title: Eprosartan effect on fibrinolytic/hemostatic variables in arterial hypertension: a comparative study to losartan.
abstract: Essential hypertension is often accompanied by abnormalities of the coagulation/fibrinolytic system predisposing to a procoagulant state. The aim of the present study was to examine the comparative efficacy of the angiotensin II type 1 receptor antagonists eprosartan and losartan on plasma levels of hemostatic/fibrinolytic and endothelial function markers in a cohort of previously untreated hypertensive patients. A total of 86 patients whose hypertension was controlled by monotherapy with eprosartan 600 mg (45 patients) or losartan 100 mg (41 patients) were studied. The plasma levels of plasminogen activator inhibitor-1 (PAI-1) antigen, tissue plasminogen activator inhibitor (tPA) antigen, thrombomodulin (TM), tissue factor pathway inhibitor (TFPI) antigen, and fibrinogen were determined before and after 6 months of therapy. Age, sex distribution, body mass index, lipid profile, systolic and diastolic blood pressure levels, and baseline values of the measured markers were similar in both groups. After 6 months of therapy, systolic blood pressure was significantly lower in patients treated with eprosartan, while no differences were observed with respect to diastolic blood pressure. Treatment with both drugs was associated with a significant decrease in PAI-1 antigen, TM, fibrinogen plasma levels and an increase in tPA antigen. The favorable modification of all the above parameters was significantly greater in the eprosartan than in the losartan group, while TFPI plasma levels were decreased to a similar extent with both drugs. In conclusion, the results of our study indicate that 6-month monotherapy with a new angiotensin II type 1 receptor blocker, eprosartan, is associated with a more favorable modification of hemostatic/fibrinolytic status than with losartan.
authors.affiliation: Department of Cardiology, Laiko Hospital of Athens, Athens, Greece.
authors.forename: T K
authors.initials: TK
authors.lastname: Makris
authors.forename: G
authors.initials: G
authors.lastname: Stavroulakis
authors.forename: D P
authors.initials: DP
authors.lastname: Papadopoulos
authors.forename: P
authors.initials: P
authors.lastname: Krespi
authors.forename: A
authors.initials: A
authors.lastname: Hatzizacharias
authors.forename: A
authors.initials: A
authors.lastname: Zilidis
authors.forename: C
authors.initials: C
authors.lastname: Tsoukala
authors.forename: V E
authors.initials: VE
authors.lastname: Votteas
mesh_terms: D000179:Acrylates / Q000494:pharmacology / Q000627:therapeutic use*; D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers; D004334:Drug Administration Schedule; D005260:Female; D005340:Fibrinogen / Q000737:chemistry / Q000187:drug effects; D005342:Fibrinolysis / Q000187:drug effects* / Q000502:physiology; D005500:Follow-Up Studies; D006487:Hemostasis / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D007093:Imidazoles / Q000494:pharmacology / Q000627:therapeutic use*; D008074:Lipoproteins / Q000097:blood; D019808:Losartan / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D044140:Receptor, Angiotensin, Type 1 / Q000627:therapeutic use; D013876:Thiophenes / Q000494:pharmacology / Q000627:therapeutic use*; D018180:Thrombomodulin / Q000097:blood / Q000187:drug effects; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000037:antagonists & inhibitors / Q000097:blood / Q000187:drug effects
chemical_list: D000179:Acrylates; D047228:Angiotensin II Type 1 Receptor Blockers; D007093:Imidazoles; D008074:Lipoproteins; D017395:Plasminogen Activator Inhibitor 1; D044140:Receptor, Angiotensin, Type 1; D013876:Thiophenes; D018180:Thrombomodulin; C051928:lipoprotein-associated coagulation inhibitor; C068373:eprosartan; D005340:Fibrinogen; D010959:Tissue Plasminogen Activator; D019808:Losartan