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This study examines the response of 3 different groups of patients to anticoagulants: 50 patients previously treated with streptokinase for acute myocardial infarction (AMI) (group 1), 24 patients with AMI who had received anticoagulants without prior thrombolysis (group 2) and 11 subjects who received anticoagulants for noncoronary indications (group 3). No significant differences were detected between groups 2 and 3; therefore, they were combined for analysis. After streptokinase, patients required 37,755 [+ or -] 1,516 (mean [+ or -] standard error of the mean) U of heparin per day to achieve the desired activated partial thromboplastin time (APTT). The dosage was 30,294 [+ or -] 1,089 U/day in patients without antecedent thrombolysis (p (Am J Cardiol 1990;66:28-30), Thrombosis or the formation of blood clots within the coronary arteries, the major blood vessels supplying the heart, may block the flow of blood to the heart. The cessation of blood supply results in myocardial infarction (heart attack), and causes the deterioration of heart tissue. Acute myocardial infarction (AMI) may be treated with thrombolytic therapy, the use of agents that break down blood clots. Reperfusion or the restoration of blood flow to the heart muscle can be achieved in 75 percent of patients, but re-occlusion remains a problem. Most thrombolytic agents are combined with anticoagulants, which prevent the formation of blood clots. Treatment with the thrombolytic agent streptokinase may be followed by therapy with the anticoagulants heparin and warfarin (coumadin). However, patients treated with streptokinase may be resistant to anticoagulants. The response to anticoagulant treatment was assessed in 50 patients who had a history of a previous AMI which was treated with streptokinase; 24 patients with AMI; and 11 patients with non-heart-related conditions requiring anticoagulant therapy. Because there were no differences in the responses of patients given anticoagulants for heart- and non-heart-related conditions, these two groups of patients were combined for purposes of data analysis. Patients treated with streptokinase required a greater dose of heparin and more time to achieve an adequate blood clotting time, as indicated by the activated partial thromboplastin time (APTT), when compared with patients who did not receive prior thrombolytic therapy. Although streptokinase-treated patients required a higher dose of heparin, they had lower APTT values. Streptokinase-treated patients also required more time to reach anticoagulation with warfarin, compared with patients who were not treated with streptokinase. The findings demonstrate that AMI patients who receive streptokinase may be partially resistant to anticoagulation, and this may contribute to an increased risk of recurrent occlusion. (Consumer Summary produced by Reliance Medical Information, Inc.)

We report two cases of pulmonary edema due to scorpion sting. Radionuclide ventriculography (MUGA scan) showed localized cardiac dysfunction. The cardiac injury induced by the scorpion venom persisted for a [...]

We describe a patient with acute inferior myocardial infarction who developed a 'saddle' aortic embolus during streptoldnase infusion. Three months previously, this patient had sustained an anterior infarction, and an [...]

The pattern of reverse redistribution on the day 10 poststreptokinase resting thallium-201 myocardial scintigrams is a common finding in patients who have undergone streptokinase therapy in evolving myocardial infarction. To investigate this phenomenon, 67 patients who underwent streptokinase therapy were studied preand 10 days poststreptokinase therapy resting thallium-201 studies, poststreptokinase therapy resting radionuclide ventriculography and coronary arteriography (60 of the 67 patients). Of the 67 patients, 50 (75%) showed the reverse redistribution pattern on the day 10 thallium-201 study (Group I), 9 (13%) had a nonreversible defect (Group II) and the remaining 8 (12%) had a normal study or showed a reversible defect (Group III). The reverse redistribution pattern was associated with patency of the infarct-related artery (100%), quantitative improvement in resting thallium-201 defect size from day 1 to day 10 study (94%) and normal or near normal wall motion on day 10 radionuclide ventriculography (80% of segments with marked and 54% of those with mild reverse redistribution). In contrast, nonreversible defects were associated with significantly less frequent patency of the infarct-related artery (67%, p = 0.01), improvement in defect size (11%, p < 0.001) and normal or near normal wall motion (21%, p < 0.05). Group III patients were similar to Group I with respect to these variables. The quantitated thallium-201 percent washout was higher in the regions with the reverse redistribution pattern (49 ± 15%) compared with the contralateral normal zone (24 ± 15%, p < 0.001).

Thirty-four patients with acute myocardial infarction were treated prospectively using a new strategy of prehospital intravenous streptokinase given by a physician-operated mobile intensive care unit. The 29 prehospital-treated patients who had experienced no previous myocardial infarction were compared to a similar group treated with streptokinase inhospital. Patients receiving streptokinase in the prehospital phase of acute myocardial infarction had smaller infarcts and better residual myocardial function than the group given streptokinase inhospital in terms of peak creatinine phospholdnase, ejection fraction, computer-derived dysfunction index, and electrocardiographic QRS score. The only difference between these groups at baseline was the duration of pain prior to initiation of streptokinase therapy. There were no major complications related to prehospital administration of streptokinase.