Looking Beyond Reperfusion
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چکیده
The root cause of acute myocardial infarction (AMI) was postulated way back in in 1912 by James Herrick who proposed it to be thrombotic occlusion of the coronary artery [1,2]. This hypothesis prioritized thrombolytic agents into the line of treatment which could remove thrombotic occlusion, restore blood supply to myocardium and prevent or limit the extent of myocardial damage. Hume et al in 1958 was the first to propose this treatment of acute MI based on fibrinolysis [3]. By the late 1970s Reimer, Jennings et al. [4,5] laid down, evidence of reperfusion therapy for the treatment of AMI. In their classical experiment a canine model was subjected to coronary occlusion. The myocardial cell death began within 15 minutes of occlusion and proceeded rapidly in a wave front from endocardium to epicardium. On releasing the occlusion within a narrow time frame (<3-6 hrs) myocardial salvage could be achieved. The degree of salvage was inversely proportional to the duration of ischemia and occurred in a reverse wave front from epicardium to endocardium. The extent of necrosis could be modified by changing metabolic demands and varying collateral blood supply as well as the duration of occlusion. Subsequent to this finding, in 1975 Chazov et al. [6] initiated the phase of reperfusion for the patients of AMI wherein thrombi were lysed by infusing streptokinase directly into the blocked coronary arteries [6]. Subsequently it was also demonstrated that timely reperfusion actually salvaged severely ischemic myocardium [7]. The experimental evidence however, of thrombotic occlusion in the coronary artery of AMI patients was obtained in 1980. It was a landmark study conducted by Marcus DeWood and colleagues who performed coronary angiography in the early hours of AMI and found thrombotic occlusion to be present in the coronary arteries in 87% of patients studied within 4 hours of symptom onset [8,9].
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