VEGFA and myocardial infarction: In the context of the lag in neovascularization induced by VEGF relative to the more rapid time course of myocardial infarction, and our observations of an equivalent extent of fibrosis in animals treated with vs without VEGF, the (comparatively limited) improvement in EF observed after VEGF administration (without GMT) is potentially attributable to the antiapoptotic properties of VEGF, as well as its angiogenic properties in promoting the viability and/or function of border zone cells.43–50