The risk of developing heart disease is determined not only by our genes, but also by the state of the intrauterine environment that we experience before birth. Fetal hypoxia is a common complication of pregnancy and is responsible for programming cardiac and endothelial dysfunction in offspring in later life. The mechanisms by which this happens remain elusive, preventing the identification of potential therapy.

 Research carried out by speaker Dino Giussani has led to the hypothesis that oxidative stress in the fetal heart and vasculature underlies how prenatal hypoxia programmes cardiac dysfunction in later life. His talk will detail the physiology underlying this hypothesis, what he has discovered, and how these can be applied to modify the risk of heart disease not only in our children but also in further generations.