Clinical ramifications of anticoagulant therapy in suspected severe myocardial infarction: organized summary of randomised trials. Exclusions to the are when there is certainly evidence of brand-new development of still left bundle branch stop or a genuine posterior myocardial infarction (proven by JI-101 ST portion depression with prominent R waves within network marketing leads V1 and V2). These circumstances need thrombolytic treatment. Signs and contraindications for thrombolysis in severe myocardial infarction IndicationsClinical background and presentation highly suggestive of myocardial infarction within 6 hours and something or even more of:1?mm ST elevation in several contiguous limb leads2?mm ST elevation in several contiguous upper body leadsNew still left bundle branch stop2?mm ST depression in V1-4 suggestive of true posterior myocardial infarction Sufferers delivering with above within 7-12 hours of onset with persisting upper body aches and ST portion elevation Sufferers aged 75 years delivering within 6 hours of anterior wall structure myocardial infarction is highly recommended for recombinant tissues plasminogen activator Contraindications5.83%, P=0.04). Significantly, clopidogrel was aswell tolerated as aspirin. As a result, it might be reasonable to provide sufferers clopidogrel after severe myocardial infarction if aspirin had been contraindicated or not really tolerated. Risk elements for systemic embolisation when anticoagulation is highly recommended Large anterior wall myocardial infarction Myocardial infarction complicated by severe left ventricular dysfunction Congestive heart failure Echocardiographic evidence of mural thrombus or left ventricular aneurysm Previous emboli Atrial fibrillation The glycoprotein IIb/IIIa antagonists have been tried in conjunction with thrombolysis in acute myocardial infarction, but the various regimens used in recent trials did not confer any additional benefit over conventional treatment. However, there was some evidence of more rapid and complete reperfusion, and these agents warrant further evaluation and refinement. Anticoagulant treatment Long term anticoagulation with heparin followed by warfarin is not needed routinely except in patients at higher risk of venous or systemic thromboembolism. Intracardiac thrombi usually occur within 48 hours after acute myocardial infarction and tend to embolise within the first few weeks. Low dose dalteparin has been shown to reduce the incidence of intramural thrombus (21.9% 14.2%, P=0.03) in patients given thrombolytic treatments, although this is at a risk of small increase in minor bleeding complications. Thus, in patients ARFIP2 at high risk of mural thrombus formation, dalteparin should be started as soon as possible after the diagnosis of acute myocardial infarction. Warfarin should be continued for two to three months, except in the case of atrial fibrillation, when it may be maintained indefinitely. While a patient is taking warfarin, aspirin use may increase the risk of bleeding, but, pending further evidence, many clinicians still continue to use low dose aspirin for its antiplatelet effect. Although thrombus is commonly associated with left ventricular aneurysm (up to 60%), systemic emboli are uncommon (4-5%), and long term anticoagulation does not seem to further reduce the risk of systemic embolisation; thus, anticoagulant treatment is not currently indicated in these patients in the long term. Further reading Cairns JA, Theroux P, Lewis JI-101 D, Ezekowitz M, Meade TW. Antithrombotic agents in coronary artery disease. Collins R, MacMahon S, Flather M, Baigent C, Remvig L, Mortensen S, et al. Clinical effects of anticoagulant therapy in suspected acute myocardial infarction: systematic overview of randomised trials. 1996;313:652-9 ISIS-2 Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. 1988;II:349-60 Oldroyd KG. Identifying failure to achieve complete (TIMI 3) reperfusion following thrombolytic treatment: how to do it, when to do it, and why it’s worth doing. 2000;84:113-5 Mounsey JP, Skinner JS, Hawkins T, MacDermott AF, Furniss SS, Adams PC, et al. Rescue thrombolysis: alteplase as adjuvant treatment after streptokinase in acute myocardial infarction. 1995;74:348-53 The GUSTO Investigators. An international randomized trial comparing 4 thrombolytic strategies for acute myocardial infarction. 1993;329:673-82 National Institute for Clinical Excellence. London: NICE, 2002 Ohman EM, Harrington RA, Cannon CP, Agnelli G, Cairns JA, Kennedy JW. Intravenous thrombolysis in acute myocardial infarction. 