Heparin-induced thrombocytopenia from venous thromboembolism treatment.
OBJECTIVE
We aimed to characterize the clinical experiences of patients in whom heparin-induced thrombocytopenia (HIT) complicated heparin therapy for venous thromboembolism (VTE) and who switched to argatroban.


METHODS
A retrospective analysis of previously reported prospective, multicentre, historical-controlled Argatroban-911 and Argatroban-915 studies of argatroban therapy in HIT.


METHODS
Inpatient.


METHODS
Patients (n = 145) administered heparin for VTE and who developed HIT were identified.


METHODS
Patients were treated with argatroban 2 mcg kg(-1) min(-1) for up to 14 days, adjusted to maintain activated partial thromboplastin times 1.5 to three times baseline. Patient characteristics, anticoagulation and outcomes were summarized. The primary end-point was a composite of death, amputation, or new thrombosis within 37 days of argatroban initiation.


RESULTS
During heparin therapy, platelet counts decreased (mean +/- SD nadir: 78 +/- 67 x 10(9) L(-1)), and 75 (52%) patients developed thrombosis. After heparin was discontinued, patients received argatroban (mean dose 2.1 +/- 1.2 mcg kg(-1) min(-1)) for 6.8 +/- 4.3 days. By day 6 of argatroban therapy, the mean platelet count rose to >150 x 10(9) L(-1). The primary end-point occurred in 41 (28.3%) patients (values of 26-44% are reported for argatroban therapy of HIT from any heparin indication). Seventeen (11.7%) patients, including 12 who had also experienced thrombosis whilst on heparin, developed new thrombosis after argatroban initiation, typically on the day argatroban was discontinued or later (n = 10). Seven (4.8%) patients experienced major bleeding.


CONCLUSIONS
For VTE patients with HIT, argatroban provides effective anticoagulation, with outcomes comparable with those reported for other argatroban-treated HIT patients. New thrombosis in this setting occurred most often in patients with existing HIT-associated thrombosis, before HIT recognition or either at/after argatroban discontinuation.
Begelman
S M
SM
Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, OH 44195, USA. begelms@ccf.org
Hursting
M J
MJ
Aghababian
R V
RV
McCollum
D
D
D000671:Amputation, Surgical / Q000379:methods; D000925:Anticoagulants / Q000008:administration & dosage / Q000009:adverse effects*; D001120:Arginine / Q000031:analogs & derivatives; D004334:Drug Administration Schedule; D005260:Female; D006470:Hemorrhage / Q000209:etiology; D006493:Heparin / Q000008:administration & dosage / Q000009:adverse effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010875:Pipecolic Acids / Q000008:administration & dosage / Q000627:therapeutic use; D010976:Platelet Count; D016032:Randomized Controlled Trials as Topic; D012008:Recurrence; D012189:Retrospective Studies; D013449:Sulfonamides; D013921:Thrombocytopenia / Q000139:chemically induced* / Q000401:mortality / Q000601:surgery; D013923:Thromboembolism / Q000188:drug therapy* / Q000601:surgery; D016896:Treatment Outcome; D014859:Warfarin / Q000627:therapeutic use
D000925:Anticoagulants; D010875:Pipecolic Acids; D013449:Sulfonamides; D014859:Warfarin; D006493:Heparin; D001120:Arginine; C031942:argatroban