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Among treated patients with LDL-C levels of 1.8 mmol/l (70 mg/dl) or higher and hsCRP levels of 2 mg/l or higher, the risk of recurrent MI of CHD death was 4.6 per 100 person-years, and 2.4 per 100 person-years for patients with LDL-C levels [http://www.selleckchem.com/products/abt-199.html learn more] inflammatory protein in the inflammatory cascade and a more specific target of therapy (7). Median secretory PLA2 and hsCRP levels were [http://www.selleckchem.com/products/ABT-263.html Selleck Navitoclax] elevated at baseline in both treatment groups, but the levels of these inflammatory proteins were even higher among those subjects who had a secondary event during the course of the study: sPLA2 23.9 pmol/l versus 26.9 pmol/l, and hsCRP 8.6 mg/l versus 16.5 mg/l, respectively. Of the various sPLA2 isoenzymes, sPLA2-IIA is an acute phase reactant [http://en.wikipedia.org/wiki/Bumetanide Bumetanide] expressed in arterial smooth muscle cells and hepatocytes that activates transcription factors that induce synthesis of proinflammatory cytokines such as tumor necrosis factor-��, IL-1��, and IL-6 (8). These proinflammatory cytokines induce hepatic and myocardial CRP. We observed an increase in sPLA2-IIA levels in ACS patients that preceded the rise in hsCRP levels. These temporal differences in inflammatory markers are inconsistent with the earlier activation of sPLA2 from leukocytes after acute tissue injury than is observed from hepatic synthesis of CRP evident 48 to 72 h after an acute event (39). In this trial, varespladib reduced acute phase mediated increases in sPLA2-IIA concentrations. As on-trial sPLA2-IIA levels were highest among subjects with recurrent major cardiovascular events, these data are consistent with the prognostic significance of elevated sPLA2-IIA levels shown in ACS patients (15?and?16). Another phospholipase A2 inhibitor under clinical investigation is lipoprotein-associated phospholipase A2 (Lp-PLA2) (7). The Lp-PLA2 inhibitor represents a calcium-independent phospholipase that is predominantly synthesized by macrophages. In plasma, Lp-PLA2 is bound to LDL and high-density lipoprotein, with a greater affinity for the polar surface of LDL particles, particularly electronegative small LDL particles that have been minimally oxidatively modified.