title: Regression of left ventricular mass with captopril and metoprolol, and the effects on glucose and lipid metabolism.
abstract: OBJECTIVE
  Angiotensin II and insulin have been suggested to promote the development of hypertensive left ventricular (LV) hypertrophy. We compared the effects of captopril and metoprolol on the regression of LV mass and the relation to insulin sensitivity.
  
  
  METHODS
  51 previously untreated non-diabetic hypertensive patients (mean age 51 +/- 8 years, body mass index, BMI 25.9 +/- 3.2 kg/m2, office blood pressure, 158/102 mmHg) were randomized to captopril or metoprolol; a low-dose diuretic and/or a calcium cannel antagonist were added, if needed.
  
  
  METHODS
  LV mass index (LVMI; by echocardiography) and 24-h ambulatory blood pressure were examined at baseline, 6 and 12 months. At baseline and 12 months, insulin sensitivity index (MI) was calculated by a hyperinsulinemic-euglycemic insulin clamp technique.
  
  
  RESULTS
  Blood pressures were reduced similarly in both groups. LVMI (115 +/- 21 g/m2 at baseline) was reduced in both groups (p < 0.01), but more with captopril than with metoprolol (e.g. -16 vs -7 g/m2, i.e. -13 vs -6%, at 12 months, p < 0.01). MI decreased by 6% with captopril (p = 0.05) and by 23% with metoprolol (p < 0.01), with no difference between the groups. Changes in LVMI were not related to changes in MI in the two groups, or when all patients were analyzed together. High-density lipoprotein (HDL)-cholesterol decreased (p < 0.05) by both drugs, with small effects on low-density lipoprotein (LDL), and triglycerides increased by 30% with metoprolol (p < 0.01).
  
  
  CONCLUSIONS
  Blockade of the renin-angiotensin-aldosterone system has a role beyond that of blood pressure reduction in the regression of LV mass. There was no relationship between regression of LV mass and improvement in insulin sensitivity. We could not confirm a beneficial effect of ACE inhibition on insulin sensitivity. Thus, our results do not support the importance of insulin in the control of LV geometry.
authors.affiliation: Division of Internal Medicine, Karolinska Institutet, Danderyd Hospital, Sweden. karin.malmqvist@med.ds.sll.se
authors.forename: K
authors.initials: K
authors.lastname: Malmqvist
authors.forename: T
authors.initials: T
authors.lastname: Kahan
authors.forename: H
authors.initials: H
authors.lastname: Isaksson
authors.forename: J
authors.initials: J
authors.lastname: Ostergren
mesh_terms: D000328:Adult; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage / Q000494:pharmacology; D000959:Antihypertensive Agents / Q000008:administration & dosage* / Q000494:pharmacology; D001786:Blood Glucose / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects; D018660:Blood Pressure Monitoring, Ambulatory; D002216:Captopril / Q000008:administration & dosage* / Q000494:pharmacology; D004452:Echocardiography; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000188:drug therapy*; D007328:Insulin / Q000008:administration & dosage / Q000494:pharmacology; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood*; D008297:Male; D008790:Metoprolol / Q000008:administration & dosage* / Q000494:pharmacology; D008875:Middle Aged
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D001786:Blood Glucose; D007328:Insulin; D008055:Lipids; D002216:Captopril; D008790:Metoprolol