Myocardial infarction heparin therapy

J Heparin-induced thrombocytopenia (HIT) is a serious immune-mediated problem that requires immediate intervention. For patients receiving therapeutic UFH doses, a baseline platelet count should be obtained before therapy is initiated and then every-other-day for 14 days or until therapy is stopped, whichever occurs first. HIT should be suspected if a patient develops a thromboembolic event (e.g., DVT, PE, stroke, myocardial infarction, limb artery occlusion) during or soon after receiving UFH. The platelet... 

Collen, D. (1998). Staphylokinase a potent, uniquely fibrin-selective thrombolytic agent. Nature Med. 4(3), 279-284. Collins, R. et al. (1997). Drug therapy—aspirin, heparin and fibrinolytic therapy in suspected acute myocardial infarction. N. Engl. J. Med. 336(12), 847-860. 

Drug therapy of acute coronary syndromes including unstable angina and non-Q-wave myocardial infarction includes use of aspirin, heparin and anti-ischaemic drugs and is similar in older patients to other age groups. Activation of platelet thromboxane production in the coronary circulation has been demonstrated in unstable angina. The risk of myocardial infarction or death is reduced by approximately 50% by early aspirin therapy in recommended doses of 160-325 mg per day and continued... 

Krumholz HM, Hennen J, Ridker PM, Murillo JE, Wang Y, Vaccarino V et al. Use and effectiveness of intravenous heparin therapy for treatment of acute myocardial infarction in the elderly. J Am Coll Cardiol 1998 31(5) 973-9. 

Randomized comparison of direct thrombin inhibition versus heparin in conjunction with fibrinolytic therapy for acute myocardial infarction results from the GUSTO-lib Trial. Global Use of Strategies to Open Occluded Coronary Arteries in Acute Coronary Syndromes (GUSTO-lib) Investigators. J Am Coll Cardiol, 1998.31(7) 1493-8. 

Small subcutaneous closes of heparin have been found to be effective in high-nsk post-surgical patients and in patients with acute myocardial infarction. The preventive treatment is commenced a few hours before an operative procedure and continued postoperatively for 4 to 5 days. As the result of a study in 1975. low-dose heparin prophylaxis in high-nsk patients who undergo abdomina-thoracic surgery has become a widely accepted practice, However, preventive anticoagulant therapy, to date, has been unsatisfactory and controversial in the instances of hip surgery or prostatectomy. 

Efficacy and safety oftenecteplase in combination with enoxaparin, abciximab, or unfractionated heparin the ASSENT-3 randomized trial in acute myocardial infarction. Lancet 2001 358 605. LincoffAM, Califf RM, Van De WerfE etal. Mortality at I year with combination platelet glycoprotein llb/llla inhibition and reduced-dose fibrinolytic therapy vs conventional fibrinolytic therapy for acute myocardial infarction GUSTO V randomized trial. JAMA 2002 288 2130. 

Behar S, Hod H, Kaplinsky E, et al, Argatroban versus heparin as adjuvant therapy to thrombolysis for acute myocardial infarction safety considerations-ARGAMI-2 study. Circulation 1998 98 1-453-1-454. 

The Hirulog and Early Reperfusion or Occlusion (HERO) -2 Trial Investigators. Thrombin-specific anticoagulation with bivalirudin versus heparin in patients receiving fibrinolytic therapy for acute myocardial infarction the HERO-2 randomised trial. Lancet 2001 3 58 1 855-1 863,... 

Patients with acute coronary syndromes such as acute myocardial infarction and unstable angina remain at risk for recurrent myocardial ischemia despite therapy with antiplatelet agents and heparin. Although first clinical trials indicate a possible use of oral direct TIs for the prevention of cardiovascular events in patients after acute myocardial infarction, the presently available data are still limited and it has not... 

Acute myocardial infarction (MI) Fibrinolytic therapy Streptokinase Alteplase Reteplase Heparin Aspirin Reduced coronary and all-cause mortality GISSI-1 ISIS-2 GISSI-2/ISG ISIS-3 GUSTO >120,000 10... 

Pharmacokinetics Streptokinase therapy is instituted within 4 hours of a myocardial infarction and is infused for 1 hour. Its ti/2 is less than a half-hour. Thromboplastin time is monitored and maintained at two to five times control value. On discontinuation of treatment, either heparin or oral anticoagulants may be administered. 

Antiplatelet therapy (aspirin or clopidogrel) reduces the incidence of fatal and of nonfatal myocardial infarction in patients with unstable angina, used alone or with low-dose heparin. 

Adverse effects. Haemorrhage occurs but is less of a problem with low doses of heparin it remains a particular risk in patients treated after failed fibrinol5 c therapy for acute myocardial infarction. Platelet transfusion after cessation of abciximab is necessary for refractory or life threatening bleeding. After transfusion, the antibody redistributes to the transfused platelets, reduces the mean level of receptor blockade and improves platelet function. Thrombocytopenia may occur from 1 hour to days after commencing treatment in up to 1% of patients. This necessitates platelet counts at 2-4 hours and then daily if severe, therapy must be stopped and, if necessary, platelets transfused. EDTA-induced pseudothrombocytopenia has been reported and a low platelet count should prompt examination of a blood film for agglutination before therapy is stopped. 

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. 

Two forms of heparin-induced thrombocytopenia (HIT) have been observed. The first (HIT I) is a transient, mild, and benign thrombocytopenia seen soon after initiation of heparin therapy (normally within 2 days) and is felt to be due to inherent plateletaggregating properties of heparin. A second, more severe form of HIT (HIT II) is typically seen later and is immune-mediated. The incidence of HIT II is estimated at 3-5%. The onset is generally 3-14 days after initiation of heparin therapy but may occur sooner with repeat exposure. HIT II may occur with any dose and type of heparin, but the frequency is highest with continuous intravenous infusions of unfractionated heparin. HIT with subsequent thrombosis is a feared complication. These thrombi can form in the venous or arterial circulation. Thrombotic complications include necrotic skin lesions, myocardial infarction, stroke, and gangrene. Hyperkalemia may be seen with heparin therapy due to aldosterone synthesis inhibition. 

Y. Uchida, A. Yanagisawa-Miwa, F. Nakamura, K. Yamada, T. Tomaru, K. Kimura, and T. Morita, Angiogenic therapy of acute myocardial infarction by intrapcricardial injection of basic fibroblast growth factor and heparin sulfate an experimental study, Am Heart J130, 1182-1188 (1995). 

Theroux P, Welsh RC. Meta-analysis of randomized trials comparing enoxaparin versus unfractionated heparin as adjunctive therapy to fibrinolysis in ST-elevation acute myocardial infarction. Am J Cardiol... 

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