cgp-39393 has been researched along with bivalirudin* in 8 studies
7 review(s) available for cgp-39393 and bivalirudin
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Looking back into the future: desirudin in acute coronary syndromes and coronary stenting.
Although percutaneous coronary intervention (PCI) is a highly effective modality for the management of acute coronary syndromes, it can potentiate the existing prothrombotic state around lesion areas and lead to ischaemic complications. Adjunctive pharmacologic treatment with heparin reduces the risk of ischaemic events, but the utility of heparin is limited by its unpredictable pharmacodynamic effects and its inability to modulate fibrin-bound thrombin. Additionally, a potential risk of heparin-induced thrombocytopenia is associated with heparin use. Direct thrombin inhibitors (DTIs) have emerged as potential alternatives to heparin in patients undergoing PCI. Bivalirudin is a DTI indicated for use in PCI. Results from various studies have suggested clinical benefit associated with the use of bivalirudin, driven primarily by the reduction in bleeding risks compared with the standard treatment regimens. Of concern, however, is a significant increase in acute stent thrombosis with bivalirudin monotherapy compared with heparin plus GPIIb/IIIa inhibitors following primary PCI for ST-segment elevation myocardial infarction (STEMI). Desirudin is a highly potent DTI with greater binding affinity than bivalirudin for thrombin. This report provides a comparative overview of the pharmacology and clinical utility of desirudin and bivalirudin in the setting of PCI. Topics: Acute Coronary Syndrome; Angioplasty, Balloon, Coronary; Antithrombins; Clinical Trials as Topic; Hirudins; Humans; Peptide Fragments; Recombinant Proteins; Stents | 2011 |
Heparin-induced thrombocytopenia and cardiac surgery.
Heparin-induced thrombocytopenia (HIT) is an important, increasingly recognized antibody-mediated complication of heparin therapy occurring in approximately 0.5-5% of patients receiving heparin for at least 5 days. HIT is a prothrombotic disorder that typically presents with a 50% platelet count drop, thrombotic event manifesting usually 5-14 days after starting heparin, or both. HIT antibodies usually decrease to negative titers/levels within 3 months. When there is clinical suspicion of HIT, heparin should be discontinued and alternative anticoagulation should be considered, as well as laboratory evaluation for HIT.. HIT immunoassay results should be used for clinical decision-making about initial anticoagulation management. Recent data reevaluate the importance of absolute titers of HIT antibodies as a risk factor for clinical occurrence. Although laboratory assays are routinely used, current data suggest that increasing optical densities are more likely associated with a positive 14C-serotonin release assay and HIT. HIT is also associated with a greater risk for adverse events, so even though alternative anticoagulation is used, clinicians should be aware of this hypercoagulable syndrome.. For patients with HIT, alternative anticoagulation is available, but for cardiovascular surgery, if the operation cannot be delayed until HIT antibodies have become negative, alternative anticoagulation strategies are recommended, although patients with HIT are at a greater risk for adverse outcomes. Topics: Anticoagulants; Arginine; Cardiovascular Surgical Procedures; Heparin; Hirudins; Humans; Peptide Fragments; Pipecolic Acids; Platelet Activation; Platelet Count; Platelet Factor 4; Recombinant Proteins; Sulfonamides; Thrombin; Thrombocytopenia | 2010 |
[Direct thrombin inhibitors: pharmacology and application in cardiovascular anesthesia].
The options for drug-controlled anticoagulation are becoming noticeably more manifold. In the area of anaesthesiology and intensive care, there are furthermore special disease patterns, such as heparin-induced thrombocytopenia (HIT) to be known, diagnosed and treated. This article gives a review of the substance groups of the direct thrombin inhibitors (DTI) as alternative anticoagulants for HIT in combination with cardiovascular diseases. For the administration of DTIs, experience and the correct dose are the keys to success and are the deciding factors for the two sides of haemostasis: thrombosis and haemorrhage. Topics: Anesthesia; Anticoagulants; Cardiovascular Surgical Procedures; Critical Care; Hemorrhage; Hemostasis; Heparin; Heparin Antagonists; Hirudins; Humans; Peptide Fragments; Recombinant Proteins; Thrombin; Thrombosis | 2008 |
New anticoagulant agents: direct thrombin inhibitors.
