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Hypertension. 2004;44:22-24
Published online before print June 1, 2004, doi: 10.1161/01.HYP.0000132768.19056.33
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(Hypertension. 2004;44:22.)
© 2004 American Heart Association, Inc.


Editorial Commentaries

The Dietary Sodium-Blood Pressure Plot "Stiffens"

Alexei Y. Bagrov; Edward G. Lakatta

From the Laboratory of Cardiovascular Science, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, Md.

Correspondence to E.G. Lakatta, Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, 5600 Nathan Shock Dr, Baltimore, MD 21224. E-mail LakattaE@grc.nia.nih.gov


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

Nearly 50% of our population by 65 years of age has a systolic pressure within a "risky" range, that is, has predominantly systolic hypertension (PSH),1 attributable, in part, to a reduction in large artery compliance because of an increased stiffness of the arterial wall. For a given pattern of left ventricular ejection, arterial stiffening reduces diastolic pressure and increases pulse pressure. Although increased arterial stiffness elevates pulse pressure, it is not itself sufficient to raise systolic pressure to hypertensive levels, unless accompanied by an increase in stroke volume or peripheral vascular resistance (PVR).2 Whereas the former is not increased in older persons with PSH, the latter is higher (by {approx}15% on average) than in age-matched normotensive persons.3 This mild-moderate elevation of PVR is usually unrecognized because it is not routinely assessed. The increased large artery stiffness that accompanies PSH precedes the elevation of arterial pressure to clinically defined hypertensive values,4 giving rise to the notion that this form of hypertension, at least in part, is a disease of the arterial wall. Moreover, elevated pulse wave velocity, an index of arterial stiffness, and reduced total systemic compliance, assessed by stroke volume/pulse pressure, are themselves independent predictors of future cardiovascular events, even after accounting for the effect of the concomitant increase in blood pressure.5,6

There is substantial evidence to indicate that the NaCl dependence of arterial pressure increases with advancing age and that this age effect is exaggerated in older hypertensive patients.7 In this issue of Hypertension, Gates et al8 add . . . [Full Text of this Article]




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