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(Hypertension. 2004;44:257.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

Hypertension: A Novel Regulator of Adaptive Immunity in Atherosclerosis?

From INSERM U541, Hôspital Lariboisière, Paris, France.

Correspondence to Alain Tedgui, PhD, INSERM U541, 41, Bd de la Chapelle, 75010 Paris, France. E-mail tedgui@larib.inserm.fr

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

Epidemiological investigations clearly pointed out that hypertension is a powerful cardiovascular risk factor. Elevated blood pressure levels have been found to be highly predictive of cardiovascular events, including ischemic coronary disease, stroke, and peripheral arterial disease.¹ These ischemic cardiovascular events have a predominant vascular origin resulting from atherosclerosis.

Hypertension is known to act on the arterial wall to promote both vascular remodeling and atherosclerosis, resulting in diminished arterial wall compliance and elevated stiffness. Clinical and experimental investigations have shown that increased blood pressure is associated with exaggerated atherosclerosis. In human subjects, carotid artery intima-media thickness, measured with high-resolution B-mode ultrasound, is highly correlated with blood pressure levels and well-reflects atherosclerosis and tracks its progression.² Previous experimental studies have demonstrated that hypertension increases the rate of atherosclerotic plaque development in hypercholesterolemic rabbits,³ monkeys,⁴ and more recently in mouse models of atherosclerosis.⁵

Several mechanisms can account for hypertension-induced atherosclerosis. Pressure-induced stretch of the wall increases endothelial permeability to low-density lipoprotein and accentuates low-density lipoprotein accumulation in the intima, which is central to the atherogenic process.⁶ Hypertension also promotes or aggravates endothelial dysfunction, and our current understanding of the pathobiology of atherosclerosis suggests that alterations of endothelial function play a pivotal role in the development and progression of atherosclerosis and its clinical complications.⁷ Monocyte adhesion, an early hallmark of atherosclerosis, is enhanced by hypertension.⁸ Finally, inflammation associated to hypertension is of particular relevance to atherosclerosis, because it is well-accepted that atherosclerosis is an inflammatory disease of the arterial wall where interactions between vascular . . . [Full Text of this Article]