Heparin Binds Plasma Proteins; Angiomax® (bivalirudin) Binds Specifically to Thrombin Heparin (long strand) binds to other plasma proteins (colored molecules)

Slides:



Advertisements
Similar presentations
Heparin Resistance “Heparin resistance is a term used to describe the situation when patients require unusually high doses of heparin to achieve a therapeutic.
Advertisements

Major Hemorrhagic Events (Acute Phase) No significant increase in rate of major hemorrhage ESSENCE n = 3171 TIMI 11B n = 3910.
1 PERIPROCEDURAL PHARMACOTHERAPHY IN PRIMARY ANGIOPLASTY SM Ashraf PROFESSOR MD DM FSCAI FESC FACC Sahakarana Hrudayalaya Pariyaram Medical College Hospital.
Heparin Binds Plasma Proteins: Angiomax ® (Bivalirudin) Binds Specifically to Thrombin Heparin (long strand) binds to other plasma proteins (colored molecules)
1 Replace Heparin and Improve Outcomes New Antithrombotic Strategies in ACS Patients Undergoing PCI ANG-PSL-XXX-XXX.
Applications of bivalirudin in interventional cardiology
Ho PM, et al. JAMA 2009;301: Baseline Characteristics of Patients Taking Clopidogrel After Hospital Discharge a Ho PM, et al. JAMA 2009;301:
STEMI < 6 h Lytic eligible Lytic choice by MD (TNK, tPA, rPA, SK) ENOX < 75 y: 30 mg IV bolus SC 1.0 mg / kg q 12 h (Hosp DC) ≥ 75 y: No bolus SC 0.75.
Noble High School Red Maple 1 Ecology. There were roughly 85% of green leaves on the red maple and there were a lot of leaves that were in the process.
Dr Jonathan Day Senior Director Global Medical The Medicines Company Bivalirudin Advancing Anticoagulation in ACS.
Anticoagulation to the max A Michael Lincoff MD Cardiologist Division of Cardiology Cleveland Clinic Cleveland, OH.
Bivalirudin: Myths vs Reality? Dr Reman McDonagh Nycomed UK Ltd Conflict of Interest: Senior Manager working for Nycomed UK Ltd.
You have 10 seconds to name…
Www. Clinical trial results.org Heparin Increases Platelet Activation Heparin (yellow strands) makes platelets more reactive to activation by other agonists.
Bivalirudin Drugbank ID : DB00006
William O. Suddath, M. D. Director, Interventional Cardiology Training
HIT: The Consequences of Heparin’s Nonspecific Binding to Platelet Factor 4 Heparin is neutralized by platelet factor 4, (PF4), which is present in high.
Antibodies to Heparin–Platelet Factor 4 Complex: Pathogenesis, Epidemiology, and Management of Heparin-Induced Thrombocytopenia in Hemodialysis  Andrew.
A model of the protein C activation complex
Arterioscler Thromb Vasc Biol
Characteristics of High and Low Molecular Weight Heparin Chains
Anti-Coagulants Physical Process of Clotting
Glenn N. Levine et al. JACC 2016;68:
by Nadine Martel, James Lee, and Philip S. Wells
Indirect vs Direct Thrombin Inhibition
Angiomax® (bivalirudin) Inhibits Clot-Bound Thrombin
Nat. Rev. Cardiol. doi: /nrcardio
Cg-OxyR disulfide formation reorganizes its tetrameric conformation.
Name: _______________________________
Figure 3 Management of acute coronary syndrome with intact fibrous cap
Bivalirudin is Cleaved by Thrombin so that there is a Rapid Return to Hemostasis and a Safety Advantage Heparin’s effects on platelets and its reappearance.
Antibodies to Heparin–Platelet Factor 4 Complex: Pathogenesis, Epidemiology, and Management of Heparin-Induced Thrombocytopenia in Hemodialysis  Andrew.
Figure 2 Ischaemic and bleeding outcomes in the major clinical trials
!'!!. = pt >pt > \ ___,..___,..
by Alexey Dementiev, Abel Silva, Calvin Yee, Zhe Li, Michael T
Surface depiction of cluster II epitopes on the surface of ricin toxin
Antithrombin Therapy in the Management of ACS
Parenteral Anticoagulants
The conundrum of acute chest pain in general practice: a nationwide survey in The Netherlands by Ralf Harskamp, Petra van Peet, Jettie Bont, Suzanne Ligthart,
High Sensitivity Troponin (hsTnT) : Result Interpretation Matrix*
OASIS-5: Study Design Randomize N=20,078 Enoxaparin (N=10,021)
Localization of putative cholesterol-binding motifs in the homology model of human glucose transporter 1 (GLUT1) protein. Localization of putative cholesterol-binding.
Francesco Prati et al. JIMG 2013;6:
