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(Circulation. 1997;95:1749-1751.)
© 1997 American Heart Association, Inc.

Articles

Interrelated Risk Factors for Venous Thromboembolism

Martin D. Phillips, MD

the Division of Hematology, University of Texas–Houston.

Correspondence to Martin D. Phillips, MD, Division of Hematology, University of Texas–Houston, 6431 Fannin St, Room 5.278 MSB, Houston, TX 77030. E-mail martinp@heart.med.uth.tmc.edu

Key Words: Editorials • homocysteine • risk factors • thrombosis, venous • activated protein C resistance

	Introduction

 
The concept of multiple risk factors interacting to cause arterial thrombotic disease is well established. Conversely, venous thrombotic events are often described as discrete events, even though many of the known risk factors for venous thrombosis are lifelong. In most cases, it remains enigmatic why any particular thrombosis occurs. Unanswered questions include why there is often a 30- or 40-year lag before the first thrombosis in many patients with documented congenital hypercoagulable states. Why do first-degree relatives of affected patients who share the defective gene generally have only a 50% lifetime risk of developing thrombosis?

In part, the answers to these questions are that several factors, congenital and acquired, must operate in concert to defeat the redundancy of antithrombotic mechanisms. An article in this issue of Circulation¹ demonstrates an interaction of two such risk factors: activated protein C resistance and moderate hyperhomocyst(e)inemia. Alone, each factor carries a modest risk of thrombosis. Together, they exponentially increase the probability of thrombosis. In addition, unlike the previously described risk factors, homocyst(e)inemia is potentially treatable.

Both of these mechanisms that contribute to the development of venous thrombosis have been described recently. The first is factor V Leiden, the cause of most cases of resistance to activated protein C.² This point mutation in the factor V molecule greatly decreases the rate of inactivation of factor Va by activated protein C.³ The factor V Leiden point mutation does not alter the plasma concentration or coagulant activity of factor V but only stabilizes it against proteolytic inactivation. . . . [Full Text of this Article]

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