Changes in wave reflection with advancing age in normal subjects.

Changes in Wave Reflection With Advancing Age in Normal Subjects To the Editor: From their study of a small selected group (521 of 2640 persons) within the Framingham cohort, Mitchell et al1 conclude that increase in central aortic stiffness rather than wave reflection is responsible for the increase in pulse pressure with advancing age in healthy men and women. The authors state that changes in wave reflection with advancing age are consistent with the hypothesis that a marked increase in elastic artery pulse wave velocity (PWV) with little change in muscular artery PWV leads to impedance matching between central aorta and proximal muscular arteries, which reduces proximal wave reflection and shifts reflecting sites distally. This view runs counter to classic studies that say the characteristic feature of the pressure pulse waveform with aging is attributable to early wave reflection resulting from increased elastic artery PWV and shifts of reflecting sites closer to (not further from) the heart.2 Mitchell’s calculation of reflection wave transit time (RWTT) was based on identification of an inflection point (or foot of the reflected wave) on the rising limb of the carotid pressure wave. RWTT duration (129 SD28 ms) was consistently lower than time to the end of systole (312 to 320 ms). Yet the authors acknowledged in young adults the “reflected pressure wave arriving centrally during diastole,” that is, more than 300 ms after the wave foot and some 200 ms and 6 standard deviations after their calculated RWTT! Were there no young adults in this study? The average value of RWTT found by Mitchell et al (129 ms) was considerably higher than the mean of 102 to 116 ms found by us in a normal cohort.3 Also, in their study, there was no change in RWTT from the mid-50s to the mid-60s, then RWTT decreased in males but increased in females. In most older subjects ( 60 years), especially females (because they are shorter), there is no visible reflected wave foot or inflection point on the pressure wave, because the forward wave and the reflected wave blend (merge) together. We have pointed out the problems in identification of the reflected wave onset2,3 and in calculation of augmentation, which depends on pressure at this point in time. Mitchell’s calculations of augmentation index, forward and reflected pressure wave amplitudes, and averaged distance to wave reflection site are based on inflection point identification, and hence are suspect. The consistency of their calculations (with unprecedented correlation coefficients between 0.968 to 0.999) denote similarity in identification but not necessarily accuracy in identifying features of the reflected wave. We have been unable to achieve such consistency. Mitchell et al conclude that the major aging change in arteries is a consequence of increased aortic stiffness with wave reflection unchanged or decreased. We agree with the former statement but not the latter. Apparent decrease in wave reflection with age was not seen by Mitchell in men, and shown only for women 60-years-old, and statistical significance was not apparent over the full age range studied (authors’ Figure 3).1 Conclusions are at odds not only with Kelly’s detailed study in 1000 normal subjects3 but with the older sphygmographic studies of Marey, Mahomed, Broadbent, and Mackenzie and clinical teachings of Osler, all of which showed that aging in humans is characterized by increased amplitude of the secondary systolic pressure wave, which we now recognize as caused by exaggerated early wave reflection from the lower body.2,3 Michael F. O’Rourke University of New South Wales/VCCRI St. Vincent’s Clinic Sydney, Australia