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Pathological changes after intravenous streptokinase treatment in eight patients with acute myocardial infarction
S G Richardson1, D C Allen, P Morton
1Histopathology Department, Belfast City Hospital.
Insights
Following streptokinase treatment for myocardial infarction, patent coronary arteries were found in most patients. Thrombus on complex lesions may resist lysis, but myocardial hemorrhage is typically confined to necrotic areas.
Area of Science:
- Cardiology
- Pathology
Background:
- Severe acute myocardial infarction requires effective treatment.
- Intravenous streptokinase was used to treat acute myocardial infarction.
- Coronary artery patency post-treatment is a key indicator of reperfusion success.
Purpose of the Study:
- To investigate the histological findings of infarct-related coronary arteries after streptokinase treatment.
- To determine the characteristics of myocardial infarcts and associated hemorrhage.
Main Methods:
- Necropsy examination of eight patients treated with intravenous streptokinase for severe acute myocardial infarction.
- Histological analysis of infarct-related coronary arteries to assess patency, plaque morphology, and intimal lesions.
- Evaluation of infarct thickness and myocardial hemorrhage.
Main Results:
- Five of eight patients had a patent infarct-related coronary artery, with stenoses caused by fibrofatty atheromatous plaques.
- No residual thrombi or acute intimal lesions were found in patent arteries.
- Three infarcts were partial thickness, while two were transmural.
- Six infarcts showed noticeable myocardial hemorrhage confined to necrotic areas.
Conclusions:
- Thrombus overlying complex atherosclerotic lesions may be more resistant to lysis by streptokinase than thrombus on simple plaques.
- Myocardial hemorrhage outside the infarct area, potentially leading to cardiac rupture or delayed healing, is uncommon.
Abstract:
At necropsy five of eight patients (mean age 57 years) who died after intravenous streptokinase treatment for severe acute myocardial infarction (mean Peel index = 18) were found to have a patent infarct related coronary artery. Coronary artery stenoses were caused by fibrofatty atheromatous plaques; there were no residual thrombi in the lumen or acute intimal lesions. Three of these infarcts were of partial thickness (less than two thirds wall width) with sparing of the outer third of the myocardium and subendocardial zones. In the other three patients the infarct related coronary arteries remained histologically closed with residual lumen thrombi and underlying intimal lesions. Two infarcts were transmural. Six of the eight infarcts were noticeably haemorrhagic. Myocardial haemorrhage was confined to areas of necrotic myocardium and did not affect viable regions. These findings suggest that thrombus overlying a complex lesion may be more difficult to lyse than thrombus overlying a simple fibrofatty plaque. They also suggest that myocardial haemorrhage outside the infarct area, which might lead to cardiac rupture or delayed healing, does not usually occur.