on February 24, 2005
Arteriosclerosis, Thrombosis, and Vascular Biology. 2005
Published online before print February 24, 2005, doi: 10.1161/01.ATV.0000160548.78317.29
Published online before print February 24, 2005, doi: 10.1161/01.ATV.0000160548.78317.29
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Submitted on December 9, 2004
Accepted on February 11, 2005
Mechanisms, Pathophysiology, and Therapy of Arterial Stiffness
Susan J. Zieman *;
From the Department of Medicine (S.J.Z., V.M., D.A.K.), Gerontology Research Center (V.M.), Cardiology Division, National Institute on Aging, Johns Hopkins Medical Institutions, Baltimore, Md.
* To whom correspondence should be addressed. E-mail: szieman{at}jhmi.edu.
Abstract--Arterial stiffness is a growing epidemic associated with increased risk of cardiovascular events, dementia, and death. Decreased compliance of the central vasculature alters arterial pressure and flow dynamics and impacts cardiac performance and coronary perfusion. This article reviews the structural, cellular, and genetic contributors to arterial stiffness, including the roles of the scaffolding proteins, extracellular matrix, inflammatory molecules, endothelial cell function, and reactive oxidant species. Additional influences of atherosclerosis, glucose regulation, chronic renal disease, salt, and changes in neurohormonal regulation are discussed. A review of the hemodynamic impact of arterial stiffness follows. A number of lifestyle changes and therapies that reduce arterial stiffness are presented, including weight loss, exercise, salt reduction, alcohol consumption, and neuroendocrine-directed therapies, such as those targeting the renin-angiotensin aldosterone system, natriuretic peptides, insulin modulators, as well as novel therapies that target advanced glycation end products.
Key words: arterial stiffness • isolated systolic hypertension • mechanisms • therapeutics • pathophysiology
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