Aging is associated with increased central aortic systolic pressure (CSP) and pulse pressure which are predictive of cardiovascular events. Mechanisms implicated for higher central pressures include a higher forward incident pressure wave (P1), higher augmented pressure (AP), and shorter reflected wave round trip travel time (Tr). African-Americans (AA) have more frequent and deleterious blood pressure elevation. Using applanation tonometry, we studied the association of age and CSP with P1 and AP in 900 AA subjects. Data showed that in subjects ≤50 years old, CSP was mediated by AP but not P1 or Tr, whereas in those >50, CSP was mediated by both AP and P1 and to a lesser extent by Tr. Predictive models were significant ( ) for both age groups. In conclusion, wave reflection is the primary determinant of CSP in younger AA, while in older subjects, CSP is mediated by both the magnitude and timing of wave reflection as well as aortic impedance. 1. Introduction Vascular aging and remodeling predominantly affects the large elastic arteries, with the unfavorable consequence of increased aortic stiffness and higher central systolic (CSP) and pulse pressure (PP) [1]. In recent years, it has been demonstrated that central pressures are more closely related to cardiovascular outcomes as compared to peripheral pressures [2]. Pathological changes within the arterial system lead to hemodynamic alterations that are reflected in the aortic waveform. The growing use of applanation tonometry has rejuvenated interest in the mechanisms of blood pressure elevation. Several mechanisms have been proposed for the higher central pressures observed with aging. There may be an increased forward incident pressure wave (P1), a higher augmented pressure (AP) and augmentation index (AI), and a shorter round trip travel time of the reflected wave (Tr) [3]. Aortic characteristic impedance also increases with age, thereby increasing P1. Greater AP due to increased wave reflection is the conventional explanation of why CSP increases with age, with age-related increases in aortic stiffness shortening Tr and causing the reflected wave to sum on the incident wave during systole [4–8]. Other investigators have found P1 to be the more important determinant of central pressure [9, 10]. A recent study in a large cohort of normal subjects found the contribution of AP and P1 to the CSP to vary between those younger and older than 60 years [11]. Thus, the reasons for higher CSP and PP with advancing age have not been fully clarified. African-Americans (AA) have a high prevalence of hypertension,
References
[1]
S. S. Franklin, W. Gustin, N. D. Wong et al., “Hemodynamic patterns of age-related changes in blood pressure: the Framingham Heart Study,” Circulation, vol. 96, no. 1, pp. 308–315, 1997.
[2]
B. Williams, P. S. Lacy, S. M. Thom et al., “Differential impact of blood pressure-lowering drugs on central aortic pressure and clinical outcomes: principal results of the Conduit Artery Function Evaluation (CAFE) study,” Circulation, vol. 113, no. 9, pp. 1213–1225, 2006.
[3]
R. S. Vasan, “Pathogenesis of elevated peripheral pulse pressure: some reflections and thinking forward,” Hypertension, vol. 51, no. 1, pp. 33–36, 2008.
[4]
J. P. Murgo, N. Westerhof, J. P. Giolma, and S. A. Altobelli, “Aortic input impedance in normal man: relationship to pressure wave forms,” Circulation, vol. 62, no. 1, pp. 105–116, 1980.
[5]
A. V. Chobanian, “Isolated systolic hypertension in the elderly,” The New England Journal of Medicine, vol. 357, no. 8, pp. 789–796, 2007.
[6]
W. W. Nichols and M. F. O'Rourke, McDonald's Blood Flow in Arteries, Hodder Arnold, London, UK, 5th edition, 2005.
[7]
S. Laurent, J. Cockcroft, L. Van Bortel et al., “Expert consensus document on arterial stiffness: methodological issues and clinical applications,” European Heart Journal, vol. 27, no. 21, pp. 2588–2605, 2006.
[8]
I. B. Wilkinson, H. MacCallum, P. C. Hupperetz, C. J. van Thoor, J. R. Cockcroft, and D. J. Webb, “Changes in the derived central pressure waveform and pulse pressure in response to angiotensin II and noradrenaline in man,” Journal of Physiology, vol. 530, no. 3, pp. 541–550, 2001.
[9]
G. F. Mitchell, H. Parise, E. J. Benjamin et al., “Changes in arterial stiffness and wave reflection with advancing age in healthy men and women: the Framingham Heart Study,” Hypertension, vol. 43, no. 6, pp. 1239–1245, 2004.
[10]
J. L. Izzo, “Arterial stiffness and the systolic hypertension syndrome,” Current Opinion in Cardiology, vol. 19, no. 4, pp. 341–352, 2004.
[11]
M. Namasivayam, B. J. McDonnell, C. M. McEniery, and M. F. O'Rourke, “Does wave reflection dominate age-related change in aortic blood pressure across the human life span?” Hypertension, vol. 53, no. 6, pp. 979–985, 2009.
