Related Experiment Video

Updated: Feb 19, 2026

Combined Near-infrared Fluorescent Imaging and Micro-computed Tomography for Directly Visualizing Cerebral Thromboemboli
13:10

Combined Near-infrared Fluorescent Imaging and Micro-computed Tomography for Directly Visualizing Cerebral Thromboemboli

Published on: September 25, 2016

10.4K

[Involvement of thrombophilia in coronary thrombosis]

C Bal Dit Sollier1, L Drouet1

  • 1CREATIF (centre de référence et d'éducation aux antithrombotiques d'Île-de-France), service de cardiologie, hôpital Lariboisière, 2, rue Ambroise-Paré, 75010 Paris, France.

Annales De Cardiologie Et D'Angeiologie
|November 4, 2017
PubMed

Insights

This review explores thrombophilia, examining classical and exceptional factors contributing to both venous and arterial thrombosis, particularly coronary thrombosis. It highlights specific arterial thrombophilia like homocystein and serotonin, and includes conditions such as cancer and inflammation.

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Pathophysiology

Background:

  • Thrombophilia encompasses conditions predisposing to thrombosis.
  • Classical thrombophilia is primarily associated with venous pathology.
  • Arterial thrombosis, especially coronary thrombosis, requires understanding specific thrombotic factors.

Purpose of the Study:

  • To review classical and exceptional thrombophilia in the context of coronary thrombosis.
  • To identify thrombophilic factors relevant to arterial versus venous pathology.
  • To explore the role of specific agents like homocystein and serotonin in arterial thrombosis.

Main Methods:

  • Literature review of thrombophilia and thrombosis.
  • Analysis of classical and exceptional thrombophilic conditions.
  • Examination of specific arterial thrombotic factors and associated conditions.

Main Results:

  • Classical thrombophilia can be relevant to coronary thrombosis.
  • Exceptional thrombophilias contribute to both venous and arterial thrombosis.
  • Homocystein and serotonin are identified as specific arterial thrombotic agents, with homocystein also causing arterial wall lesions and serotonin inducing coronary spasm.
  • Cancer and inflammatory conditions are recognized as thrombophilic states.

Conclusions:

  • Understanding diverse thrombophilia is crucial for managing arterial thrombosis, including coronary events.
  • Specific factors like homocystein and serotonin warrant attention in arterial thrombotic disease.
  • Thrombophilic conditions such as cancer and inflammation are integral to the broader scope of thrombophilia.

Keywords:
Acute coronary syndromeCardiovascular risk factorsCoagulationCoronary thrombosisFacteurs de risque cardiovasculaireInfartus du myocardeMyocardial infarctionSyndrome coronarien aiguThrombophiliaThrombophilie ;Thrombose coronaire

More Related Videos

Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel07:26

Ferric Chloride-induced Thrombosis Mouse Model on Carotid Artery and Mesentery Vessel

Published on: June 29, 2015

18.8K
Ferric Chloride-induced Murine Thrombosis Models10:37

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

23.3K

Related Concept Videos

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...
2.0K
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...
13.7K
Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
519
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
646
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.
2.4K
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.
9.4K