title: Surgical revascularisation in patients with severe limb ischaemia induces a pro-thrombotic state.
abstract: Platelet and coagulation activation are implicated in the increased incidence of ischaemic events seen in patients with peripheral arterial disease. This study aimed to assess the effect of surgical revascularisation on platelet aggregation and coagulation in patients with severe limb ischaemia (SLI). Twenty-two patients had blood samples taken: prior to surgery, on reperfusion, 2, 24 and 48 h post-surgery. Platelet aggregation through COX-mediated and thrombin receptor activator peptide (TRAP)-stimulated GPIIb/IIIa pathways was measured by the Ultegra point of care system. Thrombin-antithrombin III Complex (TAT) and D-dimer were measured by ELISA. COX-mediated aggregation increased significantly at reperfusion and remained elevated at 24 h [median increase from baseline of 9% (range -16 to 33%) P = 0.011]. TRAP-stimulated aggregation increased significantly at reperfusion and remained elevated at 2 h post-surgery [median increase 18% (range -71 to 45%); P = 0.007]. TAT levels were significantly elevated from reperfusion and remained so at 48 h (P < 0.003), whereas D-dimer only increased at 24 h (P = 0.014). For the first time, we have demonstrated that in patients with SLI, platelet aggregation is increased following surgery and there is a mismatch in the balance between the coagulation and fibrinolytic pathways despite the use of aspirin and heparin. Thus in the early post-operative these patients exhibit a pro-thrombotic state.
authors.affiliation: Department of Vascular Surgery, University of Aberdeen, Scotland, UK.
authors.forename: P
authors.initials: P
authors.lastname: Collins
authors.forename: I
authors.initials: I
authors.lastname: Ford
authors.forename: M
authors.initials: M
authors.lastname: Greaves
authors.forename: E
authors.initials: E
authors.lastname: Macaulay
authors.forename: J
authors.initials: J
authors.lastname: Brittenden
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000990:Antithrombin III / Q000032:analysis; D001157:Arterial Occlusive Diseases / Q000097:blood / Q000601:surgery*; D001241:Aspirin / Q000494:pharmacology; D001777:Blood Coagulation / Q000502:physiology*; D000077144:Clopidogrel; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006801:Humans; D007511:Ischemia / Q000097:blood / Q000601:surgery*; D008297:Male; D019007:P-Selectin / Q000032:analysis; D010447:Peptide Hydrolases / Q000032:analysis; D010974:Platelet Aggregation; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D011183:Postoperative Complications / Q000503:physiopathology; D015424:Reperfusion / Q000009:adverse effects*; D013927:Thrombosis / Q000503:physiopathology; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000494:pharmacology; D014656:Vascular Surgical Procedures; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D019007:P-Selectin; D010975:Platelet Aggregation Inhibitors; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; D014841:von Willebrand Factor; D000990:Antithrombin III; D000077144:Clopidogrel; D010447:Peptide Hydrolases; D013988:Ticlopidine; D001241:Aspirin