There is increasing evidence to implicate inflammation as an important precursor of endothelial dysfunction. This mechanistic link is apparent across the entire spectrum of inflammatory status, i.e. endothelial function is apparent following acute infection, and in subjects with chronic high-grade inflammation and, perhaps most importantly, persistent low-grade inflammation. The recognition of this relationship has present therapeutic ramifications, but also requires that future longitudinal studies determining the predictive ability of endothelial function measures for vascular events should incorporate markers of inflammation as potential confounders. In this issue of Clinical Science, Fichtlscherer and co-workers describe a link between endothelial function and sPLA2 (secretory non-pancreatic type II phospholipase A2) serum activity.

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