Aortic coarctation is the fifth most common congenital heart disease. Surgical correction early in life is associated with a low surgical mortality and excellent short and mid-term outcomes. However, up to 50% of adults with a history of repaired aortic coarctation repair have hypertension at 30 to 40 years of age. The mechanism of hypertension rarely is recurrent aortic narrowing so it has been hypothesized that these patients also have systemic vascular disease, with findings from previous studies suggesting endothelial dysfunction as the culprit. These finding are refuted in a small but elegant study which has been chosen as the Editor's Choice for this issue of Heart. Dr Radke and colleagues (see page 1696) found no significant differences in endothelial function between 20 patients with a repaired aortic coarctation and 22 normal subjects based on a detailed analysis that included peripheral arterial tomographic measurement of flow-mediated vasodilation, plasma levels of inflammatory mediators and endothelial function, and numbers of circulating endothelial progenitor cells (figure 1).