title: Is vascular stiffness a target for therapy?
abstract: BACKGROUND
  Early cardiovascular disease starts in the endothelium leading to functional changes in the vasculature. These changes can be depicted by assessment of arterial stiffness or elasticity. There are several techniques to assess arterial stiffness. Increased arterial stiffness or decreased arterial elasticity has been associated with cardiovascular risk factors. There is now evidence that small artery elasticity is a strong predictor for arterial hypertension. Moreover arterial elasticity provides extra prognostic information beyond arterial blood pressure measurement. Arterial stiffness attenuation may reflect the true reduction of arterial wall damage.
  
  
  RESULTS
  ACE-inhibitors, angiotensin II receptor blockers, aldosterone antagonists and calcium antagonists have favorable effects in improving arterial elasticity, while beta-blockers have an inverse effect. Diuretics have not been evaluated. Lipid lowering therapy, some antidiabetic therapy have shown to reduce arterial stiffness. Inflammatory and infectious diseases have been associated with vascular inflammation and consequently increase in arterial stiffness. The effect of anti-inflammatory agents and antiretroviral therapy on arterial stiffness is under investigation.
  
  
  CONCLUSIONS
  Measurement of arterial stiffness will not only be helpful in the detection of early vascular disease but also as a tool in the selection and follow-up monitoring of therapeutic strategies aimed at preventing or delaying progression of vascular disease.
authors.affiliation: Cardiovascular Division, Medical School, University of Minnesota, VCRC Room 270, 420 Delaware St SE, MMC 508, Minneapolis, MN 55455, USA. dupre007@umn.edu
authors.forename: Daniel A
authors.initials: DA
authors.lastname: Duprez
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D057911:Angiotensin Receptor Antagonists / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D001158:Arteries / Q000737:chemistry / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology; D001167:Arteritis / Q000188:drug therapy / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002318:Cardiovascular Diseases / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control*; D003141:Communicable Diseases / Q000150:complications; D042241:Early Diagnosis; D004548:Elasticity / Q000187:drug effects* / Q000502:physiology*; D004730:Endothelium, Vascular / Q000737:chemistry / Q000473:pathology / Q000502:physiology / Q000503:physiopathology; D006801:Humans; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology; D011379:Prognosis; D012216:Rheumatic Diseases / Q000150:complications; D012307:Risk Factors; D014655:Vascular Resistance / Q000187:drug effects* / Q000502:physiology*
chemical_list: D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002121:Calcium Channel Blockers; D000451:Mineralocorticoid Receptor Antagonists