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viewpoints SALVAGING THE MYOCARDIUM IN ACUTE MI BY THROMBOLYSIS Prompt streptokinase treatment can succeed Acute myocardial infarction (MI) as a manifestation of ischaemic heart disease is a leading cause of hospital admission. Thrombus formation in a coronary artery causes a marked reduction in regional blood flow and myocardial necrosis ensues if vital intracellular metabolic function is stopped for long enough. Many treatments have been directed towards preservation of the jeopardised myocardium but none have resulted in substantial salvage. Two studies have investigated the use of thrombolytic treatment with streptokinase in salvaging the myocardium following acute MI [see Therapy section p.6]. Both studies involved patients who were treated soon after the onset of chest pain symptoms. The study by Anderson et al. managed to treat patients within 4 hours of symptom onset, arid streptokinase was given with supportive heparin. This study produced a higher reperfusion success rate than that of Khaja et a/., who did not give supportive heparin and had a 5.4-hour lag time between onset of symptoms and treatment. The study by Anderson et al. also showed a more clear-cut and significant benefit in a number of objective assessments. It would seem that the differences in success rates and objective parameters between the studies is caused by the time taken to initiate treatment and possibly the use of supportive heparin to prevent rethrombosis. Essentially, these 2 studies are complementary and underline the success that can be obtained with streptokinase so long as treatment is initiated soon after symptoms arise and before extensive myocardial necrosis occurs. Swan. H.J.C.: New England Journal of Medicine 308: 1354 (2 Jun 1983) 2 INPHARMA 9 Jul 1983 0156-2703/83/0709-0002/0$01 .00/0 @) ADIS Press

SALVAGING THE MYOCARDIUM IN ACUTE MI BY THROMBOLYSIS

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viewpoints SALVAGING THE MYOCARDIUM IN ACUTE MI BY THROMBOLYSIS

Prompt streptokinase treatment can succeed Acute myocardial infarction (MI) as a manifestation of ischaemic heart disease is a leading cause of hospital admission. Thrombus formation in a coronary artery causes a marked reduction in regional blood flow and myocardial necrosis ensues if vital intracellular metabolic function is stopped for long enough. Many treatments have been directed towards preservation of the jeopardised myocardium but none have resulted in substantial salvage. Two studies have investigated the use of thrombolytic treatment with streptokinase in salvaging the myocardium following acute MI [see Therapy section p.6]. Both studies involved patients who were treated soon after the onset of chest pain symptoms. The study by Anderson et al. managed to treat patients within 4 hours of symptom onset, arid streptokinase was given with supportive heparin. This study produced a higher reperfusion success rate than that of Khaja et a/., who did not give supportive heparin and had a 5.4-hour lag time between onset of symptoms and treatment. The study by Anderson et al. also showed a more clear-cut and significant benefit in a number of objective assessments. It would seem that the differences in success rates and objective parameters between the studies is caused by the time taken to initiate treatment and possibly the use of supportive heparin to prevent rethrombosis. Essentially, these 2 studies are complementary and underline the success that can be obtained with streptokinase so long as treatment is initiated soon after symptoms arise and before extensive myocardial necrosis occurs. Swan. H.J.C.: New England Journal of Medicine 308: 1354 (2 Jun 1983)

2 INPHARMA 9 Jul 1983 0156-2703/83/0709-0002/0$01 .00/0 @) ADIS Press