Recent advances in arterial stiffness and wave reflection in human hypertension

S Laurent, P Boutouyrie - Hypertension, 2007 - Am Heart Assoc
Hypertension, 2007Am Heart Assoc
Indeed, data from the Framingham study suggest that reduced aortic diameter may play an
important role in the genesis of increased functional stiffness of the aorta. Mitchell et al13
demonstrated, in older subjects with uncomplicated systolic hypertension, that aortic
stiffness, determined by carotid-femoral PWV, was not significantly higher in hypertensives
than in normotensives after adjustment to MBP, whereas increased characteristic
impedance, calculated from the ratio of change in carotid pressure and aortic flow in early …
Indeed, data from the Framingham study suggest that reduced aortic diameter may play an important role in the genesis of increased functional stiffness of the aorta. Mitchell et al13 demonstrated, in older subjects with uncomplicated systolic hypertension, that aortic stiffness, determined by carotid-femoral PWV, was not significantly higher in hypertensives than in normotensives after adjustment to MBP, whereas increased characteristic impedance, calculated from the ratio of change in carotid pressure and aortic flow in early systole, remained highly significant. 13 Increased characteristic impedance in hypertensive men was attributable to decreased aortic effective diameter, with no difference in aortic stiffness at comparable MBP. These findings are not consistent with the hypothesis of secondary aortic degeneration, dilation, and wall stiffening. They rather suggest that reduced aortic diameter could be an initiating mechanism of systolic hypertension, leading to an impedance mismatch between ventricular ejection and large artery properties. However, aortic diameter was not directly measured in this work, 13 and these results should be confirmed by further studies. Although the role played by large artery stiffness in the generation of systolic hypertension is well accepted, the role of small artery stiffness has been less studied, particularly in humans. This is likely because of the difficulty in obtaining gluteal subcutaneous tissue from patients. The inward remodeling of resistance vessels in hypertensive patients is associated with an increased wall stiffness. 14 Wall stiffness is a limiting factor of wall strain for a given loading blood pressure. Thus, any increase in wall stiffness tends to reduce the lumen diameter for a given smooth muscle tone and blood pressure, leading to increased wave reflections and central PP, which in turn may represent a trigger for hypertrophic remodeling of small arteries. However, arterial stiffness of resistive arteries did not correlate with systolic blood pressure, media/lumen ratio, or left ventricular mass index, in hypertensive and normotensive subjects. 15 This important area remains to be further investigated. The damaging effect of local pulse pressure has been well demonstrated on large arteries, but to a lesser extent on small arteries. Elevated PP may stimulate hypertrophy, remodeling, or rarefaction in the microcirculation, leading to increased resistance to mean flow. An illustration of such pathogenic mechanism may be given by the demonstration, in the Framingham Heart Study offspring cohort, that aortic stiffness and increased pressure pulsatility were closely related with blunted microvascular reactivity to ischemic stress, in multivariable models that adjusted for cardiovascular disease risk factors. 16 However, alternative explanations include:(1) a common pathogenesis, which may explain the damage of both large and small arteries;(2) an inward remodeling and altered vasodilatation of small arteries, which may enhance wave reflections and central pulse pressure. Recent studies showed a close relationship between microvascular damage in brain and kidney and either pulse pressure or arterial stiffness. Indeed, significant and independent relationships have been demonstrated between carotid stiffness and glomerular filtration rate (GFR) in patients with mild to moderate chronic kidney disease, 17 between brachial pulse pressure and GFR in elderly patients with never-treated isolated systolic hypertension, 18 and between arterial stiffness and cognitive impairment in elderly subjects attending a geriatric outpatient clinic. 19 However, the mechanism of such association has not yet been firmly established. O’Rourke and …
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