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[Thrombolysis in acute myocardial infarct of embolic origin]
H R Meléndez1, J L Leiva Pons, S Simón
1Departamento de Urgencias, INCICH.
Insights
Embolic myocardial infarction, though uncommon, shares similarities with atherosclerotic causes and responds to thrombolysis. Intravenous streptokinase effectively treated acute embolic myocardial infarction in three patients, improving outcomes.
Area of Science:
- Cardiology
- Vascular Medicine
- Thrombotic Disorders
Context:
- Embolic myocardial infarction (MI) accounts for 5-13% of MIs.
- Patients with embolic MI are at high risk for systemic embolism.
- Pathogenesis is similar to atherosclerotic MI, suggesting susceptibility to thrombolysis.
Purpose:
- To evaluate the efficacy of intravenous streptokinase in treating acute myocardial infarction of embolic origin.
- To report on the clinical outcomes of three patients with embolic MI due to various underlying conditions.
Summary:
- Three patients with embolic MI (causes: rheumatic heart disease, coarctation of aorta, mechanical valve prosthesis) received intravenous streptokinase.
- All patients achieved myocardial reperfusion; two experienced post-infarction angina.
- Management included coronary artery bypass grafting for reocclusion and anticoagulant therapy for persistent thrombus.
Impact:
- Thrombolytic therapy with streptokinase is effective in acute embolic MI, preventing ischemic damage progression.
- Early suspicion of embolic MI in patients with embolism risk factors and normal coronary arteries is crucial.
- Improved clinical outcomes are observed with timely thrombolytic intervention.
Abstract:
Myocardial infarctions which are derived from embolic source have an incidence of 5-13%. They are at risk of systemic embolism. The pathogenesis of myocardial infarction is similar to that of those myocardial infarction whose etiology is atherosclerosis. This make it susceptible to thrombolysis. We report 3 patients with either inactive rheumatic heart disease, coarctation of the aorta or mechanical valvular prosthesis as the probable causes of an embolic infarction. It was located in the posterior-inferior region with a dorsal extension. These patients were treated with intravenous streptokinase. The three of them fulfilled criteria for myocardial reperfusion. Two of them suffered post-infarction angina. In the first case reocclusion of the righ coronary artery was observed; thus a saphenous vein graft was undertaken. In the second, the persistence of thrombus required three month treatment with anticoagulants. The third patient showed not coronary lesions. In conclusion, thrombolytic therapy with streptokinase in acute infarction of embolic origin prevents the progression of ischemic damage and betters the clinical outcome of the patient. Furthermore such disease should be suspected in patients that have risk factors for systemic embolism and normal coronary arteries and with obstruction of a single vessel.