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Peripheral Artery Disease: causes and consequences

Coronary Artery Disease: causes and consequences

Thrombus Formation

This section introduces haemostasis, the coagulation cascade, venous and arterial thrombi and thrombus formation

  • A thrombus can block the flow of blood through a vein or artery
  • If it detaches from the vessel wall and lodges in the lungs or other vital organs, it can become a life-threatening embolus1,2
  • The coagulation system depends on a delicate balance between:
    • Natural coagulant and anticoagulant factors
    • The coagulation and fibrinolytic system
  • A pathological thrombus forms when there is an imbalance in the blood coagulation system leading to a number of serious health conditions, including heart attacks and cardioembolic stroke in patients with AF, and VTE1,3,4
  • VTE can manifest as DVT and/or PE – two distinct but related aspects of the same disease
  • Over 150 years ago, the German pathologist Rudolph Virchow postulated that thrombus formation and propagation resulted from abnormalities in three key areas:
    • Blood flow
    • The vessel wall
    • Blood components
  • These three factors are known as Virchow’s triad5
  • The features of Virchow’s triad have now been further refined:6,7
    • Circulatory stasis – abnormalities of haemorheology and turbulence at vessel bifurcations and stenotic regions
    • Vascular wall injury – abnormalities in the endothelium, such as atherosclerosis and associated vascular inflammation
    • Hypercoagulable state – abnormalities in coagulation and fibrinolytic pathways and in platelet function associated with an increased risk of VTE and other cardiovascular diseases (including CAD and heart failure, and stroke in patients with AF)7
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Virchow’s Triad – the pathologist Rudolph Virchow was the first to describe the three main factors that predispose to thrombosis

  • Two different types of thrombus can form, which differ in composition and appearance:8
    • Arterial thrombus – typically composed of platelet aggregates (white thrombus)
    • Venous thrombus – largely consists of fibrin and red blood cells (red thrombus)
References
  • Tapson VF. Acute pulmonary embolism. N Engl J Med 2008;358:1037–1052. Return to content
  • Lyaker MR, Tulman DB, Dimitrova GT et al. Arterial embolism. Int J Crit Illn Inj Sci 2013;3:77–87. Return to content
  • Fuster V, Moreno PR, Fayad ZA et al. Atherothrombosis and high-risk plaque: part I: evolving concepts. J Am Coll Cardiol 2005;46:937–954. Return to content
  • Waldo AL. Anticoagulation: stroke prevention in patients with atrial fibrillation. Med Clin North Am 2008;92:143–159. Return to content
  • Merli GJ. Pathophysiology of venous thrombosis, thrombophilia, and the diagnosis of deep vein thrombosis-pulmonary embolism in the elderly. Clin Geriatr Med 2006;22:75–92, viii-ix. Return to content
  • Jerjes-Sanchez C. Venous and arterial thrombosis: a continuous spectrum of the same disease? Eur Heart J 2005;26:3–4. Return to content
  • Lip GYH, Blann AD. Thrombogenesis and fibrinolysis in acute coronary syndromes. Important facets of a prothrombotic or hypercoagulable state? J Am Coll Cardiol 2000;36:2044–2046. Return to content
  • Mackman N. Triggers, targets and treatments for thrombosis. Nature 2008;451:914–918. Mackman N. Triggers, targets and treatments for thrombosis. Nature 2008;451:914–918. Return to content

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