[12]
V. E. Friedewald, S. D. Nesbitt, C. V. S. Ram, and W. C. Roberts, “Hypertension in African Americans and other non-caucasian ethnic groups,” American Journal of Cardiology, vol. 106, no. 10, pp. 1466–1472, 2010.
[13]
K. S. Heffernan, S. Y. Jae, K. R. Wilund, J. A. Woods, and B. Fernhall, “Racial differences in central blood pressure and vascular function in young men,” American Journal of Physiology—Heart and Circulatory Physiology, vol. 295, no. 6, pp. H2380–H2387, 2008.
[14]
C. M. McEniery, Yasmin, I. R. Hall, A. Qasem, I. B. Wilkinson, and J. R. Cockcroft, “Normal vascular aging: differential effects on wave reflection and aortic pulse wave velocity—the Anglo-Cardiff Collaborative Trial (ACCT),” Journal of the American College of Cardiology, vol. 46, no. 9, pp. 1753–1760, 2005.
[15]
W. Wojciechowska, J. A. Staessen, T. Nawrot et al., “Reference values in white Europeans for the arterial pulse wave recorded by means of the SphygmoCor device,” Hypertension Research, vol. 29, no. 7, pp. 475–483, 2006.
[16]
C. H. Chen, E. Nevo, B. Fetics et al., “Estimation of central aortic pressure waveform by mathematical transformation of radial tonometry pressure: validation of generalized transfer function,” Circulation, vol. 95, no. 7, pp. 1827–1836, 1997.
[17]
A. L. Pauca, M. F. O'Rourke, and N. D. Kon, “Prospective evaluation of a method for estimating ascending aortic pressure from the radial artery pressure waveform,” Hypertension, vol. 38, no. 4, pp. 932–937, 2001.
[18]
W. W. Nichols, “Clinical measurement of arterial stiffness obtained from noninvasive pressure waveforms,” American Journal of Hypertension, vol. 18, no. 1, part 2, pp. 3S–10S, 2005.
[19]
K. J. Preacher and A. F. Hayes, “Asymptotic and resampling strategies for assessing and comparing indirect effects in multiple mediator models,” Behavior Research Methods, vol. 40, no. 3, pp. 879–891, 2008.
[20]
J. A. Staessen, J. Gasowski, J. G. Wang et al., “Risks of untreated and treated isolated systolic hypertension in the elderly: meta-analysis of outcome trials,” The Lancet, vol. 355, no. 9207, pp. 865–872, 2000.
[21]
M. J. Roman, R. B. Devereux, J. R. Kizer et al., “Central pressure more strongly relates to vascular disease and outcome than does brachial pressure: the Strong Heart Study,” Hypertension, vol. 50, no. 1, pp. 197–203, 2007.
[22]
R. Pini, M. C. Cavallini, V. Palmieri et al., “Central but not brachial blood pressure predicts cardiovascular events in an unselected geriatric population,” Journal of the American College of Cardiology, vol. 51, no. 25, pp. 2432–2439, 2008.
[23]
G. F. Mitchell, P. R. Conlin, M. E. Dunlap et al., “Aortic diameter, wall stiffness, and wave reflection in systolic hypertension,” Hypertension, vol. 51, no. 1, pp. 105–111, 2008.
[24]
R. Kelly, C. Hayward, A. Avolio, and M. O'Rourke, “Nonivasive determination of age-related changes in the human arterial pulse,” Circulation, vol. 80, no. 6, pp. 1652–1659, 1989.
[25]
M. Namasivayam, A. Adji, and M. F. O'Rourke, “Aortic augmentation index and aging: mathematical resolution of a physiological dilemma?” Hypertension, vol. 56, no. 1, pp. e9–e10, 2010.
[26]
M. F. O'Rourke and J. Hashimoto, “Mechanical factors in arterial aging: a clinical perspective,” Journal of the American College of Cardiology, vol. 50, no. 1, pp. 1–13, 2007.
[27]
G. F. Mitchell, “Effects of central arterial aging on the structure and function of the peripheral vasculature: implications for end-organ damage,” Journal of Applied Physiology, vol. 105, no. 5, pp. 1652–1660, 2008.
[28]
G. M. London, “Large artery function and alterations in hypertension,” Journal of Hypertension, Supplement, vol. 13, no. 2, pp. S35–S38, 1995.
[29]
J. Hashimoto, W. W. Nichols, M. F. O'Rourke, and Y. Imai, “Association between wasted pressure effort and left ventricular hypertrophy in hypertension: influence of arterial wave reflection,” American Journal of Hypertension, vol. 21, no. 3, pp. 329–333, 2008.
