Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 17 unaesthetized dogs several side branches of the left descending coronary artery were ligated. The ST-segment elevation in the epicardial ECG ascended to 22 mV after 5 min and to 19 mV after 20 min. Aortic pressure, left ventricular enddiastolic pressure, heart rate and hemostasiological parameters (thrombin-time, thrombin-coagulase-time, reptilase-time, plasma-fibrinogen, staphylococcal clumping test) did not change significantly. 20 min after the beginning of coronary occlusion, the vessels were reopened. When ST-segment elevation had disappeared, a controlled fibrinolytic therapy (Streptokinase 1.5 Mega I.E. in 30 min, later on 0.75 Mega I.E./h) was induced. When an effective fibrinolysis could be demonstrated by the hemostasiological parameters, the same vessels were occluded again. Now the hemodynamic parameters too did not change significantly, but the ST-segment elevation was significantly diminished for more than 50% compared with simple ligation. A control group, which only got the solvent of the streptokinase, showed the same ST-segment elevation. This effect, induced by streptokinase is ascribed to fibrinogen degradation products and a diminution in the amount of fibrinogen which cause an improvement of microcirculation.
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PMID:[Influence of a streptokinase-induced fibrinolysis on the extent of the acute experimental myocardial infarction (author's transl)]. 116 21

We report our early experience in the use of intravenous Streptokinase in acute coronary occlusion in a peripheral hospital. From 1st November 1988 to 20th July 1989, 30 patients were treated with Streptokinase. The hospital mortality was 1/30 (3.3%) from a non-streptokinase related event. The commonest complication following streptokinase infusion was transient hypotension, affecting 10/30 patients. From a total of 30 patients, 3 had transient bleeding complications and was self limiting. Follow up coronary angiograms were performed on 17/30 patients, demonstrating a patent infarct related artery in 12/17 patients (70.6%). We concluded that it is both feasible and safe to use intravenous streptokinase in a peripheral setting in the treatment of acute myocardial infarction.
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PMID:The use of intravenous streptokinase (SK) in a peripheral hospital in the treatment of acute myocardial infarction. 232 18

Variation in major coagulation parameters was assessed in 87 patients with acute myocardial infarction, treated with streptokinase and/or heparin under angiographic control. Streptokinase treatment was associated with a drop in plasma fibrinogen, plasminogen and alpha 2-antiplasmin, and an increase in serum fibrin/fibrinogen degradation products. The magnitude of coagulation shifts was greater in case of intravenous streptokinase infusion (1,000,000 units over 60 min), as compared to intracoronary streptokinase administration in lower doses (120,000-180,000 units over 60-90 min). In all patients with regained coronary flow, fibrinogen, plasminogen and alpha 2-antiplasmin levels began to decline significantly earlier and/or became normal significantly later, as compared to patients with persisting coronary occlusion. The rates and severity of hemorrhagic complications were basically similar in intravenous and intracoronary routes of administration, in spite of different doses and magnitude of coagulation shifts.
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PMID:[Blood coagulation shifts in patients with myocardial infarction treated with streptokinase]. 306

To assess the efficacy of intravenous streptokinase in patients with acute myocardial infarction, 40 patients (30 men and 10 women, mean age 54 years) with acute myocardial infarction were given 1.5 million U of streptokinase intravenously in 1 hour, and coronary arteriography was performed repeatedly to assess reperfusion. Streptokinase treatment was begun 270 +/- 86 (mean +/- SD) minutes after the onset of chest pain. Of the 40 patients, 34 had total or near total coronary occlusion before streptokinase administration. In 14 (41%) of these 34 patients, some reperfusion occurred during the 90 minutes after the administration of streptokinase, but in only 11 of the 14 was reperfusion present at 90 minutes. After streptokinase administration, all patients received heparin for 8 to 10 days; they were subsequently administered aspirin and dipyridamole. Clinical evidence of reocclusion during the first 24 hours of heparin therapy occurred in one patient. Thus, when given to patients with acute myocardial infarction and total coronary occlusion an average of 4 1/2 hours after the onset of chest pain, high dose intravenous streptokinase achieves reperfusion in only about 40% and results in sustained reperfusion in only about 30%.
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PMID:High dose intravenous streptokinase for acute myocardial infarction: preliminary results of a multicenter trial. 404 46

Despite variable efficacy in achieving recanalization, different thrombolytic agents demonstrate similar abilities to reduce mortality following myocardial infarction. We investigated whether factors other than the ability to achieve coronary artery recanalization are important in mediating the beneficial effects associated with thrombolytic therapy during acute myocardial infarction using anaesthetized rabbits. Coronary artery occlusion was produced using either a single ligature (which was released to initiate reperfusion) or by placing two ligatures 5 mm apart to allow the formation of an intraluminal thrombus. In this case, ligature removal followed by thrombolysis was required for recanalization to occur. Experiments were performed in the presence and absence of streptokinase. Streptokinase was most effective in reducing myocardial necrosis when associated with thrombolytic recanalization (total left ventricular infarct size was reduced from 37 +/- 7% to 13 +/- 1%, P < 0.01). However, streptokinase also reduced infarct size in the absence of reperfusion (45 +/- 4% vs 35 +/- 2%, P < 0.05), although further work is needed to clarify the mechanisms.
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PMID:Effects of streptokinase on infarct size in rabbits in the presence and absence of coronary artery recanalization. 805 13

Myocardial infarction and thrombolysis are proven to be associated with platelet activation. However, the time relationship of platelet activation with the onset of symptoms and with thrombolysis, and the response to aspirin are not well defined. In this study we measured platelet activity in the early phase of myocardial infarction treated with either streptokinase or recombinant tissue-type plasminogen activator (rt-PA) and evaluated whether and to what extent it may be counteracted by aspirin. Fourty-one patients (mean age 57 +/- 6 years) received thrombolytic therapy after coronary occlusion: 1.5 million units of streptokinase (Group 1; 21 patients) or 100 mg of rt-PA (Group 2; 20 patients). Ten randomly selected patients in either group were given 500 mg aspirin i.v. prior to infusion of the thrombolytic compound and, then, 325 mg/die of aspirin orally. Beta-thromboglobulin (BTG), a marker of platelet activity, was determined at admission, after thrombolysis and in the subsequent 48 hours. At admission, BTG plasma levels averaged 125 +/- 31 IU/ml in Group 1 and 134 +/- 35 IU/ml in Group 2 (NS). Thrombolysis produced a similar increase in platelet activity in both groups, and maximal values were reached at the third hour (196 +/- 43 IU/ml in Group 1 and 192 +/- 39 in Group 2, p < 0.001 vs baseline and NS between groups). Levels of BTG were higher in streptokinase-treated group starting from 24 hours (p < 0.05). Differences in BTG levels between aspirin-treated and aspirin-untreated patients became significant at 48 hours after thrombolysis in both groups. An inverse correlation was found between time elapsed from onset of symptoms and BTG value on admission (r = -0.86, p < 0.001); in patients admitted within 2 hours after the beginning of symptoms, and having the higher BTG levels, thrombolysis did not induce a significant increase in platelet activity; this, on the contrary, was observed in patients admitted later. Platelet activation is greater early after myocardial infarction and is differently influenced by thrombolytic treatment, depending on the delay of the patient's admission. Streptokinase and rt-PA induce a similar increase in platelet activity which is more persistent after streptokinase; cycloxygenase inhibition with aspirin seems to influence platelet activity only starting from the second day.
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PMID:[Platelet activation in the early phases of acute myocardial infarction]. 980 73