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Course of thrombin activation markers in patients implanted with Palmaz-Schatz stents: first experiences with a
A Haushofer1, W M Halbmayer, M Dittel
1Zentrallabor, Krankenhaus Lainz, Vienna, Austria.
Insights
This study shows that a combined heparin, phenprocoumon, and aspirin regimen effectively manages anticoagulation after coronary stent implantation. Monitoring via activated partial thromboplastin time (aPTT) and International Normalized Ratio (INR) ensures therapeutic levels, though prothrombin fragment F1.2 levels may rise initially.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Biochemistry
Background:
- Coronary stent implantation necessitates effective anticoagulation to prevent thrombosis.
- Standard protocols often involve a combination of anticoagulant agents.
- Monitoring anticoagulation levels is crucial for patient safety and treatment efficacy.
Purpose of the Study:
- To evaluate the efficacy of a combined anticoagulation protocol (heparin, phenprocoumon, aspirin) following coronary Palmaz-Schatz stent implantation.
- To assess the effectiveness of routine monitoring methods, including activated partial thromboplastin time (aPTT) and International Normalized Ratio (INR), in managing this combined therapy.
- To investigate the correlation between coagulation markers, such as prothrombin fragment F1.2 (F1.2) and thrombin-antithrombin III complexes (TAT), and clinical outcomes like restenosis and stent thrombosis.
Main Methods:
- A cohort of 29 patients received Palmaz-Schatz stents and were treated with a combination of intravenous heparin, oral phenprocoumon, and aspirin.
- Heparin dosage was adjusted to maintain aPTT within the therapeutic range.
- Phenprocoumon therapy was initiated the day after stenting and continued for 3 months.
- Coagulation parameters including aPTT, Heptest, F1.2, and TAT were monitored for 10 days post-implantation.
- Follow-up angiography was performed on 25 patients after discontinuing phenprocoumon therapy.
Main Results:
- The combined anticoagulation therapy achieved therapeutic levels of aPTT and INR within 9 and 8 days, respectively.
- Prothrombin fragment F1.2 levels increased significantly on day 4 post-stenting but decreased thereafter, correlating negatively with Heptest and INR.
- Higher mean F1.2 levels were observed in patients with restenosis at follow-up angiography.
- In a case of subacute stent thrombosis, F1.2 and TAT levels were lower than in other patients, suggesting they are not predictive of thrombotic events.
Conclusions:
- The combination of heparin, phenprocoumon, and aspirin provides efficient anticoagulation for coronary stent implantation.
- Routine monitoring methods (aPTT, INR) are effective in managing this combined anticoagulation therapy.
- While F1.2 levels indicate thrombin generation, they did not predict stent thrombosis in this study, and higher levels were associated with restenosis.
Abstract:
Following implantation of coronary Palmaz-Schatz stents, 29 patients were anticoagulated with a combination of heparin, phenprocoumon and aspirin following a standard protocol. After removing the arterial and venous 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 thromboplastin time (aPTT) and adjusted by increasing or reducing i.v. heparin by 250 IU/h to maintain the aPTT within the therapeutic range. Phenprocoumon therapy began the day after stent implantation (day 2) and lasted for 3 months. aPTT, Heptest, 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). Anticoagulation was efficient with aPTT levels remaining within the therapeutic range on day 9 and the simultaneous, moderate-onset oral anticoagulation within the therapeutic range of the International Normalized Ratio (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 from day 8 on (P < 0.05). F1.2 was negatively correlated with the Heptest (P < 0.05) and fell significantly as a function of the INR during phenprocoumon administration (P < 0.001). After phenprocoumon therapy was discontinued over 3 weeks, 25 patients were followed up by angiography. Despite adequate anticoagulation, mean F1.2 levels in patients showing restenosis at follow-up angiography were significantly higher (P < 0.005) than in those without restenosis. In one patient who developed 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 micrograms/l vs 3.21 +/- 3.38 micrograms/l). Thus, neither F1.2 nor TAT predicted the occurrence of thrombotic stent failure in individuals. Efficient anticoagulation by a combination of anticoagulants is imperative for stent implantation. Using only current routine methods, this way of monitoring anticoagulation is effective for managing combined anticoagulation therapy.