Comparative Pharmacology
Head-to-head clinical analysis: ANGIOMAX versus HEPARIN SODIUM 20 000 UNITS IN DEXTROSE 5.
Peer-Reviewed Evidence
Head-to-head clinical analysis: ANGIOMAX versus HEPARIN SODIUM 20 000 UNITS IN DEXTROSE 5.
ANGIOMAX vs HEPARIN SODIUM 20,000 UNITS IN DEXTROSE 5%
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Direct thrombin inhibitor that reversibly binds to the active site of thrombin, blocking its interaction with substrates, thereby inhibiting fibrin formation and activation of coagulation factors V, VIII, and XIII.
Heparin sodium binds to antithrombin III, causing a conformational change that accelerates the inactivation of thrombin and factor Xa, and to a lesser extent factors IXa, XIa, and XIIa, thereby inhibiting coagulation. It also inhibits platelet aggregation and prolongs clotting times.
1 mg/kg intravenous bolus followed by 0.1 mg/kg/hour continuous intravenous infusion for duration of procedure; alternatively, 0.75 mg/kg intravenous bolus followed by 1.75 mg/kg/hour continuous intravenous infusion for up to 4 hours during percutaneous coronary intervention.
Adults: Initial IV bolus 80 units/kg, then continuous IV infusion at 18 units/kg/hour. For therapeutic anticoagulation, adjust to target aPTT 1.5-2.5 times control. Dosing per institutional nomogram.
None Documented
None Documented
Terminal elimination half-life: 25-30 minutes in patients with normal renal function; increased to 2-3 hours in dialysis-dependent patients
Terminal half-life 1.5 hours (range 1-3 hours) for therapeutic doses; dose-dependent, with higher doses prolonging half-life; half-life prolonged in hepatic or renal impairment.
Renal: ~90% unchanged; biliary/fecal: negligible (<1%)
Renal: 50-60% as unchanged drug via glomerular filtration; hepatic metabolism (desulfation) accounts for minor clearance; fecal elimination negligible (<1%).
Category C
Category A/B
Anticoagulant
Anticoagulant