Author + information
- Adam J. Nelson, BMedSc, MBBS⁎ (, )
- Matthew I. Worthley, MBBS, PhD⁎ and
- James D. Cameron, MBBS, MD, MBE(Elec), MEngSc
- ↵⁎Cardiovascular Investigation Unit, Royal Adelaide Hospital, North Terrace, Adelaide 5000, South Australia, Australia
We refer to Hickson et al.'s (1) recent interesting report on regional differences in aortic stiffness. As they note, their results are in contrast to 3 other reports in the literature (2,3), including our own (4), raising themes that warrant further discussion. First, Hickson et al. (1) make a very important point, specifically, that aortic diameter is an important, but usually overlooked, influence on pulse wave velocity. This is particularly relevant since pulse wave velocity, despite being a surrogate marker, has become the noninvasive gold standard for assessment of arterial stiffness. Second, our study used cardiac magnetic resonance to calculate the local distensibility directly, not the pulse wave velocity, and found the predominant effect of aging was an increase in the difference between the distensibility of the ascending compared with that of the distal aorta.
Both our own and Hickson et al.'s (1) report show that ageing appears to have its predominant absolute effect in the distal descending aorta, although in our cohorts, the greatest proportional change occurred in the proximal (elastic) aorta. Hickson et al. (1) are probably correct in that changes in aortic diameter tend to compensate for primary distensibility changes, and this may be responsible for their variant results.
In this context, a serious dilemma remains as to whether distensibility (and possibly diameter changes per se) or the deranged hemodynamic effects mediated through pulse wave velocity is the important pathophysiological factor. Furthermore, the issue still remains whether this phenomenon acts either as a primary determinant of adverse outcomes or simply as a biomarker of systemic disease. The increase in ascending aortic diameter (decreasing pulse wave velocity) and increase in regional length (increasing transit time at a given pulse wave velocity) with very little change in other segments, as reported by Hickson et al. (1) (their Fig. 4), would have a significant effect on the relative timing of any reflected pressure wave within the cardiac cycle and therefore on central blood pressure. The net influence of these changes would be to delay return of any reflected wave; although these could be seen as compensatory changes, they apparently generally fail, as aging is associated with earlier (systolic) pressure augmentation. It therefore remains uncertain whether the established deleterious effect of aortic stiffening (age or disease related) is mediated by the effect of local changes in mechanics and geometry as has been suggested (5), secondary effects related to suboptimal hemodynamic coupling, or whether increased aortic stiffening is merely acting as a biomarker of a progressive systemic condition (e.g., ageing, atherosclerosis, arteriosclerosis).
The influence of aortic diameter as opposed to wave reflection and pulse wave velocity in determining cardiovascular risk have been debated, and we would suggest that the most relevant issue is how these factors are related to central blood pressure. The work by Hickson et al. (1) offers further insight into these issues and, equally relevant, highlights the potential for cardiac magnetic resonance to individualize cardiovascular risk prediction and management.
- American College of Cardiology Foundation