title: Antithrombotic treatment (argatroban vs. heparin) in coronary angioplasty in angina pectoris: effects on inflammatory, hemostatic, and endothelium-derived parameters.
abstract: To evaluate the suitability of two anticoagulants (heparin vs. argatroban) as adjunctive drugs during and after elective conventional percutaneous transluminal coronary angioplasty, we compared the changes in inflammatory, hemostatic, and endothelium-derived markers in groups of patients with stable angina treated with the two drugs during percutaneous transluminal coronary angioplasty. Twenty-seven patients were randomly allocated to either group 1 (15 patients who received an empiric dose of heparin and aspirin as anticoagulant), or group 2 (12 patients who received an alternative regimen of argatroban and aspirin). Both drugs were administered as a bolus followed by continuous infusion for 96 hours during and after percutaneous transluminal coronary angioplasty. There were no differences in the inflammatory response induced by percutaneous transluminal coronary angioplasty in both groups, but the fibrinogen concentration significantly decreased during percutaneous transluminal coronary angioplasty in group 2. Decreased platelet counts and increased mean platelet volume were observed during percutaneous transluminal coronary angioplasty in both groups. The levels of prothrombin fragment 1+2 and thrombin antithrombin III complex increased markedly during percutaneous transluminal coronary angioplasty. Group 2 showed a more rapid return to the baseline levels of these two markers than group 1. Secondary fibrinolysis was evidenced by a steep increase of D-dimer after percutaneous transluminal coronary angioplasty in both groups. In contrast to the significant decrease in antithrombin activities during percutaneous transluminal coronary angioplasty in group 1, no marked change in these markers was found in group 2. Although the levels of von Willebrand factor and plasminogen activator inhibitor-1 showed essentially the same changes in both groups during and after percutaneous transluminal coronary angioplasty, more markedly increased levels of tissue type plasminogen activator and type plasminogen activator-plasminogen activator inhibitor-1 complex after percutaneous transluminal coronary angioplasty were found in group 1 than in group 2. While neither drug had any effect on the percutaneous transluminal coronary angioplasty-induced inflammatory response, argatroban may more effectively inhibit the generated thrombin and prevent antithrombin consumption during and after percutaneous transluminal coronary angioplasty.
authors.affiliation: Hyogo Prefectural Awaji Hospital, 1-6-6, Shimogamo, Hyogo 656-0013, Sumoto, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Suzuki
authors.forename: T
authors.initials: T
authors.lastname: Matsuo
authors.forename: H
authors.initials: H
authors.lastname: Kobayashi
authors.forename: M
authors.initials: M
authors.lastname: Matsuo
authors.forename: C
authors.initials: C
authors.lastname: Shimamo
authors.forename: M
authors.initials: M
authors.lastname: Koide
authors.forename: S
authors.initials: S
authors.lastname: Sakamoto
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000188:drug therapy / Q000628:therapy*; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D000925:Anticoagulants / Q000627:therapeutic use*; D000990:Antithrombin III / Q000032:analysis; D001120:Arginine / Q000031:analogs & derivatives; D001241:Aspirin / Q000627:therapeutic use; D015415:Biomarkers; D003131:Combined Modality Therapy; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism; D005260:Female; D005341:Fibrinolysin / Q000032:analysis; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006487:Hemostasis / Q000187:drug effects*; D006493:Heparin / Q000627:therapeutic use*; D015844:Heparin Cofactor II / Q000032:analysis; D006801:Humans; D007249:Inflammation / Q000209:etiology; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000032:analysis; D010447:Peptide Hydrolases / Q000032:analysis; D010875:Pipecolic Acids / Q000627:therapeutic use*; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D017396:Plasminogen Activator Inhibitor 2 / Q000032:analysis; D010976:Platelet Count; D011516:Prothrombin / Q000032:analysis; D013449:Sulfonamides; D010959:Tissue Plasminogen Activator / Q000032:analysis; D000979:alpha-2-Antiplasmin / Q000032:analysis; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D000925:Anticoagulants; D015415:Biomarkers; D005343:Fibrinolytic Agents; D010446:Peptide Fragments; D010875:Pipecolic Acids; D017395:Plasminogen Activator Inhibitor 1; D017396:Plasminogen Activator Inhibitor 2; D013449:Sulfonamides; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C045879:prothrombin fragment 1.2; D014841:von Willebrand Factor; D015844:Heparin Cofactor II; D000990:Antithrombin III; D011516:Prothrombin; D006493:Heparin; D001120:Arginine; D010447:Peptide Hydrolases; D010959:Tissue Plasminogen Activator; D005341:Fibrinolysin; C031942:argatroban; D001241:Aspirin