Abstract
A growing understanding of the importance of the rupture of atherosclerotic plaque in the pathogenesis of coronary events has led to the identification of an expanding array of markers of plaque vulnerability.1,2 Reports of markers of inflammation and coronary risk are appearing with increasing frequency; such markers include adhesion molecules, metalloproteinases, and as described in this issue of the Journal, myeloperoxidase (reported by Brennan et al., pages 1595–1604) and glutathione peroxidase 1 (reported by Blankenberg et al., pages 1605–1613). What should the clinician look for in these reports to determine their implications for patient care?First, the measure should . . .