Prothrombotic fibrin clot phenotype as a risk factor for persistent left ventricular thrombus following acute

Krystian Mróz1, Elżbieta Paszek2, Maciej Polak3

  • 1Clinical Department of Interventional Cardiology, St. John Paul II Hospital, Kraków, Poland.

Insights

Dense, poorly lysable fibrin clots are linked to anticoagulation failure in ST-segment elevation myocardial infarction (MI) patients with left ventricular thrombus (LVT). These prothrombotic clot properties may be associated with NETosis, impacting treatment outcomes.

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Biochemistry

Background:

  • Left ventricular thrombus (LVT) affects up to 15% of ST-segment elevation myocardial infarction (MI) patients.
  • LVT can persist in 30% of patients despite anticoagulation therapy.
  • Dense, poorly lysable fibrin clots are hypothesized to contribute to LVT persistence.

Purpose of the Study:

  • To investigate if unfavorable fibrin clot properties are associated with LVT resolution.
  • To identify determinants of these fibrin clot properties in MI patients.

Main Methods:

  • 149 patients with LVT post-MI were studied.
  • Fibrin clot permeability (Ks), clot lysis time (CLT), plasminogen activator inhibitor-1 (PAI-1), and citrullinated histone H3 (citH3) were measured.
  • LVT resolution was assessed at 3 and 6 months after MI.

Main Results:

  • Patients with persistent LVT at 3 months had lower Ks, longer CLT, and higher PAI-1 and citH3 levels.
  • Persistent LVT at 6 months also showed an unfavorable clot phenotype.
  • Lower Ks and longer CLT were independently associated with LVT persistence.

Conclusions:

  • Prothrombotic fibrin clot properties are associated with anticoagulation failure in LVT complicating acute MI.
  • Enhanced NETosis may contribute to these unfavorable clot properties.
  • This finding is the first to link clot phenotype to treatment resistance in LVT.
Abstract

Related Concept Videos

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.
4.9K
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...
652
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...
5.3K
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.
740
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
6.5K
Coagulation01:09

Coagulation

The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
5.6K