Mechanisms, pathophysiology, and therapy of arterial stiffness

Susan J. Zieman, Vojtech Melenovsky, David A Kass

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Pages (from-to)932-943
Number of pages12
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume25
Issue number5
DOIs
StatePublished - May 2005

Fingerprint

Vascular Stiffness
Salts
Natriuretic Peptides
Advanced Glycosylation End Products
Extracellular Matrix Proteins
Therapeutics
Renin-Angiotensin System
Chronic Renal Insufficiency
Oxidants
Alcohol Drinking
Compliance
Dementia
Life Style
Weight Loss
Atherosclerosis
Arterial Pressure
Endothelial Cells
Perfusion
Hemodynamics
Insulin

Keywords

  • Arterial stiffness
  • Isolated systolic hypertension
  • Mechanisms
  • Pathophysiology
  • Therapeutics

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Mechanisms, pathophysiology, and therapy of arterial stiffness. / Zieman, Susan J.; Melenovsky, Vojtech; Kass, David A.

In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 25, No. 5, 05.2005, p. 932-943.

Research output: Contribution to journalArticle

@article{551f99600adb44e3b7f0e8572c218a92,
title = "Mechanisms, pathophysiology, and therapy of arterial stiffness",
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.",
keywords = "Arterial stiffness, Isolated systolic hypertension, Mechanisms, Pathophysiology, Therapeutics",
author = "Zieman, {Susan J.} and Vojtech Melenovsky and Kass, {David A}",
year = "2005",
month = "5",
doi = "10.1161/01.ATV.0000160548.78317.29",
language = "English (US)",
volume = "25",
pages = "932--943",
journal = "Arteriosclerosis, Thrombosis, and Vascular Biology",
issn = "1079-5642",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

TY - JOUR

T1 - Mechanisms, pathophysiology, and therapy of arterial stiffness

AU - Zieman, Susan J.

AU - Melenovsky, Vojtech

AU - Kass, David A

PY - 2005/5

Y1 - 2005/5

N2 - 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.

AB - 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.

KW - Arterial stiffness

KW - Isolated systolic hypertension

KW - Mechanisms

KW - Pathophysiology

KW - Therapeutics

UR - http://www.scopus.com/inward/record.url?scp=18244373458&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=18244373458&partnerID=8YFLogxK

U2 - 10.1161/01.ATV.0000160548.78317.29

DO - 10.1161/01.ATV.0000160548.78317.29

M3 - Article

C2 - 15731494

AN - SCOPUS:18244373458

VL - 25

SP - 932

EP - 943

JO - Arteriosclerosis, Thrombosis, and Vascular Biology

JF - Arteriosclerosis, Thrombosis, and Vascular Biology

SN - 1079-5642

IS - 5

ER -