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Antikoagulační léčba doc. MUDr. Jaromír Chlumský, PhD.

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Prezentace na téma: "Antikoagulační léčba doc. MUDr. Jaromír Chlumský, PhD."— Transkript prezentace:

1 Antikoagulační léčba doc. MUDr. Jaromír Chlumský, PhD.

2 1.Antitrombotická léčba = ACP, ticlodipin, clopidogrel 2.Trombolytická léčba = streptokináza, TPA 3.Antikoagulační léčba =heparin, warfarin

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10 Other High Risk 32%  Antiplatelet Trialists’ Collaboration Efficacy in Prevention of Ischemic Events * OR = Odds reduction, a percentage reduction of an outcome measure comparing treatment to control group. Antiplatelet Trialists’ Collaboration. BMJ. 1994;308:81–106. Antiplatelet Therapy Control % of Patients Having Stroke, MI, or Vascular Death Prior Stroke/TIA Acute MI Prior MI High Risk 0% 5% 10% 15% 20%25% 22%  29%  25%  27%  All Patients Odds Reduction*

11 ASA – 7 dní, indobufen- 12 hodin ticlopidin - neutropenie clopidogrel- rezistence prasugrel

12 Coagulation Cascade XIIa XIa IXas Intrinsic Pathway (surface contact) Xa Extrinsic Pathway (tissue factor) VIIa Thrombin (IIa) Thrombin-Fibrin Clot aPTT PTa Heparin / aLMWH (AT-III dependent) Hirudin/Hirulog (direct antithrombin) Courtesy of VTI

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14 The Procoagulant State in Thrombolysis Amplification Vascular Injury Activation of Platelets And Coagulation Xa Thrombin (IIa)

15 Role of Platelets in Thrombus Formation in Acute Ischemic Events Atherosclero tic Vessel Plaque Ruptur e Platelet Adhesion, Activation, and Aggregation Thrombu s Formatio n Thromboti c Occlusion MI MI Stroke Stroke Vascular VascularDeath Lipid Core Schafer AI. Am J Med. 1996;101:199–209. Vessel wall injury  Plaque rupture  Exposure of subendothelial collagen and other platelet-adhering ligands

16 Inactivation of Thrombin by Heparin-AT Complexes When thrombin binds to fibrin, it becomes resistant to inactivation by heparin. AT Heparin Fibrin Thrombin HF S C

17 AT Unfractionated Heparin Differential inhibitory activity against factor Xa and IIa activity Thrombin (IIa) HF S C AT LMWH Thrombin (IIa) HF S C By binding to AT, most UH and LMWH can inhibit Xa activity. Fewer than half the chains of LMWH are of sufficient length to also bind factor IIa, therefore has decreased anti-IIa activity.

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22 Délka antikoagulační léčby doživotněHŽT + AT III def., homozygot aPC, kombinované TF, životohrožující příhoda 6-18 měsícůHŽT+ nádor, protein C nebo S deficience, žilní insuficiencie 6 měsícůHŽT + věk do 45 let, recidiva nebo RA, PE 3 měsíceHŽT po operaci doživotněHŽT + AT III def., homozygot aPC, kombinované TF, životohrožující příhoda 6-18 měsícůHŽT+ nádor, protein C nebo S deficience, žilní insuficiencie 6 měsícůHŽT + věk do 45 let, recidiva nebo RA, PE 3 měsíceHŽT po operaci

23 Physiologic Fibrinolytic System (plasmin - key to fibrinolysis) Plasminogen –synthesized in the liver –circulates in high concentrations –significant homology with LP(a) Plasminogen Activator –t-Pa and u-PA released by endothelium –converts plaminogen to plasmin –fibrin surface facilitates fibrinolysis by providing the binding site for the formation of plasminogen-tPA complex –free floating t-PA has low activity Fibrinolytic Inhibitor –PAI-1 is the main inhibitor of tPA & uPA Plasminogen activators (t-PA, u-PA) Plasminogen Plasminogen activator inhibitors (PAI-1, PAI-2)  2-Antiplasmin FibrinFDP Plasmin

24 Trombolytická léčba Streptokináza: j bolus dále j /l hod Nebo j/ hod hod tPA: 15 mg bolus, 50 mg l hod, 35 mg l hod

25 Indikace IM plicní embolie lokálně – embolie či trombosy


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