title: Local pulse pressure is a major determinant of large artery remodelling.
abstract: 1. The aim of the present brief review is to show that the pulsatile component of blood pressure is a stronger determinant of large artery remodelling than the steady component (i.e. mean blood pressure). 2. Pulse pressure, which is a strong determinant of cardiovascular events, including coronary heart disease and stroke, is increased when large arteries stiffen. Local pulse pressure, measured with applanation tonometry in normotensives and patients with essential hypertension, explains a significant part of the variance of intima-media thickness at the site of the carotid artery, a proximal elastic artery, whereas mean blood pressure does not contribute. Local pulse pressure has no influence on intima-media thickness at the site of the radial artery, a distal muscular artery that undergoes very little stroke change in diameter. 3. The decrease in carotid pulse pressure is also a major determinant of the regression of carotid intima-media thickness after antihypertensive treatment. Local pulse pressure can influence not only intima-media thickness, but also internal diameter. Indeed, there is a significant association between the lumen enlargement of the ascending aorta in patients with Marfan syndrome and pulse pressure. In addition, carotid pulse pressure is positively correlated with carotid internal diameter in normotensives and hypertensives, and the decrease in carotid internal diameter during long-term antihypertensive treatment is influenced by the decrease in carotid pulse pressure and not by the reduction in mean blood pressure. 4. We suggest that the effects of pulse pressure on large artery remodelling may explain part of its predictive value on cardiovascular events.
authors.affiliation: Department of Pharmacology and EMI INSERM 0107, Hôpital Européen Georges Pompidou, Paris, France. stephane.laurent@egp.ap-hop-paris.fr
authors.forename: S
authors.initials: S
authors.lastname: Laurent
authors.forename: A I
authors.initials: AI
authors.lastname: Tropeano
authors.forename: A
authors.initials: A
authors.lastname: Lillo-Lelouet
authors.forename: G
authors.initials: G
authors.lastname: Jondeau
authors.forename: B
authors.initials: B
authors.lastname: Laloux
authors.forename: P
authors.initials: P
authors.lastname: Boutouyrie
mesh_terms: D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use; D001158:Arteries / Q000033:anatomy & histology* / Q000187:drug effects / Q000254:growth & development*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology; D008382:Marfan Syndrome / Q000503:physiopathology; D017539:Tunica Intima / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology
chemical_list: D000959:Antihypertensive Agents