Various models and derived measures of arterial function have been proposed to describe and quantify pulsatile hemodynamics in humans. A major distinction can be drawn between lumped models based on circuit theory that assume infinite pulse wave velocity versus distributed, propagative models based on transmission line theory that acknowledge finite wave velocity and account for delays, wave reflection, and spatial and temporal pressure gradients within the arterial system. Although both approaches have produced useful insights into human arterial pathophysiology, there are important limitations of the lumped approach. The arterial system is heterogeneous and various segments respond differently to cardiovascular disease risk factors including advancing age. Lumping divergent change into aggregate summary variables can obscure abnormalities in regional arterial function. Analysis of a limited number of summary variables obtained by measuring aortic input impedance may provide novel insights and inform development of new treatments aimed at preventing or reversing abnormal pulsatile hemodynamics.
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