LAUSR

Vascular remodeling in pulmonary hypertension (PH) causes increased ventricular afterload, resulting in right ventricular failure and high mortality.1 Afterload is the mechanical impedance imposed by the arterial tree, against which the ventricle must work to eject blood. Despite the tendency to conflate afterload with blood pressure, it cannot be reduced to a single number or variable. Instead it is more appropriately defined in terms of pressure-flow relations.2,3 See Article by Schafer et al Afterload is divided into several steady and pulsatile components, including vascular resistance, total arterial compliance, characteristic impedance, and wave reflections. Each of these has been shown to be abnormal in the pulmonary circulation in PH resulting in increased right ventricular afterload.4–8 However, abnormalities of the systemic vasculature that result in increased left ventricular (LV) afterload have been relatively understudied in PH. In this issue of Circulation: Cardiovascular Imaging , Schafer et al9 demonstrate elevated proximal aortic pulse wave velocity and other metrics of local aortic …