title: Reversal of pathophysiologic changes with long-term lisinopril treatment in isolated systolic hypertension.
abstract: The purpose of this study was to evaluate in a prospective, double-blind, placebo-controlled study the effect of long-term (2-year) lisinopril treatment on cardiovascular end-organ damage in patients with previously untreated isolated systolic hypertension (ISH). All patients with ISH were derived from a population screening program. End-organ damage measurements, done initially and after 6 and 24 months of treatment, included measurements of aortic distensibility and echocardiographic left ventricular mass index (LVMI) and diastolic function. Blood pressure was measured by office and ambulatory measurements. Of the 97 subjects with ISH selected from the screening, 62 (30 lisinopril) completed the study according to protocol. Office blood pressure decreased in both groups, but ambulatory results significantly decreased with lisinopril-treatment only. Aortic distensibility increased significantly with lisinopril, as opposed to a decrease in placebo-treated subjects. The main effect of increased distensibility occurred between 6 and 24 months, whereas ambulatory blood pressure changed mainly in the first 6 months of treatment. LVMI decreased in both treatment groups, with a significantly higher reduction in lisinopril-treated subjects. Left ventricular diastolic function showed no significant changes in either group. The vascular pathophysiologic alterations of ISH-a decreased aortic distensibility-can be improved with long-term lisinopril treatment, whereas values deteriorate further in placebo-treated subjects. These results, in one of the first studies including subjects with previously untreated ISH only, indicate that lisinopril treatment might favorably influence the cardiovascular risk of ISH.
authors.affiliation: Department of Cardiology, University of Groningen, The Netherlands.
authors.forename: W F
authors.initials: WF
authors.lastname: Heesen
authors.forename: F W
authors.initials: FW
authors.lastname: Beltman
authors.forename: A J
authors.initials: AJ
authors.lastname: Smit
authors.forename: J F
authors.initials: JF
authors.lastname: May
authors.forename: P A
authors.initials: PA
authors.lastname: de Graeff
authors.forename: J H
authors.initials: JH
authors.lastname: Muntinga
authors.forename: T K
authors.initials: TK
authors.lastname: Havinga
authors.forename: F H
authors.initials: FH
authors.lastname: Schuurman
authors.forename: E
authors.initials: E
authors.lastname: van der Veur
authors.forename: B
authors.initials: B
authors.lastname: Meyboom-de Jong
authors.forename: K I
authors.initials: KI
authors.lastname: Lie
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D000959:Antihypertensive Agents / Q000008:administration & dosage*; D001024:Aortic Valve Stenosis / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D016009:Chi-Square Distribution; D004311:Double-Blind Method; D005260:Female; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology*; D017706:Lisinopril / Q000008:administration & dosage*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D014463:Ultrasonography; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology
chemical_list: D000959:Antihypertensive Agents; D017706:Lisinopril