Killing Me Unsoftly

The aorta, as the major conduit artery of the human body, is primarily thought of as a blood vessel that provides a low-resistance path for blood flow directed from the heart to peripheral organs and tissues. However, the aorta has another central hemodynamic function, whereby the elastic nature of the aortic wall provides a significant biomechanical buffering capacity complementing the pulsatile cardiac blood flow, and this is often referred to as Windkessel function. In systole, the compliant aortic wall stretches to accommodate the bolus of blood ejected by the left ventricle, thereby dampening an increase in systolic arterial pressure (SAP). In diastole, the aortic wall’s elastic recoil enables continued aortic blood flow and limits the diastolic drop in arterial pressure. As a consequence, stiffening of the arterial wall—that is, the loss of Windkessel properties—leads to fundamental alterations in central hemodynamics, with widespread detrimental implications for organ function. In this Recent Highlights article, we describe recent contributions in ATVB that have highlighted the novel mechanisms and consequences of arterial stiffness, the relevance to clinical conditions, and recent advancements in the field (Figure).