Decades of research have been devoted to developing effective, safe, and convenient anticoagulant agents. In recent years, much emphasis has been placed on the development of direct thrombin inhibitors (DTIs) that offer benefits over agents like heparin and warfarin including the inhibition of both circulating and clot-bound thrombin; a more predictable anticoagulant response, because they do not bind to plasma proteins and are not neutralized by platelet factor 4; lack of required cofactors, such as antithrombin or heparin cofactor II; inhibiting thrombin-induced platelet aggregation; and absence of induction of immune-mediated thrombocytopenia. Various injectable DTIs are currently available and used for many indications. In addition, research is now focusing on oral DTIs that seem promising and offer various advantages, such as oral administration, predictable pharmacokinetics and pharmacodynamics, a broad therapeutic window, no routine monitoring, no significant drug interactions, and fixed-dose administration. Topics: Anticoagulants; Arginine; Atrial Fibrillation; Benzimidazoles; Dabigatran; Fibrinolytic Agents; Half-Life; Hirudins; Humans; Peptide Fragments; Pipecolic Acids; Pyridines; Recombinant Proteins; Stroke; Sulfonamides; Thrombin | 2008 |
Anticoagulation for acute coronary syndromes: from heparin to direct thrombin inhibitors.
The anticoagulant properties of heparin were discovered in 1916, and by the 1930s researchers were evaluating its therapeutic use in clinical trials. Treatment of unstable angina with unfractionated heparin (UFH), in addition to aspirin, was introduced into clinical practice in the early 1980s. UFH was combined with aspirin to suppress thrombin propagation and fibrin formation in patients presenting with acute coronary syndromes (ACS) or patients undergoing percutaneous coronary intervention (PCI). However, UFH stimulates platelets, leading to both activation and aggregation, which may further promote clot formation. Clinical trials have demonstrated that newer agents, such as the low-molecular-weight heparins (LMWHs), are superior to UFH for medical management of unstable angina or non-ST-segment elevation myocardial infarction. Increasingly, the LMWHs have been used as the anticoagulant of choice for patients presenting with ACS. For patients undergoing PCI, LMWH provides no sub-stantial benefit over UFH for anticoagulation; however, direct thrombin inhibitors (DTIs) have demonstrated safety and efficacy in this setting. UFH is likely to be replaced by more effective and safer antithrombin agents, such as DTIs. DTIs have antiplatelet effects, anticoagulant action, and most do not bind to plasma proteins, thereby providing a more consistent dose-response effect than UFH. The FDA has approved 4 parenteral DTIs for various indications: lepirudin, argatroban, bivalirudin, and desirudin. The antiplatelet, anticoagulant, and pharmacokinetic properties of bivalirudin support its use as the anticoagulant of choice for both lower- and higher-risk patients, including those undergoing PCI. Topics: Acute Disease; Angina Pectoris; Angina, Unstable; Angioplasty, Balloon, Coronary; Anticoagulants; Arginine; Fondaparinux; Hemorrhage; Heparin; Heparin, Low-Molecular-Weight; Hirudins; Humans; Models, Molecular; Molecular Structure; Myocardial Ischemia; Peptide Fragments; Pipecolic Acids; Platelet Activation; Polysaccharides; Recombinant Proteins; Sulfonamides; Syndrome; Thrombin; Thrombosis | 2007 |
[Clinical use of a new class of anticoagulant drugs: the direct thrombin inhibitors].
The coagulation cascade, and particularly thrombin, plays a very important role in arterial and venous thrombosis. Thereby, it is clear that thrombin inactivation is an optimal strategy for thrombotic disease prevention and treatment. The direct thrombin inhibitors are a new class of anticoagulant drugs directly binding thrombin and blocking its interaction with fibrinogen. The group of direct thrombin inhibitors includes recombinant hirudin (lepirudin and desirudin), bivalirudin, melagatran and its oral precursor, ximelagatran, argotraban and dabigatran. These drugs have several advantages compared to other anticoagulant drugs, and the particular pharmacokinetic properties of some of them could be very important for future management of thromboembolic prophylaxis. The efficacy and safety of these new drugs are evaluated in several clinical trials; however today only few clinical indications are available for the majority of them. Topics: Anticoagulants; Antithrombins; Azetidines; Benzylamines; Clinical Trials as Topic; Drug Therapy, Combination; Fibrinolytic Agents; Hirudins; Humans; Peptide Fragments; Recombinant Proteins; Thromboembolism; Treatment Outcome | 2006 |
Thrombin-directed inhibitors: pharmacology and clinical use.
Topics: Anticoagulants; Arginine; Azetidines; Benzylamines; Blood Coagulation; Fondaparinux; Heparin; Hirudins; Humans; Peptide Fragments; Pipecolic Acids; Polysaccharides; Recombinant Proteins; Sulfonamides; Thrombin; Thrombosis; Warfarin | 2005 |
1 other study(ies) available for cgp-39393 and bivalirudin
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USAN Council. List No. 374. New names. Bivalirudin. Desirudin.
Topics: Amino Acid Sequence; Anticoagulants; Hirudins; Molecular Sequence Data; Peptide Fragments; Recombinant Proteins | 1995 |