title: Regression of left ventricular hypertrophy in human hypertension with irbesartan.
abstract: BACKGROUND
  The Swedish irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA).
  
  
  OBJECTIVE
  Angiotensin II induces myocardial hypertrophy. We hypothesized that blockade of angiotensin II subtype 1 (AT1) receptors by the AT1-receptor antagonist irbesartan would reduce left ventricular mass (as measured by echocardiography) more than conventional treatment with a beta blocker.
  
  
  METHODS
  This double-blind study randomized 115 hypertensive men and women with left ventricular hypertrophy to receive either irbesartan 150 mg q.d. or atenolol 50 mg q.d. for 48 weeks. If diastolic blood pressure remained above 90 mmHg, doses were doubled, and additional medications (hydrochlorothiazide and felodipine) were prescribed as needed. Echocardiography was performed at weeks 0, 12, 24 and 48.
  
  
  RESULTS
  Baseline mean blood pressure was 162/ 104 mmHg, and mean left ventricular mass index was 157 g/m2 for men and 133 g/m2 for women. Systolic and diastolic blood pressure reductions were similar in both treatment groups. Both irbesartan (P < 0.001) and atenolol (P< 0.001) progressively reduced left ventricular mass index, e.g. by 26 and 14 g/m2 (16 and 9%), respectively, at week 48, with a greater reduction in the irbesartan group (P = 0.024). The proportion of patients who attained a normalized left ventricular mass (i.e. < or = 131 g/m2 for men and < or = 100 g/m2 for women) tended to be greater with irbesartan (47 versus 32%, P = 0.108).
  
  
  CONCLUSIONS
  Left ventricular mass was reduced more in the irbesartan group than in the atenolol group. These results suggest that blocking the action of angiotensin II at AT1-receptors may be an important mechanism, beyond that of lowering blood pressure, in the regulation of left ventricular mass and geometry in patients with hypertension.
authors.affiliation: Division of Internal Medicine, Karolinska Institutet Danderyd Hospital, Sweden.
authors.forename: K
authors.initials: K
authors.lastname: Malmqvist
authors.forename: T
authors.initials: T
authors.lastname: Kahan
authors.forename: M
authors.initials: M
authors.lastname: Edner
authors.forename: C
authors.initials: C
authors.lastname: Held
authors.forename: A
authors.initials: A
authors.lastname: Hägg
authors.forename: L
authors.initials: L
authors.lastname: Lind
authors.forename: R
authors.initials: R
authors.lastname: Müller-Brunotte
authors.forename: F
authors.initials: F
authors.lastname: Nyström
authors.forename: K P
authors.initials: KP
authors.lastname: Ohman
authors.forename: M D
authors.initials: MD
authors.lastname: Osbakken
authors.forename: J
authors.initials: J
authors.lastname: Ostergern
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000009:adverse effects / Q000627:therapeutic use; D000328:Adult; D000368:Aged; D057911:Angiotensin Receptor Antagonists; D001262:Atenolol / Q000009:adverse effects / Q000627:therapeutic use; D001713:Biphenyl Compounds / Q000009:adverse effects / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D004311:Double-Blind Method; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D000077405:Irbesartan; D008297:Male; D008875:Middle Aged; D044140:Receptor, Angiotensin, Type 1; D012449:Safety; D013777:Tetrazoles / Q000009:adverse effects / Q000627:therapeutic use*; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D001713:Biphenyl Compounds; D044140:Receptor, Angiotensin, Type 1; D013777:Tetrazoles; D001262:Atenolol; D000077405:Irbesartan