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1 ifibatide); or DTIs (r-hirudin, bivalirudin, argatroban).
2 outcome were lower in the patients receiving argatroban.
3 ing which was not impacted by bivalirudin or argatroban.
4 t thrombin inhibitors (DTIs) bivalirudin and argatroban.
5 fluorogenic substrate, and (iv) titration of argatroban (0-1.5 microg/mL) into plugs and measurement
8 age was similar in the three groups (4% with argatroban, 3% with eptifibatide, and 2% with placebo).
10 core: eptifibatide, 6.47; 95% CI, 5.79-7.15; argatroban, 5.35; 95% CI, 4.13-6.58; placebo, 6.68; 95%
11 tal of 514 patients were assigned to receive argatroban (59 patients), eptifibatide (227 patients), o
12 fied Rankin scale scores were 5.2+/-3.7 with argatroban, 6.3+/-3.2 with eptifibatide, and 6.8+/-3.0 w
14 study evaluating the efficacy and safety of argatroban, a direct thrombin inhibitor, as anticoagulan
15 44) received 2 microgram. kg(-1). min(-1) IV argatroban, adjusted to maintain the activated partial t
17 y of combining intravenous thrombolysis with argatroban (an anticoagulant agent) or eptifibatide (an
18 urred in 37.5% of heparin, 32.0% of low-dose argatroban and 25.5% of high-dose argatroban patients (p
19 onal costs, fondaparinux prevailed over both argatroban and bivalirudin in terms of cost ($151 vs $12
20 inux has similar effectiveness and safety as argatroban and danaparoid in patients with suspected HIT
25 ice were given the direct thrombin inhibitor argatroban approximately 15 mg/kg/day or its vehicle via
27 e conducted a cost-effectiveness analysis of argatroban, bivalirudin, and fondaparinux for the treatm
28 rin agents such as fondaparinux, danaparoid, argatroban, bivalirudin, or one of the new direct-acting
34 m onset were assigned to receive intravenous argatroban, eptifibatide, or placebo within 75 minutes a
35 nearly a half, whereas doubling the dose of argatroban from its IC50 would decrease coagulation acti
37 in the placebo group [83%]; 17 of 27 in the argatroban group [63%], and 82 of 98 in the eptifibatide
38 bectomy (110 in the placebo group, 31 in the argatroban group, and 113 in the eptifibatide group).
41 c analyses demonstrated that permeation with argatroban had no significant effects on clot structure.
42 In vitro and in vivo studies have shown that argatroban has advantages over heparin for the inhibitio
45 lowing attenuation of thrombin generation by argatroban in a serum-transfer nephrotoxic model identif
47 were hemorrhagic (one per group, none during argatroban infusion); 30 (86%) were present at or within
48 m was developed to titrate an anticoagulant (argatroban) into blood samples and to measure the clotti
49 clot permeation system have also shown that argatroban is a potent inhibitor of clot-bound thrombin,
51 nd is not approved in the United States; and argatroban is contraindicated in patients with impaired
52 84 (43.1%) had been treated first-line with argatroban, lepirudin, danaparoid, and fondaparinux, res
54 29 patients (21.5%) received treatment with argatroban, lepirudin, or fondaparinux: 10 of 10 heparin
55 a small-molecule, direct thrombin inhibitor, argatroban, on reperfusion induced by tissue plasminogen
57 onset, adjunctive treatment with intravenous argatroban or eptifibatide did not reduce poststroke dis
58 d clinical trial reveal that the addition of argatroban or eptifibatide to intravenous thrombolysis w
59 hin 6 h were randomized to heparin, low-dose argatroban or high-dose argatroban in addition to TPA.
60 arin with a direct thrombin inhibitor (e.g., argatroban or lepirudin) or the heparinoid danaparoid (w
63 d with normal saline (control), bivalirudin, argatroban, or heparin and outcomes were assessed on pos
64 ieved in 42.1% of heparin, 56.8% of low-dose argatroban (p = 0.20 vs. heparin) and 58.7% of high-dose
74 creased the available thrombin activity, yet argatroban still inhibited this clot-associated thrombin
78 tio, 4.10; 95% CI, 1.12-15.01; p =.033), and argatroban-treated patients had significantly reduced od
79 new thrombosis, was reduced significantly in argatroban-treated patients versus control subjects with
81 s with heparin-induced thrombocytopenia (767 argatroban-treated patients, 193 historical controls).
82 analysis of the composite end point favored argatroban treatment in HIT (P=0.010) and HITTS (P=0.014
83 was significantly more frequent in high-dose argatroban versus heparin patients: 57.1% versus 20.0% (
86 all molecule active site inhibitors, such as argatroban, were the observation that fibrinopeptide A h
87 ns of heparin, danaparoid, fondaparinux, and argatroban with VITT-Ab/PF4 complexes using an ex vivo m