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Background  The hemodynamic basis for increased pulse pressure ( PP ) with aging remains controversial. The classic paradigm attributes a predominant role to increased pulse wave velocity ( PWV ) and premature wave reflections ( WR s). A controversial new paradigm proposes increased forward pressure wave amplitude ( FWA ), attributed to proximal aortic characteristic impedance (Z c ), as the predominant factor, with minor contributions from  WR s. Based on theoretical considerations, we hypothesized that (rectified)  WR s drive the increase in  FWA , and that the forward pressure wave does not depend solely on the interaction between flow and Z c  ( QZ c product).    Methods and Results  We performed 3 substudies: (1) open‐chest anesthetized dog experiments (n=5); (2) asymmetric T‐tube model‐based study; and (3) human study in a diverse clinical population (n=193). Animal experiments demonstrated that  FWA  corresponds to peak  QZ c only when  WR s are minimal. As  WR s increased,  FWA  was systematically greater than  QZ c and peaked well after peak flow, analogous to late‐systolic peaking of pressure attributable to  WR s. T‐tube modeling confirmed that increased/premature  WR s resulted in increased  FWA . Magnitude and timing of  WR s explained 80.8% and 74.3% of the variability in the difference between  FWA  and peak  QZ c in dog and human substudies, respectively.    Conclusions  Only in cases of minimal reflections does  FWA  primarily reveal the interaction between peak aortic flow and proximal aortic diameter/stiffness.  FWA  is strongly dependent on rectified reflections. If interpreted out of context with the hemodynamic principles of its derivation, the  FWA  paradigm inappropriately amplifies the role of the proximal aorta in elevation of  FWA  and PP.

Misinterpretation of the Determinants of Elevated Forward Wave Amplitude Inflates the Role of the Proximal Aorta