Correlation between plasma C reactive protein (CRP) and angiopoietin-like protein 4 (ANGPTL4). Correlation between plasma C reactive protein (CRP) and.
Growth factor release from LP-PRP system preparations.
Absolute ST segment elevation at the beginning of the primary percutaneous coronary intervention procedure (A), after guidewire passage (B), after thrombus.
The conundrum of acute chest pain in general practice: a nationwide survey in The Netherlands by Ralf Harskamp, Petra van Peet, Jettie Bont, Suzanne Ligthart,
Clustering of residues for which PREs unaccounted for by the main state were measured. Clustering of residues for which PREs unaccounted for by the main.
Jeffrey L. Anderson et al. JACC 2007;50:e1-e157
Any, acute and subacute stent thrombosis with bivalirudin versus unfractionated heparin (UFH) in predominantly ST segment elevation myocardial infarction.
Adjusted relative risk Adjusted odds ratio
Plasma angiopoietin-like protein 4 (ANGPTL4) in healthy controls (Controls), patients with metabolic syndrome without (MetS−I) and with low-grade inflammation.
Major bleeding with bivalirudin versus unfractionated heparin (UFH) in predominantly ST segment elevation myocardial infarction (STEMI) studies; (A) glycoprotein.
LC8 is structurally variable but conserved in sequence.
Motif sequence logo and surface analysis of LC8.
Decision tree (using the CHAID algorithm) for predicting participation in a cardiac prevention and rehabilitation programme (CPRP) among 420 Jewish and.
Major bleeding with bivalirudin versus unfractionated heparin (UFH) in predominantly non-ST segment elevation acute coronary syndrome (NSTE-ACS) studies;
Fig. 1 Data collection at a 40° tilt angle enabled reconstruction of a cryo-EM map of the NRTN-GFRα2-RET complex at a 5.7-Å resolution. Data collection.
Multifactorial processes involving a wide range of mechanisms of obstructive sleep apnea causing increased risk of future coronary events and poor prognosis.
Use of evidence-based cardiac medications before, during and after hospitalisation for the index event in (A) overall ACS population and (B) patients with.
DNA methylation status is heritable but requires maintenance
Comparison of the predicted binding models of mHA1, mHA6, and mHA 11 to the tubulin protein with that of DAMA-colchicine in the crystal structure. Comparison.
A binding relationship with thrombin
Specificity profiling, activity in human plasma, and x-ray structure
Composition of the most common clusters at the a) onset of the first acute respiratory tract infection (swab A) and b) 3 weeks later (swab B) illustrated.
DNA-binding and double-strand break formation by Vpr.
Competition by G3139 for binding of ClRNH32P-OdT18 to collagen I (A), FGF2 (B), PDGF BB (C), and VEGF (D). Competition by G3139 for binding of ClRNH32P-OdT18.
Structure of the HLA-DR10 β subunit and ligand binding sites.
Study flow chart and diagnosis at discharge from ED
Cardioprotective effects of ivabradine administration in the setting of acute coronary syndromes and myocardial infarction. Cardioprotective effects of.
Presentation transcript:

Heparin Binds Plasma Proteins; Angiomax® (bivalirudin) Binds Specifically to Thrombin Heparin (long strand) binds to other plasma proteins (colored molecules) and platelets, reducing heparin’s availability to bind to AT. Heparin-binding proteins are elevated in acute coronary syndromes (ACS). Angiomax (bright blue) binds only to thrombin (orange). Angiomax is not neutralized by other plasma proteins or platelets; it remains fully active near thrombus. Key Message: Angiomax binding is specific to thrombin. The left panel shows that heparin (depicted as the long strand) binds to other plasma proteins (depicted as colored molecules) and platelets, and reduces heparin’s availability to bind to AT. Heparin-binding proteins are elevated in acute coronary syndromes. Angiomax (depicted as bright blue) binds only to thrombin (depicted as orange). Angiomax is not neutralized by other plasma proteins or platelets and it remains fully active near thrombus. Weitz JI et al. Thromb Res. 2002;106:V275-V284. Wittkowsky AK. Pharmacother. 2002;22(6 Pt 2):97S-104S. Hirsh J et al. Chest. 2001;119(1 suppl):64S-94S. CM Gibson 2006