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Conjunctive antithrombotic therapy for thrombolysis in myocardial infarction
J H Chesebro1, J J Badimon, A F Ortiz
1Cardiac Unit, Massachusetts General Hospital, Boston 02114.
Insights
Potent antithrombotic therapy, including heparin and aspirin, is crucial for managing acute myocardial infarction. This treatment aims to reduce thrombus formation, prevent recurrent events, and minimize the need for revascularization procedures.
Area of Science:
- Cardiology
- Thrombosis Research
- Pharmacology
Background:
- Acute coronary thrombosis and myocardial infarction typically result from atherosclerotic plaque disruption.
- Understanding arterial thrombosis involves local arterial wall substrates, blood flow rheology, systemic factors, and thrombin's role.
Purpose of the Study:
- To discuss the pathogenesis of arterial thrombosis.
- To highlight the benefits of potent antithrombotic therapy in acute myocardial infarction.
- To outline maximal antithrombotic treatment strategies.
Main Methods:
- Review of the pathogenesis of arterial thrombosis.
- Description of maximal antithrombotic therapy regimens for acute myocardial infarction.
- Guidelines for transitioning from intravenous to subcutaneous heparin and initiating warfarin therapy.
Main Results:
- Potent antithrombotic therapy can accelerate thrombolysis and reduce recurrent ischemia, infarction, death, and need for revascularization.
- Maximal therapy involves specific heparin dosing, aspirin, and potentially warfarin for high-risk patients.
- Maintaining activated partial thromboplastin time (aPTT) at 2-3 times control for 5-7 days is key for heparin therapy.
Conclusions:
- Aggressive antithrombotic therapy is essential for improving outcomes in acute myocardial infarction.
- Warfarin therapy post-acute phase can prevent recurrent events in high-risk individuals.
- Optimized antithrombotic strategies reduce mortality and morbidity associated with coronary artery disease.
Abstract:
Disruption of an atherosclerotic plaque in coronary arteries with a minor stenosis is the usual stimulus for acute coronary thrombosis and myocardial infarction. In this article the pathogenesis of arterial thrombosis and contributions of local arterial wall substrates, the rheology of blood flow, systemic factors, and the critical role of thrombin in the formation of thrombus are discussed. More potent antithrombotic therapy may accelerate exogenous thrombolysis, allows endogenous thrombolysis, and should reduce recurrent infarction and ischemia and death, as well as need for coronary revascularization. Maximal antithrombotic therapy for acute myocardial infarction includes an intravenous bolus of heparin at 100 U/kg followed by an intravenous infusion--at 1,200 U/hr for patients weighing 60-80 kg, 1,300 U/hr for those weighing > 80 kg, and 1,000 U/hr for those weighing < 60 kg (or 17 U/kg/hr)--to maintain the activated partial thromboplastin time at 2-3 times control (60-90 sec) for at least 5-7 days. To convert intravenous to subcutaneous administration, use 14,000-17,000 U every 12 hours and initially overlap the intravenous infusion by 2 hours. The loading dose of aspirin on admission to the hospital is 160 mg followed by 80 mg/day. High-risk patients should be considered for conversion of heparin to warfarin therapy for at least 3 months at an international normalized ratio of 2.5-4.0 for the prevention of recurrent ischemia, reinfarction, death, thromboembolism, reactivation of thrombosis, and reduced necessity for revascularization.