PMID- 11869846 OWN - NLM STAT- MEDLINE DCOM- 20020320 LR - 20190708 IS - 0735-1097 (Print) IS - 0735-1097 (Linking) VI - 39 IP - 5 DP - 2002 Mar 6 TI - Rebound thrombin generation after heparin therapy in unstable angina. A randomized comparison between unfractionated and low-molecular-weight heparin. PG - 811-7 AB - OBJECTIVES: This study compared rebound coagulation in patients with acute coronary syndrome patients after discontinuation of unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH). BACKGROUND: Up to a quarter of patients hospitalized for unstable angina experience recurrent ischemia after discontinuation of UFH or LMWH therapy, which may be the result of rebound coagulation activation and subsequent thrombosis. It is unknown whether UFH and LMWH differ in this respect. METHODS: We randomized 71 patients admitted with unstable angina to intravenous UFH or subcutaneous LMWH (dalteparin) and measured plasma markers of coagulation before, during, and after treatment. RESULTS: A complete series of measurements was obtained in 59 patients. Plasma prothrombin fragment 1+2 (F(1+2)) levels decreased in both groups during treatment. After loss of therapeutic plasma drug levels, F(1+2) increased (within 3 h) to a maximum level at 12 to 24 h that was higher than before or during treatment in both groups (p < 0.0001). In both groups, F(1+2) levels remained higher than pretreatment up to 24 h after discontinuation. Similarly, thrombin-antithrombin (TAT) levels exceeded treatment and pretreatment levels, at a slower rate after dalteparin than after UFH. However, after dalteparin a higher peak value of TAT was observed. CONCLUSIONS: Rebound coagulation activation occurs within hours after discontinuation of both UFH and dalteparin. With both drugs, thrombin generation is significantly greater after treatment than before or during treatment. A longer duration or weaning of treatment, or continuation with another anticoagulant treatment, may reduce rebound coagulation activation and ischemic events. FAU - Bijsterveld, Nick R AU - Bijsterveld NR AD - Department of Cardiology, Academic Medical Center, Amsterdam, Netherlands. FAU - Moons, Arno H AU - Moons AH FAU - Meijers, Joost C M AU - Meijers JC FAU - Tijssen, Jan G P AU - Tijssen JG FAU - Buller, Harry R AU - Buller HR FAU - Levi, Marcel AU - Levi M FAU - Peters, Ron J G AU - Peters RJ LA - eng PT - Clinical Trial PT - Comparative Study PT - Journal Article PT - Randomized Controlled Trial PT - Research Support, Non-U.S. Gov't PL - United States TA - J Am Coll Cardiol JT - Journal of the American College of Cardiology JID - 8301365 RN - 0 (Anticoagulants) RN - 0 (Heparin, Low-Molecular-Weight) RN - 9005-49-6 (Heparin) RN - EC 3.4.21.5 (Thrombin) RN - S79O08V79F (Dalteparin) SB - IM MH - Angina, Unstable/blood/*drug therapy/physiopathology MH - Anticoagulants/blood/*therapeutic use MH - Coronary Thrombosis/blood/physiopathology/*prevention & control MH - Dalteparin/blood/*therapeutic use MH - Female MH - Fibrinolysis/drug effects/physiology MH - Heparin/blood/*therapeutic use MH - Heparin, Low-Molecular-Weight/blood/*therapeutic use MH - Humans MH - Male MH - Middle Aged MH - Recurrence MH - Thrombin/drug effects/physiology MH - Time Factors MH - *Withholding Treatment EDAT- 2002/03/01 10:00 MHDA- 2002/03/21 10:01 CRDT- 2002/03/01 10:00 PHST- 2002/03/01 10:00 [pubmed] PHST- 2002/03/21 10:01 [medline] PHST- 2002/03/01 10:00 [entrez] AID - S0735109701018253 [pii] AID - 10.1016/s0735-1097(01)01825-3 [doi] PST - ppublish SO - J Am Coll Cardiol. 2002 Mar 6;39(5):811-7. doi: 10.1016/s0735-1097(01)01825-3.