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Argatroban has been approved in the USA since 2000 for the treatment of thrombosis in patients with HIT and 2002 for anticoagulation in patients with a history of HIT or are at risk of HIT undergoing percutaneous coronary interventions (PCI). [10] [19] It was first introduced in Japan in 1990 for treatment of peripheral vascular disorders. [19]
Argatroban is used as an anticoagulant in individuals with thrombosis and heparin-induced thrombocytopenia. Often these individuals require long-term anticoagulation. If warfarin is chosen as the long-term anticoagulant, this poses particular challenges due to the falsely elevated prothrombin time and INR caused by argatroban.
Argatroban (as well as the hirudins) is used for heparin-induced thrombocytopenia, a relatively infrequent yet serious complication of heparin treatment that requires anticoagulation (as it increases both arterial and venous thrombosis risk) but not with the causative agent, heparin.
An anticoagulant, commonly known as a blood thinner, is a chemical substance that prevents or reduces the coagulation of blood, prolonging the clotting time. [1] Some occur naturally in blood-eating animals, such as leeches and mosquitoes, which help keep the bite area unclotted long enough for the animal to obtain blood.
The three major mechanisms for such an imbalance are enumerated in Virchow's triad: alterations in normal blood flow, injury to the blood vessel wall, and alterations in the constitution of blood (hypercoagulability). Most cases of cerebral venous sinus thrombosis are due to hypercoagulability. [3]
Three important clinical manifestations that may be caused by paradoxical embolism include a stroke, migraine, and acute myocardial infarction, also known as a heart attack. [7] A stroke and migraine in the setting of a paradoxical embolism are caused by the emboli disrupting blood flow in a cerebral artery .
Drug delivery to the brain is the process of passing therapeutically active molecules across the blood–brain barrier into the brain.This is a complex process that must take into account the complex anatomy of the brain as well as the restrictions imposed by the special junctions of the blood–brain barrier.
The origin of the term "Virchow's Triad" is of historical interest, and has been subject to reinterpretation in recent years. [7] While both Virchow's and the modern triads describe thrombosis, the previous triad has been characterized as "the consequences of thrombosis", and the modern triad as "the causes of thrombosis".