Ticlopidine and Aspirin Pretreatment Reduces Coagulation and Platelet Activation During Coronary Dilation Procedures

Objectives. It is unknown whether a therapeutic combination of aspirin (ASA) and ticlopidine might effectively decrease activation of hemostasis. Background. Percutaneous transluminal coronary angioplasty (PTCA), rotational atherectomy and stent implantation are procedures that fracture or ablate endothelium and plaque, a situation that activates hemostasis. Methods. In 85 patients undergoing PTCA for a 77.8 ± 1% stenosis, we measured markers of coagulation and platelet activation (thrombin-antithrombin complexes [TAT], prothrombin fragment 1 + 2 [F1+2] serotonin and the presence of circulating activated platelets reacting with monoclonal antibodies against glycoproteins exposed on platelet membranes). Blood samples were drawn from a peripheral vein and from the coronary ostium before the procedures. Both immediately and 10 min after angioplasty, and 10 min afterward, samples were collected from a probing catheter (0.018 in. [0.46 cm]) positioned beyond the stenosis. All patients were being treated with antianginal drugs and ASA, 250 mg/day. Seventy of them had taken ticlopidine, 250 mg, twice daily for ≤1 day (≤24 h) (n = 28) or for ≥3 days (≥72 h) (n = 42). Heparin (150 U/kg) was administered before angioplasty. Thirty patients underwent PTCA; 15 of them were not treated with ticlopidine and 15 were given ticlopidine (≥72 h). Thirty-five patients had stent implantation, 20 rotational atherectomy. Results. Before and during the procedures, there was greater thrombin generation (expressed by higher TAT and F1+2plasma levels) in patients not taking ticlopidine or taking it for ≤24 h (p < 0.05). Platelet activation and plasma serotonin levels were also significantly higher in the no ticlopidine or ≤24-h ticlopidine groups. Conclusions. The combined use of ticlopidine, ASA and heparin effectively controls activation of coagulation in patients with stable or unstable angina undergoing coronary dilation. (J Am Coll Cardiol 1997;29:13–20)>