Pulse Pressure: Where, How, and Why?

If one were to consider the circulatory system in terms of a simplistic model, it consists of a discontinuous pressure generator, the heart, connected to a system of elastic tubes, the arteries. The contraction of the hollow heart muscle generates an increase in pressure and, after the aortic valve opens, this travels forward into the branching arteries as a pressure (and flow) wave. The elastic properties of the arteries are not constant throughout the circulation. They vary on account of branching, diameter tapering, or changes in the underlying elastic properties of the vessel, i.e., the fibers that compose the vessel wall. Wherever this occurs, three effects will result: (i) Some of the wave energy will reflect back to its source causing wave reflections, (ii) some wave energy will be lost (dampening), and (iii) the velocity at which the wave travels will change. The different harmonic frequency components contained in the wave will be affected in different ways.1 The net effect is a change in the harmonic wave composition from the aorta to the periphery, and this is observed as an increase in pulse pressure. Mathematically, the change in a wave between two points is described as a transfer function, containing information about the change in amplitude and phase (i.e., time delay/pulse wave velocity) for each harmonic frequency component. It has been conceded that changes in phase are sufficiently different between individuals where differences in underlying arterial properties exist. However, considerable scientific debate1,2 has ensued as to whether or not the changes in amplitude between the aorta and the radial artery can be assumed to vary so little between individuals, and irrespective of the test conditions, e.g., blood pressure, pharmacological interventions, that a single “generalized” transfer function can be used for all subjects, as proposed in the paper by Nijdam et al. in this issue of the Journal.3 Nijdam et al. measured neither aortic nor radial pulse pressure.3 The underlying assumption is that (i) harmonic amplitude transfer is constant across the population,2 (ii) mean arterial pulse pressure at the brachial artery is at two-thirds of pulse plus diastolic blood pressure, and (iii) that the behavior of diastolic and mean blood pressure is predictable throughout the circulation. Using those assumptions, they demonstrated that “pulse pressure amplification” is dependent on pulse wave velocity as well as on age, blood pressure, heart rate, height, and a number of anamnestic, biochemical, and anthropometric variables. These results are similar to those of previous studies that have shown the effect of a number of similar factors on arterial properties, as well as spurious effects on measurements,4 but have nevertheless maintained that brachial arterial pressure is the better predictor of outcome.5 Does it not seem improbable that all other arterial properties would change depending on similar variables, e.g., age and blood pressure, but that transfer functions alone would remain constant? In summary, the study by Nijdam et al. in this issue of the Journal3 casts further doubt on the underlying assumption that differences between individuals can be ignored, and that a generalized transfer function can safely be used. Most importantly, it reiterates the need for a reasonably sized study in which the parameters in question, i.e., aortic and radial blood pressure, are actually measured invasively. The author declared no conflict of interest.