title: Effects of atenolol or losartan on fibrinolysis and von Willebrand factor in hypertensive patients with left ventricular hypertrophy.
abstract: OBJECTIVE
  To compare the effects of the beta-blocker atenolol with the angiotensin receptor blocker (ARB) losartan on plasma tissue-type plasminogen activator (tPA) activity and mass concentration, plasminogen activator inhibitor-1 (PAI-1) activity, tPA/PAI-1 complex, and von Willebrand factor (VWF).
  
  
  METHODS
  A prespecified, explorative substudy in 22 patients with hypertension and left ventricular hypertrophy (LVH) performed within randomized multicenter, double-blind prospective study.
  
  
  RESULTS
  After a median of 36 weeks of treatment, there were significant differences between the treatment groups, atenolol versus losartan, in plasma median levels of tPA mass (11.9 vs 7.3 ng/mL, P = .019), PAI-1 activity (20.7 vs 4.8 IU/mL, P = .030), and tPA/PAI-1 complex (7.1 vs 2.5 ng/mL, P = .015). In patients treated with atenolol, median levels of tPA mass (8.9-11.9 ng/mL, P = .021) and VWF (113.5%-134.3%, P = .021) increased significantly, indicating a change toward a more prothrombotic state. No significant changes occurred in the losartan group.
  
  
  CONCLUSIONS
  Losartan treatment was associated with preserved fibrinolytic balance compared to a more prothrombotic fibrinolytic and hemostatic state in the atenolol group. These findings suggest different fibrinolytic and hemostatic responses to treatment in hypertensive patients with LVH.
authors.affiliation: University Umeå and Department of Medicine-Geriatric, Skellefteå County Hospital, Umeå, Sweden. kurt.boman@vll.se
authors.forename: Kurt
authors.initials: K
authors.lastname: Boman
authors.forename: Jenny Hernestål
authors.initials: JH
authors.lastname: Boman
authors.forename: Jonas
authors.initials: J
authors.lastname: Andersson
authors.forename: Mona
authors.initials: M
authors.lastname: Olofsson
authors.forename: Björn
authors.initials: B
authors.lastname: Dahlöf
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use*; D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology / Q000627:therapeutic use*; D001262:Atenolol / Q000494:pharmacology / Q000627:therapeutic use*; D004311:Double-Blind Method; D005260:Female; D005342:Fibrinolysis / Q000187:drug effects*; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D019808:Losartan / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D012084:Renin-Angiotensin System / Q000502:physiology; D019851:Thrombophilia / Q000209:etiology / Q000503:physiopathology; D010959:Tissue Plasminogen Activator / Q000032:analysis; D014841:von Willebrand Factor / Q000032:analysis*
chemical_list: D000319:Adrenergic beta-Antagonists; D047228:Angiotensin II Type 1 Receptor Blockers; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D014841:von Willebrand Factor; D001262:Atenolol; D010959:Tissue Plasminogen Activator; D019808:Losartan