title: Hemostasis and fibrinolysis in patients with intermittent claudication: effects of prostaglandin E1.
abstract: There is evidence that the coagulation system is activated in patients with peripheral arterial occlusive disease (PAOD). The beneficial effects of the vasoactive drug prostaglandin E1 (PGE1) may rely in part on the modulation of the coagulation system. The study was designed to evaluate the effects of PGE1 on hemostatic and fibrinolytic variables in patients with intermittent claudication. Therefore molecular markers of thrombin (prothrombin fragment 1+2, PTF 1+2; thrombin-antithrombin III complexes, TAT) and fibrin formation (fibrinopeptide A, FPA) and markers of the fibrinolytic activity (fibrin degradation products, D-dimers) were determined before and immediately after the first PGE1 dose (60 microg in 100 ml NaCl over 2 h i.v.) as well as after 4 weeks of daily infusion therapy in 12 PAOD patients and in eight control patients before and after a single placebo infusion. Plasma levels of PTF1+2, TAT, FPA and D-dimers tended to decrease after the initial dose of PGE1. Infusion therapy with PGE1 for 4 weeks led to a decrease of all hemostatic and fibrinolytic parameters with most pronounced changes for PFT1+2, D-dimers and plasminogen activator inhibitor-1 decreasing by 11% (P<0.05), 20% (P<0.05), and 7% (P<0.05), respectively. These variables remained unchanged in controls with placebo infusion. In summary, infusion therapy with PGE1 in patients with PAOD reduces thrombin formation and results in a decrease of fibrin degradation. PGE1 may thus reduce fibrin deposition involved in the pathogenesis of atherosclerosis.
authors.affiliation: Abteilung für Sportmedizin und Abteilung für Kardiologie/Angiologie, Universität Heidelberg, Heidelberg, Germany. claus_weiss@med.uni-heidelberg.de
authors.forename: C
authors.initials: C
authors.lastname: Weiss
authors.forename: S
authors.initials: S
authors.lastname: Regele
authors.forename: T
authors.initials: T
authors.lastname: Velich
authors.forename: P
authors.initials: P
authors.lastname: Bärtsch
authors.forename: T
authors.initials: T
authors.lastname: Weiss
mesh_terms: D000368:Aged; D000527:Alprostadil / Q000627:therapeutic use*; D000990:Antithrombin III; D001157:Arterial Occlusive Diseases / Q000188:drug therapy; D016022:Case-Control Studies; D019281:Dimerization; D005337:Fibrin / Q000096:biosynthesis / Q000378:metabolism; D005342:Fibrinolysis / Q000187:drug effects*; D005344:Fibrinopeptide A / Q000096:biosynthesis; D006487:Hemostasis / Q000187:drug effects*; D006801:Humans; D007383:Intermittent Claudication / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000097:blood; D010919:Placebos; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011516:Prothrombin / Q000096:biosynthesis; D013917:Thrombin / Q000096:biosynthesis; D013997:Time Factors
chemical_list: D010919:Placebos; D017395:Plasminogen Activator Inhibitor 1; C046193:antithrombin III-protease complex; D005344:Fibrinopeptide A; D000990:Antithrombin III; D011516:Prothrombin; D005337:Fibrin; D010447:Peptide Hydrolases; D013917:Thrombin; D000527:Alprostadil