This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Cattaneo, M. Articles by Ridker, P. M. Search for Related Content PubMed PubMed Citation Articles by Cattaneo, M. Articles by Ridker, P. M.

(Circulation. 1998;97:295-296.)
© 1998 American Heart Association, Inc.

Correspondence

Interrelation of Hyperhomocyst(e)inemia, Factor V Leiden, and Risk of Future Venous Thromboembolism

Marco Cattaneo; Maria Luisa Monzani; Ida Martinelli; Cristina Rosario Falcon; ; Pier Mannuccio Mannucci

A. Bianchi Bonomi Hemophilia and Thrombosis Center, IRCCS Ospedale Maggiore, University of Milano, Milano, Italy

To the Editor:

In their large, prospective cohort study published in the April 1, 1997 issue of Circulation,¹ Ridker et al showed that hyperhomocysteinemia is a risk factor for venous thromboembolism (VTE) only when it coexists with factor V Leiden, which is responsible for most cases of resistance to activated protein C. Hyperhomocysteinemia alone did not increase the risk of any VTE, although it tended to increase the risk of idiopathic VTE (P=.06). These important findings are in partial disagreement with those of previous case-control studies, which demonstrated an increased prevalence of hyperhomocysteinemia in patients with any VTE and which demonstrated that the association between hyperhomocysteinemia and any VTE was independent of the coexistence of activated protein C resistance² or factor V Leiden.³ There are at least three possible explanations for these contrasting results: (1) Hyperhomocysteinemia is a consequence, rather than a risk factor, of VTE. Although this explanation can account for divergences in results of case-control studies and prospective cohort studies, it should be rejected, because Ridker et al showed in their prospective cohort study that hyperhomocysteinemia increases the risk of VTE in subjects with factor V Leiden. (2) The association between hyperhomocysteinemia and VTE is stronger in women than in men, as shown by den Heijer et al.³ If confirmed by further studies, this sex difference could account for the negative results of the study by Ridker et al, which included only men. (3) The inclusion of patients with cancer, which is a very strong . . . [Full Text of this Article]

Paul M. Ridker, MD

Brigham and Women's' Hospital, Harvard Medical School, Boston, Mass