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Serum immunoglobulin E response to myocardial infarction
A Szczeklik1, K Sladek, A Szczerba
1Department of Medicine, Copernicus Academy of Medicine, Cracow, Poland.
Circulation
|June 1, 1988
Summary
Serum immunoglobulin E (IgE) levels increase after myocardial infarction, potentially protecting patients with high levels from severe complications. This suggests IgE plays a role in heart disease pathogenesis.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Pathogenesis of Heart Disease
Background:
- Mast cells are implicated in coronary heart disease pathogenesis.
- Immunoglobulin E (IgE)-mediated mechanisms activate mast cells, releasing mediators affecting blood flow.
Purpose of the Study:
- To systematically determine serum IgE concentrations in patients with acute myocardial infarction.
- To investigate the relationship between serum IgE levels and myocardial infarction severity and complications.
Main Methods:
- Serum IgE concentrations were measured in 100 patients with acute myocardial infarction.
- Serum IgE levels were also assessed in 16 subjects with acute coronary insufficiency without infarction.
- Comparison of IgE changes with blood eosinophil and serum IgG levels post-infarction.
Main Results:
- Serum IgE showed a significant increase on days 3 and 5, peaking on day 7, and declining by week 3 after myocardial infarction.
- Patients with high initial IgE levels (>200 IU/ml) exhibited a greater IgE increase and fewer severe complications.
- Serum IgE levels remained unchanged in patients with acute coronary insufficiency without infarction.
Conclusions:
- Circulating IgE may sensitize mast cells and eosinophils in myocardial infarction, facilitating mediator release.
- High IgE levels might offer protection against infarction complications due to mediator ratios and decreased platelet function.