An overview of therapeutic interventions in myocardial infarction. Emphasis on secondary prevention.
The high risk of subsequent mortality and morbidity following the occurrence of a myocardial infarction (MI) underlies the importance of instituting effective preventive regimens as part of the overall management of these patients. The aim of such treatment is to prolong survival by preventing sudden and non-sudden death and further major cardiovascular events. Currently available data from randomised, controlled clinical trials in MI patients indicate that early treatment with thrombolytic agents [streptokinase, anisolyated plasminogen streptokinase activator complex (APSAC) or recombinant tissue-type plasminogen activator (rt-PA)] in the first few hours after onset of symptoms significantly reduces the short term mortality following MI, with follow-up studies at 1 year indicating that the early benefits persist long term. The optimum time for initiation of thrombolytic therapy is within 6 hours of onset, but treatment started between 7 and 24 hours after onset can also be beneficial. Similarly, there is good evidence that beta-blockers (e.g. propranolol, timolol, metoprolol, atenolol) and aspirin are effective in reducing both the mortality and reinfarction rate following MI. With beta-blockers, a policy of starting treatment early intravenously and continuing orally for 2 to 3 years seems likely to save more lives than either strategy alone; however, contraindications to beta-blockade reduce the number of patients eligible to receive this treatment. In the case of aspirin, the optimum dosage has yet to be determined, but on the basis of present evidence, it seems reasonable to start treatment early with doses of 160 to 325 mg daily and continue for a year or 2 after recovery. Other studies have shown that long term oral anticoagulant therapy is also effective in reducing the mortality and reinfarction rate after MI. Subcutaneous heparin therapy given for 10 days in patients with acute anterior MI reduces the frequency of left ventricular mural thrombosis, while intravenous heparin given for greater than or equal to 4 days improves coronary artery patency rates following administration of a thrombolytic agent. In a comparison with low dose aspirin, intravenous heparin proved more effective in maintaining coronary artery patency rates after rt-PA thrombolysis. There is also evidence that oral nitrates may reduce mortality in MI patients, especially in those with heart failure. However, current data on the use of antiarrhythmic drugs do not support the routine of these drugs following MI. Similarly, with lipid-lowering agents, the evidence that lowering cholesterol is beneficial in reducing mortality after MI is at present inconclusive. Further studies with these groups of drugs are awaited with interest.(ABSTRACT TRUNCATED AT 400 WORDS)
Hinstridge
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Adis Drug Information Services, Chester, Cheshire, England.
Speight
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D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000787:Angina Pectoris / Q000517:prevention & control; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D000925:Anticoagulants / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000517:prevention & control; D003328:Coronary Thrombosis / Q000517:prevention & control; D006333:Heart Failure / Q000517:prevention & control; D006801:Humans; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy* / Q000517:prevention & control; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D012008:Recurrence; D015912:Thrombolytic Therapy
D000319:Adrenergic beta-Antagonists; D000889:Anti-Arrhythmia Agents; D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors