoagulants and antiplatelets, carry bleeding risks.
  • Combining these drug classes can exacerbate bleeding.
  • Previous research indicates distinct effects of antiplatelet versus anticoagulant drugs on hemostatic plug formation in vivo.

Purpose of the Study:

  • To investigate if dual antithrombotic treatment (combined antiplatelet and anticoagulant) alters hemostatic plug structure and function differently compared to monotherapy.
  • To assess the impact of combined P2Y12 antagonist and Factor Xa inhibitor on hemostasis.

Main Methods:

  • Mice were treated with clopidogrel (P2Y12 antagonist) and rivaroxaban (Factor Xa inhibitor) alone or in combination at various doses.
  • Hemostatic response was evaluated using a mouse jugular vein puncture model.
  • Platelet accumulation, fibrin deposition, and bleeding times were quantified using multiphoton fluorescence microscopy.

Main Results:

  • Clopidogrel alone reduced platelet accumulation, prolonging bleeding only at high doses.
  • Rivaroxaban alone decreased fibrin deposition with no bleeding impact.
  • Dual therapy showed similar platelet/fibrin levels as monotherapy but impaired hemostasis at doses that were safe in isolation.

Conclusions:

  • Combined antiplatelet and anticoagulant therapy exacerbates bleeding risk compared to monotherapy.
  • This effect may stem from the combined inhibition of ADP- and thrombin-mediated platelet activation.
  • Findings improve understanding of bleeding risks associated with dual antithrombotic strategies.