From Arterial Stiffness to Heart Failure: Still a Long Way to Go.

A rterial stiffness has re-emerged over the past 20 years as an important predictor of cardiovascular outcomes. However, the evidence on the role of arterial stiffness in the development of heart failure (HF) is limited to 2 large studies with some conflicting resulting. Furthermore, both studies lack the distinction between HF phenotypes, which could be associated differently with arterial stiffness. Thus, it is particularly pleasing to see new data on this topic from the Framingham Heart Study 4 in this issue of the Journal of the American Heart Association. Arterial stiffness is the hallmark of arterial aging. Several measurements for quantifying arterial stiffness have been proposed, which are summarized in Figure. Carotid–femoral pulse-wave velocity (PWV) is the reference measurement of arterial stiffness, and it is calculated by measuring the time taken for the pressure wave to travel the distance between the carotid and the femoral artery, which is generally measured over the body surface. Timing is obtained by measuring the interval between the foot of the carotid and the femoral waveforms taken with a tonometer. Parameters generally referred to as arterial wave reflection are instead estimated by placing a tonometer on the surface of a peripheral vessel (ideally the radial artery) and applying mathematical processes to predict the waveform in the more proximal aortic circulation. The derived aortic pressure waveform is the result of a forward-traveling pressure wave (Pf), generated by left ventricular (LV) ejection, and a backward-traveling reflected pressure wave (Pb), generated by peripheral vascular resistance, vessels tapering, and bifurcations (Figure). These 2 components can be separated by simultaneously measuring the aortic flow waveform with echocardiography, or assuming a “triangular” aortic flow waveform (ie, pseudoflow) through the identification of the inflection point (ie, the point visible on the upward part of the aortic pressure waveform that corresponds to the foot of the backward-reflected pressure wave). Augmented pressure above the inflection point is assessed subtracting Pf from central pulse pressure, and augmentation index (AI) estimated as augmented pressure expressed as a percentage of the central pulse pressure. The reflection magnitude instead is the ratio of the magnitudes of the backward wave and the forward wave (Pb/Pf). From a physiological standpoint, the stiffer the arterial system, the higher the PWV, and the faster the reflected pressure wave returns from the periphery to the proximal aorta, adding earlier to the forward wave and eventually reaching the heart at systole instead of diastole, thus causing (1) augmentation of central systolic blood pressure increasing cardiac loading, and (2) reduction of central diastolic blood pressure decreasing coronary perfusion. Several studies linked PWV and indexes of wave reflection with LV dysfunction, which constituted the background for investigating their potential contribution to the development of HF. In an earlier analysis of 2844 participants of the Health Aging and Body Composition study (mean age 74 3 years, 48% men, 26% prevalent cardiovascular disease [CVD], median follow-up 4.6 years), Sutton-Tyrrell and colleagues failed to demonstrate an association of PWV with incident HF (n=181, 6.4%). However, it is worth noting that in this study, PWV was measured using the foot of the Doppler flow wave instead of the pressure wave, whose identification may be more challenging. More recently, in 5960 participants of the Multi-Ethnic Study of Atherosclerosis study (mean age 62 years, 48% men, no prevalent CVD, median follow-up 7.6 years), Chirinos and colleagues demonstrated an independent association between reflection magnitude and incident HF (n=104, 1.7%). On the contrary, AI and pulse pressure amplification were not associated with incident HF after multivariate adjustments. In this issue of the Journal of the American Heart Association, Tsao and colleagues aimed at examining the association between arterial stiffness and incident HF with a The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association. From the Cardiovascular Unit, Department of Internal Medicine, University of Genova, Italy (M.C.); Intramural Research Program, National Institute on Aging, NIH, Baltimore, MD (M.C., M.A.). Correspondence to: Marco Canepa, MD, PhD, Cardiovascular Unit, Department of Internal Medicine, IRCCS-AOU San Martino-IST, University of Genova, Viale Benedetto XV, 6, 16132 Genova, Italy. E-mail: [email protected] J Am Heart Assoc. 2015;4:e002807 doi: 10.1161/JAHA.115.002807. a 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.