The cellular and extracellular matrix accumulations that comprise the lesions of atherosclerosis are driven by local release of cytokines at sites of predilection for lesion formation, and by the specific attraction and activation of cells expressing rece
it may no longer be enough to measure just HDL levels without determining levels of paroxonase and platelet-activating acetylhydrolase; levels of these enzymes may determine whether HDL is proinflammatory or protective. Likewise, measuring Lp(a) and small
