Central Blood Pressure Physiology: A (More) Critical Analysis

To the Editor: The review—“Brachial vs. Central Systolic Pressure and Pulse Wave Transmission Indicators: A Critical Analysis”—by Dr Izzo1 provided a broad overview of physiology and clinical consequences of pulse wave transmission in the human arterial system. We contend that a “critical analysis” of literature in this field should include consideration of all plausible evidence on the physiology contributing to central pressure waveform morphology. For decades, the idea of discrete outgoing and reflected waves as the principal factor explaining the shape of the central pressure waveform has dominated literature, and this is the explanation provided in Dr Izzo’s review. However, there is substantial invasive human and animal data proving that the role of discrete wave reflection is much less than once thought and these data fundamentally challenge many assertions presented in the review. Firstly, the notion that “earlier return of the reflected wave leads to a fuller degree of summation of the forward and backward pressure waves” has been comprehensively debunked in the metaanalysis by Baksi et al. (incorporating more than 13,000 waveforms).2 This study clearly demonstrated a miniscule shift in wave reflection timing with increasing age (0.7 ms/year) despite a substantial increase in central blood pressure (BP) augmentation. Further, this work showed that the time of wave reflection always occurred within systole (never moving from diastole into systole with increasing age) and thus a view that reduced wave reflection time results in a fuller degree of central BP augmentation cannot be correct. Secondly, the idea that reflected waves “serve important physiological functions, such as aortic valve closure” opposes the seminal works of Parker et al.3 Using wave intensity analysis, it was shown that closure of the aortic valve is more likely due to late systolic forward-travelling suction waves generated by deceleration of left ventricular contraction, and not wave reflection from peripheral sites. Thirdly, although some wave reflection energy is discernable from wave intensity analysis of pressure and flow velocity in the ascending aorta, the idea that a discrete reflected wave returning from the periphery will substantially contribute to central BP augmentation is an interpretation that is not supported by evidence. Indeed, despite substantial increases in central BP resulting from pharmacological and exercise stress, reflected wave intensity remains unchanged.4,5 This is likely due to wave dispersion and peripheral entrapment rather than returning reflections contributing to central BP augmentation.6 These inconsistencies surrounding wave reflection theory provide impetus for more plausible explanations of central BP morphology.7 Pressure waveforms can be decomposed into a reservoir pressure component (contingent on aortic inflow, compliance, and resistance to outflow) and an excess pressure (consisting of incident and reflected waves). Parameters derived from this model are valid in humans,8 and when the reservoir function of the aorta is considered, the role of wave reflection contributing to central BP augmentation is substantially reduced. Reservoir and excess pressure (along with incident waves) dominate increases in central BP associated with aging and exercise5,9 and independently predict cardiovascular events and mortality (beyond traditional risk factors including Framingham risk, brachial and central BP).10 These new data extend our understanding on the underlying physiology of central BP and should be contemplated in any critical analysis of literature.