Abstract
In the ischemic state, which leads to myocardial infarction, there is a gradation of cardiac muscle injury and a sequence of functional loss. On coronary occlusion an immediate cellular leak of potassium occurs and the rate of relaxation declines. Within 1 to 2 minutes there is complete loss of contraction followed by the onset of contracture in 7 to 10 minutes in isolated preparations. The major problem of this initial period, if the occlusion zone is not too great, is electrical dysfunction. The next 1 to 6 hours is the period of variable reversible injury. Positron emission tomography technique and fatty acid and carbohydrate tracers quantitatively assess regions that are metabolically competent. The problem is to maintain and improve the competence of these regions during reperfusion, whether by thrombolytic therapy (streptokinase) or tissue plasminogen activator, percutaneous transluminal angioplasty, acute coronary artery bypass graft or by total vented bypass and regional reperfusion without thoracotomy (procedure under development).
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