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(Circulation. 2004;110:e37-e38.)
© 2004 American Heart Association, Inc.

Correspondence

Katharina Schroecksnadel, MD; Barbara Frick, PhD; Dietmar Fuchs, PhD

Institute of Medical Chemistry and Biochemistry, Medical University of Innsbruck, Innsbruck, Austria

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

To the Editor:

With great interest we read the article by Zylberstein and coworkers,¹ in which the authors conclude that homocysteine is an independent risk factor for myocardial infarction, in particular fatal myocardial infarction in middle-aged women. Follow-up investigations, especially long-term follow-up studies, are certainly better suited to assess the role of homocysteine in the pathogenesis of disease. However, the question of whether homocysteine itself is responsible for disease progression in vascular diseases is not yet answered; a causality between moderate hyperhomocysteinemia and atherogenesis remains to be demonstrated. This point is also discussed by the authors,¹ whereas the point that homocysteine is an independent risk factor for myocardial infarction and vascular disease requires some comment.

In studies focusing on patients with coronary heart disease, neurodegenerative diseases, and autoimmune disease, we found that moderate hyperhomocysteinemia closely correlates with increased cellular immune activation.² Moreover, in vitro production of homocysteine was found in peripheral blood mononuclear cells on stimulation with mitogens.³ These results point to a role of immune activation in the development of moderate hyperhomocysteinemia. Inflammation and cellular immune activation are crucially involved in atherogenesis⁴ and are also established as confounding risk factors for vascular diseases. A link between the pathogenesis of moderate hyperhomocysteinemia and the immunopathogenesis of atherosclerosis is very likely and would take together both concepts. Both events could relate to the overwhelming production of reactive oxygen species by activated macrophages within cellular immune activation. Antioxidants are depleted and oxidative stress develops. Decreased concentrations of antioxidants and vitamins are often . . . [Full Text of this Article]

Dimitri Edin Zylberstein, MD; Calle Bengtsson, MD, PhD; Cecilia Björkelund, MD, PhD; Valter Sundh, BSc; Dag Thelle, MD, PhD; Lauren Lissner, PhD

Sahlgrenska Academy, Göteborg University, Göteborg, Sweden

Sverre Landaas, MD, PhD

Department of Laboratory Medicine, Ullevål University Hospital, Oslo University, Oslo, Norway