COURSE OF THROMBIN ACTIVATION MARKERS IN PATIENTS IMPLANTED WITH PALMAZ-SCHATZ STENTS - FIRST EXPERIENCES WITH A POST-INTERVENTIONAL ANTICOAGULATION REGIMEN

Following implantation of coronary Palmaz-Schatz stents, 29 patients w ere anticoagulated with a combination of heparin, phenprocoumon and as pirin following a standard protocol. After removing the arterial and v enous lines, post-interventional intravenous (i.v.) heparin treatment started with 1500 IU/h for patients > 80 kg and 1250 IU/h for patients < 80 kg. Heparin was monitored by the activated partial thromboplasti n time (aPTT) and adjusted by increasing or reducing i.v. heparin by 2 50 IU/h to maintain the aPTT within the therapeutic range. Phenprocoum on therapy began the day after stent implantation (day 2) and lasted f or 3 months. aPTT, HeptestTM, prothrombin fragment F1 and 2 (F1.2) and thrombin-antithrombin III complexes (TAT) were monitored at standard intervals for 10 days (mean monitoring time: 9.7 +/- 2.3 days). Antico agulation was efficient with aPTT levels remaining within the therapeu tic range on day 9 and the simultaneous, moderate-onset oral anticoagu lation within the therapeutic range of the International Normalized Ra tio (INR; 2.15-4.80) on day 8 on average, the mean INR being 2.43 +/- 0.76. On day 4, F1.2 levels were significantly higher than on the day of stenting (1.16 +/- 0.30 nmol/l vs 1.04 +/- 0.53 nmol/l; P < 0.005). F1.2 levels fell after day 5, the difference becoming significant fro m day 8 on (P < 0.05). F1.2 was negatively correlated with the Heptest TM (P < 0.05) and fell significantly as a function of the INR during p henprocoumon administration (P < 0.001). After phenprocoumon therapy w as discontinued over 3 weeks, 25 patients were followed up by angiogra phy. Despite adequate anticoagulation, mean F1.2 levels in patients sh owing restenosis at follow-up angiography were significantly higher (P < 0.005) than in those without restenosis. In one patient who develop ed subacute stent thrombosis, clotting factors were determined 20 min before stent occlusion. The levels of F1.2 and TAT were less than all other patients on this day (F1.2:0.98 nmol/l vs 1.11 +/- 0.40 nmol/l; TAT:2.7 mu g/l vs 3.21 +/- 3.38 mu g/l). Thus, neither F1.2 nor TAT pr edicted the occurrence of thrombotic stent failure in individuals. Eff icient anticoagulation by a combination of anticoagulants is imperativ e for stent implantation. Using only current routine methods, this way of monitoring anticoagulation is effective for managing combined anti coagulation therapy.