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Let Prevention Douse the Flames

David A. Vorchheimer, MD; Valentin Fuster, MD,PhD

JAMA. 2001;286:2154-2156.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Atherothrombosis is increasingly recognized as a dynamic chronic inflammatory process of the vessel wall, in which phases of inflammatory and thrombotic activity underlie the clinical presentations of acute coronary syndromes (ACS).¹ There is also evolving evidence that circulating monocytes and white blood cells may be involved in a proinflammatory or prothrombotic circulatory state.^2-3 These 2 mechanisms—inflammatory involvement of the vessel wall and of the circulating blood—are not mutually exclusive, and both could occur within an individual patient. Two reports in this issue of THE JOURNAL draw attention to the inflammatory basis of coronary atherothrombotic disease.

Zhang et al⁴ examined the relationship between levels of myeloperoxidase (MPO), a leukocyte enzyme that promotes oxidation of lipoproteins in the atheroma, and the prevalence of coronary artery disease (CAD). In a carefully constructed case-control study performed among patients recruited from an outpatient clinic and a cardiac catheterization . . . [Full Text of this Article]

Author Affiliation: Zena and Michael A. Wiener Cardiovascular Institute, Mount Sinai School of Medicine, New York, NY.

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