There has been a long tradition of assuming that changes in brachial cuff BP are similar to those at the heart or in peripheral target organs. As discussed, this is simply not the case due to intra- and interindividual differences in forward wave transmission and wave reflection [45, 46]. Differences in systolic BP from one site to another can be traced to alterations in the timing and amplitude of the forward and reflected pressure waves (fig. 3). Unlike diastolic or mean BP, systolic BP is thus not constant throughout the arterial tree. Within an individual, smaller distal arteries have higher input impedances than large central arteries because of the combined impact of decreasing lumen diameter and increasing effective wall stiffness. This increasing arterial stiffness gradient leads to the phenomenon of true pulse pressure amplification (PPA), where the amplitude of the forward wave increases within large and medium-sized arteries, so that systolic BP is normally higher in the peripheral arteries than in the aorta. PPA is variable between individuals but follows certain rules . With normal aging, there is a reversal of the normal tendency for distal arterial stiffness (PWV) to exceed central arterial stiffness, a phenomenon that would be expected to lower the degree of PPA observed . Muscular conduit arteries (e.g. brachial or femoral arteries) in hypertension do not usually differ from normal arteries in their stiffness, probably due in large measure to the fact that they also dilate with age, presumably by the same pressure-dependent mechanisms that affect the aorta . Age-adjusted compliance of conduit arteries is also higher in hypertension compared to normals, another result of the generalized increase in arterial diameter.
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