Thrombophilia

Thrombophilia

Venous thromboembolism (VTE) is responsible for more than 300,000 hospital admissions per year, and resultant pulmonary embolism is a contributing factor in approximately 12% of deaths among hospitalized patients.1 Pulmonary embolus is the most common cause of death associated with childbirth and is, overall, the third most common cause of death in the United States.2 The coagulation laboratory plays a central roll in determining the cause of VTE and the risk of recurrence after an initial thrombotic event.

The risk factors associated with venous thromboembolism are different from those associated with arterial thrombosis that cause heart attack, stroke, and peripheral artery diseases.3 Venous and arterial thromboses are distinct clinical entities that differ in the microenvironment of clot formation and the structure of the clots formed.1 Because of their very distinct physiology, the tests used in the assessment of these two conditions are different.1

Arterial Thrombosis

  • Arterial thrombosis forms under conditions of accelerated blood flow.
  • It often occurs at the site of rupture of atherosclerotic plaques.
  • Arterial thrombosis is typically composed of platelet aggregates linked by thin fibrin strands.
  • Tests of platelet function and inflammatory markers associated with atherosclerosis are generally most useful in arterial thrombotic risk assessment.
  • Tests for hypercoagulability are not as useful in the assessment of arterial thrombosis.3

Venous Thrombosis

  • Venous thrombosis forms in regions of slow to moderate blood flow.
  • Generally, it is composed of a mixture of red cells, platelets, and fibrin.
  • Venous thrombosis often forms in the lower limbs.
  • Clinical manifestations are a response to obstructed blood flow at the original site of thrombosis or due to embolism of the pulmonary circulation.
  • Tests for congenital or acquired defects in the coagulation cascade or fibrinolysis are often useful in the assessment of venous thrombotic risk.3

It is generally thought that most cases of venous thrombosis result from the convergence of an acquired “precipitating” condition (ie, a cause of blood stasis or vessel injury) with an underlying genetic predisposition for hypercoagulability.3 For more than a century clinicians have understood that the risk of venous thrombosis is increased in individuals with any of three predisposing conditions − referred to as Virchow's triad:4

  1. Stasis of blood
  2. Vessel injury
  3. Hypercoagulability

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