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Richard Todd Light, MD
Vanderbilt University Nashville, Tenn

JAMA. 1986;255(14):1877.

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

To the Editor.—

The recent report by Grimm and co-workers¹ of the prognostic importance of white blood cell (WBC) count as an independent predictor of future coronary heart disease raises many interesting questions about the role WBCs, particularly granulocytes, could play in the etiology of atherosclerosis. In addition to the generation of toxic oxidation metabolites injuring endothelial cells as cited by the authors, the possible role of granulocyte proteinases warrants consideration.

Granulocytes contain abundant proteolytic enzymes including an elastase, a collagenase, and cathepsin G, a proteinase with chymotrypsinlike substrate specificity. Under normal circumstances these enzymes, when released, are rapidly and irreversibly inhibited by a group of plasma proteins that circulate in large-molar excess over enzyme concentrations. For example, ₁-proteinase inhibitor, formerly called ₁-antitrypsin, is present in plasma at concentrations of 20µM or more.² However, ₁-proteinase inhibitor, the principal inhibitor of granulocyte elastase, . . . [Full Text PDF of this Article]

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