Prevention of Myocardial Damage in Acute Myocardial Ischemia by Early Treatment with Intravenous Streptokinase

Abstract

We evaluated the effectiveness of early intravenous administration of 750,000 units of streptokinase in 53 patients with acute myocardial ischemia treated by a mobile-care unit at home (9 patients) or in the hospital (44 patients). Treatment was begun an average (+/- S.D.) of 1.7 +/- 0.8 hours from the onset of pain. Non-Q-wave infarctions developed subsequently in eight patients, whereas all the others had typical Q-wave infarct patterns. In 81 per cent of the patients the infarct-related artery was patent at angiography performed four to nine days after admission. Vessel patency was independent of the time of treatment, but residual left ventricular function was time dependent. Patients treated less than 1.5 hours after the onset of pain had a significantly higher ejection fraction (56 +/- 15 vs. 47 +/- 14 per cent; P less than 0.05) and infarct-related regional ejection fraction (51 +/- 19 vs. 34 +/- 20 per cent; P less than 0.01) and a lower QRS score (5.6 +/- 4.9 vs. 8.6 +/- 5.5; P less than 0.01) than patients receiving treatment between 1.5 and 4 hours after the onset of pain. Patients treated earlier by the mobile-care unit also had better-preserved left ventricular function than patients treated in the hospital. We conclude that thrombolytic therapy with streptokinase is most effective if given within the first 1.5 hours after the onset of symptoms of acute myocardial infarction.

Beneficial effects of low-flow perfusion resumed early after zero-flow ischemia on myocardial energy metabolism and mechanical function: 31P-NMR study in the isolated perfused rat heart.

“…Although due caution is necessary to extrapolate these findings to clinical settings, it may be reasonable to assume that the best way for salvage of the afflicted myocardium is the earliest possible resumption of perfusion. This conclusion is in agreement with the prevailing opinions of today (Reimer et al 1977; Koren et al 1985;Hugenholts 1987;GISSI 1987;Tomoda 1988). However, under conditions under which the immediate resumption of perfusion is not feasible for some reason or other, it is better to take some measures to reopen the flow to the afflicted myocardium, whatever low rate it may be until the time of complete perfusion than to waste time doing nothing.…”

“…With the increasing availability of thrombolytic agents (Koren et al 1985;Hugenholtz 1987;GISSI 1987) and coronary balloon angioplasty (Meyer et al 1982; O'Neill et al 1986; Rothbaum et al 1987) for emergency revascularization, early reperfusion has become a practical reality for large numbers of patients with acute myocardial infarction (AMI). However, apart from the high hospital mortality rate associated with unsuccessful angioplasty (Simoons et al 1988; Stack et al 1988; Ellis et al 1989), opinion is still divided on the immediate application of the percutaneous transluminal coronary angioplasty (PICA) in AMI because of the much-debated deleterious effects which an abrupt reperfusion might produce in the myocardium (reperfusion injury), and some recent clinical studies (Topol et al 1987a, b) have advocated delayed elective PTCA subsequent to thrombolytic therapy instead of immediate PICA.…”

Early Contrast-Enhanced MRI Predicts Late Functional Recovery After Reperfused Myocardial Infarction

“…1,2 Significant improvement in mortality and morbidity may be achieved even when reperfusion occurs up to 6 to 12 hours after acute myocardial infarction (MI). 3 However, protracted ischemia may produce an admixture of necrotic and viable myocardium.…”

Review: The revised role of ACE-inhibition after myocardial infarction in the thrombolytic/primary PCI era

“…32 Both early and late reperfusion of the infarctrelated coronary artery have been shown to reduce the extent of LV dilatation. [3][4][5][6][7][8][33][34][35][36][37] The results of almost 14,000 mainly thrombolysed patients included in the echocardiographic substudy of Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI-3) showed no relevant change in LV size after a median of 10 days following MI (Figure 1). Interestingly, even patients predicted to be at high risk of long-term LV dilatation showed only limited progression of LV dilatation after 10 days.…”

“…by administration of thrombolytic therapy or direct percutaneous coronary intervention [PCI]) proved effective in preventing or minimising LV dilatation and reducing cardiac morbidity and mortality by limiting the infarct size. [3][4][5][6][7][8] Secondly, angiotensin-converting enzyme (ACE) inhibitors attenuated LV dilatation and reduced cardiac morbidity and mortality, especially in patients with LV dysfunction and/or without thrombolytic therapy. [9][10][11][12] However, after early reperfusion, the extent of residual LV dilatation is often limited, and additional reduction of LV dilatation by ACE inhibitor (ACE-I) treatment may be negligible.…”