This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.We propose a cross-sectional study of younger patients with acute coronary syndromes (ACS) or spontaneous venous thromboembolism (VTE) and healthy controls to address 4 specific aims: 1) Investigate whether reduced CD39 activity, and increased expression of CD39 splice variant 1.5, are associated with ACS in patients with premature atherosclerosis, both in the acute and convalescent phases; 2) Evaluate relationship between CD39 activity, CD39 isoform expression, and spontaneous VTE, both in the acute and convalescent phases; 3) Determine whether, and to what degree, increased platelet reactivity is associated with spontaneous VTE, and to compare its extent to that in ACS; 4) Assess the role of blood-borne TF in premature arterial and venous thrombosis. The significance of this study is that it addresses potentially central molecules in human thromboregulation and thrombogenesis. A role for CD39 deficiency in human thrombosis would spur additional study into determinants of this reduced activity, and provide a strong rationale for testing soluble CD39 for therapeutic application. Novel therapeutic options could be opened by determining the role of blood-borne TF in the pathogenesis of premature arterial and venous thrombosis. Last, by demonstrating whether, and to what extent, platelet activation is involved in VTE, the study could re-focus research appropriately, with clear therapeutic implications.
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