title: Large artery stiffness and antihypertensive agents.
abstract: OBJECTIVE
  Since in hypertensive populations, concentration on peripheral blood pressure only does not achieve 100% of blood pressure-attributable risk reduction, taking into consideration other hemodynamic parameters than peripheral blood pressure could perhaps improve cardiovascular prevention. The main purpose of this review is to analyse the scientific data in favour of considering arterial stiffness parameters as interesting intermediate cardiovascular endpoints in order to optimise risk assessment and risk reduction strategies.
  
  
  CONCLUSIONS
  Aortic pulse wave velocity (PWV), a marker of aortic stiffness, has been shown to be a strong independent predictor of cardiovascular morbid events, cardiovascular and all-cause mortality in numerous studies in different populations. Furthermore, it has been shown in a therapeutic trial that the lack of aortic PWV attenuation despite significant drug-induced reduction in mean blood pressure was a significant predictor of cardiovascular death in subjects with end-stage renal disease. In essential hypertension, the Reason Study has shown that, despite a similar decrease in peripheral diastolic blood pressure, different effects on central hemodynamic parameters were observed between blockade of the renin-angiotensin system and atenolol. Novel therapeutic approaches available to reduce the increase of pulse pressure and arterial stiffness with age involve converting enzyme inhibitors in association with diuretic compounds; nitrate derivatives; agents acting on collagen cross-linking; and finally spironolactone and vasopeptidase inhibitors.
  
  
  CONCLUSIONS
  These results support the hypothesis that measurement of aortic PWV could then help, not only in risk assessment strategies but also in risk reduction strategies by monitoring arterial stiffness under different pharmacological regimens.
authors.affiliation: Hypertension and cardiovascular prevention unit, Centre de Diagnostic, Hotel-Dieu, AP-HP, Place du parvis Notre-Dame, 75004 Paris, France. jacques.blacher@htd.ap-hop-paris.fr
authors.forename: Jacques
authors.initials: J
authors.lastname: Blacher
authors.forename: Athanase D
authors.initials: AD
authors.lastname: Protogerou
authors.forename: Michel E
authors.initials: ME
authors.lastname: Safar
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001011:Aorta / Q000503:physiopathology*; D003187:Compliance; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000503:physiopathology; D012084:Renin-Angiotensin System / Q000502:physiology; D018570:Risk Assessment; D040242:Risk Reduction Behavior; D012982:Sodium, Dietary / Q000008:administration & dosage; D013148:Spironolactone / Q000627:therapeutic use
chemical_list: D000959:Antihypertensive Agents; D012982:Sodium, Dietary; D013148:Spironolactone