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(Circulation. 2008;118:2286-2297.)
© 2008 American Heart Association, Inc.

Contemporary Reviews in Cardiovascular Medicine

Hypercoagulable States in Cardiovascular Disease

Mark Y. Chan, MD, MHS; Felicita Andreotti, MD, PhD; Richard C. Becker, MD

From Duke Clinical Research Institute (M.Y.C., R.C.B.), Durham, NC; National University Hospital (M.Y.C.), Singapore, Singapore; Institute of Cardiology (F.A.), Catholic University, Rome, Italy; and Divisions of Cardiology and Hematology (R.C.B.), Duke University School of Medicine, Durham, NC.

Correspondence to Richard C. Becker, MD, Professor of Medicine, Divisions of Cardiology and Hematology, Duke University School of Medicine, Director, Cardiovascular Thrombosis Center, Duke Clinical Research Institute, 2400 Pratt St, Terrace Level Room 0311, Durham, NC 27705.

Key Words: coagulation • platelets • thrombosis

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Certain individuals may have an abnormal propensity to develop venous or arterial thrombosis and either experience thromboembolic events relatively early in life or suffer recurring events.¹ This well-described clinical phenomenon, paralleled by familial clustering of thrombotic phenotypes, has led to a comprehensive search for inherited and acquired forms of hypercoagulability as part of the condition known as thrombophilia. Although clearly defined associations have been described for hypercoagulable states and thrombosis within the venous system, the establishment of causative or contributing roles for these same thrombophilic conditions and the occurrence of arterial thrombosis has been considerably more elusive.²

The World Health Organization/International Society of Thrombosis and Hemostasis in 1995 defined thrombophilia as an unusual tendency toward thrombosis.¹ Frequently cited features traditionally include (1) early age of onset; (2) recurrent episodes; (3) strong family history; (4) unusual, migratory, or widespread locations; and (5) severity out of proportion to any recognized stimulus. Here, we provide an updated review of hypercoagulable states in cardiovascular disease in 3 sections: (1) inherited hypercoagulable states; (2) acquired hypercoagulable states; and (3) diagnosis and management.

	Inherited Hypercoagulable States

 
Establishment of the role of pathways that lead to heritable hypercoagulable phenotypes in multifactorial disorders such as cardiovascular diseases is complicated by the inability to adequately discern the necessity and sufficiency of proposed mediators of hypercoagulability (Figure 1).² Hyperhomocysteinemia is a good example of the challenges faced.³ Elevated homocysteine levels exert numerous vasotoxic effects on the endothelium, which lead to endothelial cell dysfunction, platelet activation, and thrombus formation and an increased . . . [Full Text of this Article]

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