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(Circulation. 1998;97:1426-1427.)
© 1998 American Heart Association, Inc.

Correspondence

Factor V Leiden and Thromboembolism

Michael Walter, MD; Holger Reinecke, MD; Günter Breithardt, MD, FESC, FACC; ; Gerd Assmann, MD

Institute for Arteriosclerosis Research, Institute of Clinical Chemistry and Laboratory Medicine, Department of Cardiology and Angiology, University Hospital of Münster, Germany

Jürgen Heinrich, PhD

Community Hospital Solingen, Germany

To the Editor:

In an excellent study, Ridker et al¹ recently demonstrated that the risk of thrombosis is greatly increased when the factor V Leiden mutation and hyperhomocysteinemia, which alone are only moderate risk factors for thrombosis, occur together. As stated in the accompanying editorial by Phillips,² a potential weakness of this study is that the activity of other anticoagulant and fibrinolytic proteins was not specifically reported. We present a case of a 33-year-old man with factor V Leiden, increased plasminogen activator inhibitor 1 (PAI-1) activity, and a history of multiple thromboembolic events.

At the age of 18 years, the patient had pulmonary embolism of unknown origin when he was hospitalized for urologic surgery. At the age of 24 years, he developed a deep venous thrombosis without evidence of trauma complicated also on this occasion by pulmonary embolism. Warfarin was administered for 6 months. However, detailed investigations of the hypercoagulable state were not performed. At the age of 29 years, the patient was admitted with chest pain and acute inferior myocardial infarction diagnosed by ECG. Despite thrombolysis, the patient developed a maximum creatinine kinase level of 515 U/L with an MB fraction of 15%. Coronary angiography was performed 3 weeks after the myocardial infarction and revealed normal coronary arteries (see Figure ), suggesting that the infarction had been caused by a thrombotic occlusion and not by rupture or dissection of an atheromatous plaque. Six months after the infarction, the patient was referred to our institution for assessment of potential risk . . . [Full Text of this Article]

Paul M. Ridker, MD

Division of Cardiovascular Diseases, Brigham and Women's Hospital, Boston, Mass