Endothelial dysfunction, the failure of vasodilatation, results from a reduction in nitric oxide bioavailability and precedes the development of atherosclerosis by many years. In post-ACS patients, the persistence of endothelial dysfunction correlates with future cardiovascular events. Structured exercise has been shown to increase endothelial function, although not all individuals demonstrate improvement. Dr Astroulakis presents the work from her PhD fellowship, exploring a potential mechanistic link between Thymidine Phosphorylase (TP), a protein implicated in the recruitment of vascular endothelial cells, exercise and alterations in endothelial function post-ACS. A clinical trial involving 40 male patients undergoing six weeks of cardiac rehabilitation post-ACS was conducted. There was marked heterogeneity in changes in endothelial function post-therapy. Those with improved endothelial function (responders) were defined by a >1.5% increase in flow mediated dilatation (FMD). A significant upregulation of serum TP was evident in responders vs non-responders.