title: Effects of candesartan on cardiac and arterial structure and function in hypertensive subjects.
abstract: OBJECTIVE
  To study the effect of candesartan cilexetil on left ventricular mass index (LVMI), left ventricular systolic and diastolic function, arterial structure and function and blood pressure (BP) in hypertensive patients.
  
  
  METHODS
  Patients (n=35), aged >20 years, with hypertension and average baseline LVMI of 89 g/m2 were treated for 24 weeks with candesartan, 16 mg o.d., following a four-week placebo run-in period. If diastolic BP remained above 95 mmHg, hydrochlorothiazide, 12.5 mg o.d.,was added. Left ventricular structure and function were assessed using transthoracic echocardiography. Arterial function and structure were assessed using pulse wave analysis to calculate augmentation index (AIx) and forearm plethysmography to calculate minimum vascular resistance. BP was measured in the office and by 24-hour ambulatory BP monitoring (ABPM).
  
  
  RESULTS
  The mean reduction in LVMI was 4.4 g/m2(p=0.022). Left ventricular systolic function was not significantly altered from baseline, but diastolic function significantly improved: the mean change in diastolic time was 54 ms (p=0.037), in peak velocity filling 6.3 cm/s (p=0.023); E:A ratio improved by 0.08 (p=0.049). The mean reduction in forearm vascular resistance was 15 units at rest (p=0.001) and 1.3 units after limb ischaemia (p=0.006). AIx decreased significantly, with a mean reduction of 9% (p<0.001). Central BP also significantly reduced(systolic blood pressure/diastolic blood pressure 31/20 mmHg; p<0.001). BP was significantly reduced, both in the office (22/16 mmHg; p<0.001) and by 24-hourABPM (18/12 mmHg; p<0.001).
  
  
  CONCLUSIONS
  Treatment with candesartan, 16 mg o.d., with or without hydrochlorothiazide, for 24 weeks, significantly reduced left ventricular mass and arterial hypertrophy in patients with hypertension. In parallel, there were significant improvements in left ventricular diastolic function and arterial function.
authors.affiliation: University of Edinburgh, UK. jamesspratt@blueyonder.co.uk
authors.forename: J C
authors.initials: JC
authors.lastname: Spratt
authors.forename: D J
authors.initials: DJ
authors.lastname: Webb
authors.forename: A
authors.initials: A
authors.lastname: Shiels
authors.forename: B
authors.initials: B
authors.lastname: Williams
mesh_terms: D000328:Adult; D000959:Antihypertensive Agents / Q000008:administration & dosage* / Q000009:adverse effects; D001158:Arteries / Q000473:pathology; D001562:Benzimidazoles / Q000008:administration & dosage* / Q000009:adverse effects; D001713:Biphenyl Compounds; D001794:Blood Pressure / Q000187:drug effects; D003187:Compliance; D004452:Echocardiography; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D013777:Tetrazoles / Q000008:administration & dosage* / Q000009:adverse effects; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D000959:Antihypertensive Agents; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D013777:Tetrazoles; C081643:candesartan