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(Hypertension. 2005;45:349.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Arterial Stiffness and Hypertension

A Two-Way Street?

From the Heart Disease Prevention Program, University of California, Irvine.

Correspondence to Dr Franklin, Heart Disease Program, C-240 Medical Sciences, University of California, Irvine, CA 92697. E-mail ssfranklinmd@earthlink.net

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

Elastic artery stiffening, an age-related process, can be accelerated in the presence of hypertension. Hypertension may produce arterial stiffening by both functional and structural mechanisms.¹ Acute and potentially reversible stiffening of the thoracic aorta and its branches occurs with an increase in arterial blood pressure (BP). Young adult hypertensive subjects have a "downstream" increase in resistance at the level of the arterioles, causing an "upstream" increase in transmural pressure at the level of the central elastic arteries; this causes weight-bearing elastic lamellae of the large arteries to stretch and become stiffer. Elevated BP over time can lead to vascular remodeling, hypertrophy, and hyperplasia—structural changes that produce intrinsic arterial stiffening. This form of hypertension in young adults typically presents with elevated diastolic BP in the subtypes of systolic–diastolic or isolated diastolic hypertension. In contrast, isolated systolic hypertension of the elderly, associated with increased systolic BP and decreased diastolic BP, typically presents with widened pulse pressure (PP) as a marker of increased arterial stiffness.^1,2 The arterial stiffness seen in elderly persons with isolated systolic hypertension is characterized by fissuring and fracturing of the elastin protein, collagen proliferation, and calcium deposition, frequently associated with a widened and torturous aorta.¹ As large arteries dilate, wall tension and pulsatile stresses increase and exacerbate artery wall degeneration, thus initiating a positive feedback whereby increased hypertension leads to further degeneration,¹

The Framingham Heart² study showed that untreated hypertension may accelerate the rate of large artery stiffness and thus perpetuate a vicious cycle of accelerated hypertension and further . . . [Full Text of this Article]

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