2001;119:253-77S Venous thromboembolism is often associated with acute myocardial infarction, although its incidence has fallen since the introduction of thrombolytic treatment. Although no trials have compared the efficacy of low molecular weight heparin with unfractionated heparin in preventing venous thromboembolism after acute myocardial infarction per se, it is likely that these agents are equally effective, and are increasingly used in clinical practice. ? Open in a separate window Figure Electrocardiogram indicating acute inferior.Indications and contraindications for thrombolysis in acute myocardial infarction IndicationsClinical history and presentation strongly suggestive of myocardial infarction within 6 hours plus one or more of:1?mm ST elevation in two or more contiguous limb leads2?mm ST elevation in two or more contiguous chest leadsNew left bundle branch block2?mm ST depression in V1-4 suggestive of true posterior myocardial infarction Patients presenting with above within 7-12 hours of onset with persisting chest pains and ST segment elevation Patients aged 75 years presenting within 6 hours of anterior wall myocardial infarction should be considered for recombinant tissue plasminogen activator Contraindications5.83%, P=0.04). ST depression in V1-4 suggestive of true posterior myocardial infarction Patients presenting with above within 7-12 hours of onset with persisting chest pains and ST segment elevation JI-101 Patients aged 75 years presenting within 6 hours of anterior wall myocardial infarction should be considered for recombinant tissue plasminogen activator Contraindications5.83%, P=0.04). Importantly, clopidogrel was as well tolerated as aspirin. Therefore, it would be reasonable to give patients clopidogrel after acute myocardial infarction if aspirin were contraindicated or not tolerated. Risk factors for systemic embolisation when anticoagulation should be considered Large anterior wall myocardial infarction Myocardial infarction complicated by severe left ventricular dysfunction Congestive heart failure Echocardiographic evidence of mural thrombus or left ventricular aneurysm Previous emboli Atrial fibrillation The glycoprotein IIb/IIIa antagonists have been tried in conjunction with thrombolysis in acute myocardial infarction, but the various regimens used in recent trials did not confer any additional benefit over conventional treatment. However, there was some evidence of more rapid and complete reperfusion, and these agents warrant further evaluation and refinement. Anticoagulant treatment Long term anticoagulation with heparin followed by warfarin is not needed routinely except in patients at higher risk of venous or systemic thromboembolism. Intracardiac thrombi usually occur within 48 hours after acute myocardial infarction and tend to embolise within the first few weeks. Low dose dalteparin has been shown to reduce the incidence of intramural thrombus (21.9% 14.2%, P=0.03) in patients given thrombolytic treatments, although this is at a risk of small increase in minor bleeding complications. Thus, in patients at high risk of mural thrombus formation, dalteparin should be started as soon as possible after the diagnosis of acute myocardial infarction. Warfarin should be continued for two to three months, except in the case of atrial fibrillation, when it may be maintained indefinitely. While a patient is taking warfarin, aspirin use may increase the risk of bleeding, but, pending further evidence, many clinicians still continue to use low dose aspirin for its antiplatelet effect. Although thrombus is commonly associated with left ventricular aneurysm (up to 60%), systemic emboli are uncommon (4-5%), and long term anticoagulation does not seem to further reduce the risk of systemic embolisation; therefore, anticoagulant treatment isn’t presently indicated in these individuals in the long run. Further reading Cairns JA, Theroux P, Lewis D, Ezekowitz M, Meade TW. Antithrombotic real estate agents in coronary artery disease. Collins R, MacMahon S, Flather M, Baigent C, Remvig L, JI-101 Mortensen S, et al. Clinical ramifications of anticoagulant therapy in suspected severe myocardial infarction: organized summary of randomised tests. 1996;313:652-9 ISIS-2 Collaborative Group. Randomised trial of intravenous streptokinase, dental aspirin, both, or neither among 17,187 instances of suspected severe myocardial infarction: ISIS-2. 1988;II:349-60 Oldroyd KG. Identifying failing to achieve full (TIMI 3) reperfusion pursuing thrombolytic treatment: how exactly to get it done, when to accomplish it, and just why it’s well worth performing. 2000;84:113-5 Mounsey JP, Skinner JS, Hawkins T, MacDermott AF, Furniss SS, Adams PC, et al. Save thrombolysis: alteplase as adjuvant treatment after streptokinase in severe myocardial infarction. 1995;74:348-53 The GUSTO Investigators. A global randomized trial evaluating 4 thrombolytic approaches for severe myocardial infarction. 1993;329:673-82 Country wide Institute for Clinical Quality. London: Great, 2002.