are favorably affected by estrogen therapy. Moreover, estrogen inhibits intimal hyperplasia and smooth muscle migration, promotes angiogenesis, and has antioxidant properties. However, HRT increases C-reactive protein levels, which suggests a possible proinflammatory effect. 6 Increases in factor VII, prothrombin fragments 1 and 2, and activated protein C resistance and a decrease in antithrombin III are also seen. 5 Although these effects might adversely affect the development of CVD, the clinical relevance of the impact of HRT on these markers is not known. In general, the majority of surrogate end-point data support a positive role of ERT/HRT in the prevention of CVD, although enhanced CVD risk is also biologically plausible.