Fibrinolytic function and atrial fibrillation

Francisco Marín1, Vanessa Roldán, Gregory Y H Lip

  • 1Haemostasis, Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, B18 7QH, Birmingham, England, UK.

Thrombosis Research
|June 24, 2003
PubMed

Insights

Atrial fibrillation (AF) increases stroke risk due to prothrombotic states. This review examines fibrinolytic function, crucial for preventing clots, and its role in AF patients.

Area of Science:

  • Cardiology
  • Hematology
  • Thrombosis Research

Background:

  • Atrial fibrillation (AF) is a common arrhythmia linked to high stroke and thromboembolism risk.
  • Patients with AF exhibit a prothrombotic state, with research focusing on clotting factors, endothelial dysfunction, and platelets.
  • The role of fibrinolytic function in AF pathophysiology remains understudied despite its importance in preventing intravascular thrombosis.

Purpose of the Study:

  • To provide an overview of fibrinolytic function.
  • To review existing studies investigating the relationship between fibrinolytic activity and atrial fibrillation.

Main Methods:

  • Literature review of studies on fibrinolysis and AF.
  • Analysis of the role of the fibrinolytic system in cardiovascular disease.

Main Results:

  • Previous research has primarily focused on prothrombotic markers rather than the fibrinolytic system in AF.
  • Emerging evidence highlights the significance of fibrinolytic imbalance in cardiovascular diseases.

Conclusions:

  • Fibrinolytic function is a critical but less explored aspect of the hypercoagulable state in atrial fibrillation.
  • Further research into fibrinolytic activity in AF is warranted to understand its contribution to thromboembolic events.

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.
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...
Venous Thrombosis III: Interprofessional Care01:29

Venous Thrombosis III: Interprofessional Care

Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants01:18

Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants

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.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
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...
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of the heart's...