Figure 1. Arterial stiffness in large arteries. In a young health individual, a compliant aorta (left): 1) protects excess pulsatility caused by the intermittent left ventricular ejection and 2) exhibits a slow pulse wave velocity (PWV), allowing that reflected waves arrive to the heart during diastole, increasing diastolic coronary perfusion pressure but not after-load. Factors like aging and lifestyle increase aortic wall stiffness, leading to adverse hemodynamic consequences. Aortic stiffness leads to a rise in aortic root impedance, with consequent increase in forward wave amplitude and earlier arrival of the reflected waves to the heart. These hemodynamic changes result in adverse patterns of pulsatile load to the left ventricle during systole and a reduction in perfusion reserve (even in the absence of epicardial coronary disease). This inverse hemodynamic pattern also causes excess pulsatility in the aorta, which is preferably transferred to low-resistance beds, such as the kidney, placenta, and brain. In these organs, microvascular pressure is more directly associated with fluctuations in aortic pressure. AIx@75: augmentation index adjusted at heart rate. Source: the authors.