Platelet thrombolytic therapy

Heparin (in doses sufficient to prolong the aPTT to 1.5-2 times control value) is usually administered in conjunction with thrombolytictherapy aspirin may also be administered to inhibit platelet aggregation during and/or following post-thrombolytic therapy... 

These agents have been tested in various conditions where platelet activation plays a major role, in particular in patients undergoing percutaneous coronary intervention (PCI), patients admitted with ACS, and patients receiving thrombolytic therapy for acute myocardial infarction (Ml) (Fig. 2). 

Combination therapy with a thrombolytic agent and GPIIb/llla inhibitor has been studied in acute Ml. Various randomized trials (TAMI-8, IMPACT INTRO AMI, TIMI-14, SPEED, GUSTO V) in the coronary literature have shown that combination therapy reduced thrombolysis time and permitted a reduction of thrombolytic doses by 25% to 50% of the normal dose, This is explained by the fact that thrombus is composed of both fibrin and platelets. Thrombolytics only address the fibrin component of acute thrombus, Furthermore, thrombolytics may actually activate platelets directly resulting in additional thrombus formation, Therefore, the addition of GPIIb/llla inhibition facilitates the efficiency of the thrombolytic agent, It is also known that GPIIb/llla inhibition alone can actually dissolve platelet rich clot (41,42,43),... 

Platelet aggregation inhibitors decrease the formation or the action of chemical signals that promote platelet aggregation. These agents have proven beneficial in the prevention and treatment of occlusive cardiovascular diseases, the maintenance of vascular grafts and arterial patency, and as adjuncts to thrombolytic therapy in myocardial infarction. 

COLLER BS. Platelets and thrombolytic therapy. NEngl JMed 322 33-42,1990. 

Type I heparin-induced thrombocytopenia is common and is characterized by a mild transient thrombocytopenia (with platelet counts that usually do not fall below 50 X 10 /1) the thrombocytopenia occurs on the first few days of heparin administration (usually 1-5 days) and requires careful monitoring but not usually withdrawal of heparin. Type I thrombocytopenia is generally harmless and very probably results from direct heparin-induced platelet aggregation. Thrombocjdopenia is most common when large doses of heparin are used, or in some particular circumstances, such as after thrombolytic therapy (35) or in the early orthopedic postoperative period (36) it can abate in spite of continued therapy. Tjrpe I thrombocytopenia is a non-immune reaction, probably due to a direct activating effect of heparin on platelets. 

Balduini CL, Noris P, Bertolino G, Previtali M. Heparin modifies platelet count and function in patients who have undergone thrombolytic therapy for acute myocardial infarction. Thromb Haemost 1993 69(5) 522-3. 

Platelet counts should be carefully monitored for any decline. If thrombocytopenia develops, the time course and severity should help differentiate which type of HIT exists. If HIT I is suspected, heparin may be continued with caution. If HIT II is suspected, heparin therapy should be discontinued and an alternate form of anticoagulation therapy begun. If a low platelet count is encountered with a thrombotic complication, heparin should be discontinued immediately. Thrombolytic therapy or embolectomy may be necessary. Lepirudin (recombinant hirudin) is... 

Patrono C, Coller B, FitzGerald GA, et al. Platelet-active drugs the relationships among dose, effectiveness, and side effects the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004 126 234S-264S. 

Kleiman NS, Ohman EM, Califf RM, George BS, Kereiakes D, Aguirre FV, Weisman H, Schaible T, Topol EJ. Profound inhibition of platelet aggregation with monoclonal antibody 7E3 Eab after thrombolytic therapy. Results of the Thrombolysis and Angioplasty in Myocardial Infarction (TAMl) 8 Pilot Study. J Am CoU Cardiol. 1993 22 381-389. 

By inhibiting fibrinolysis and preserving platelet function, aprotinin has been shown to reduce blood loss and transfusion requirements in cardiac surgery, lung, and liver transplantations, and surgery for hip replacement. Additional indications are hyperfibrinolytic hemostatic disorders and complications of thrombolytic therapies. In Europe, aprotinin has been in clinical use for about 40 years, but in the United States it has been approved for intravenous applications only since 1993 [M. Kunitz,... 

Griguer, P., Brochier, M., Leroy, J., Leclerc, M., Bertrand, A.H. and Chalons, F. (1980). Platelet aggregation after thrombolytic therapy. Angiology, 31, 91-99... 

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