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Cell Biochemistry Martinsried |
1. Introduction:
- General risk indicators like overweight, smoking, high blood pressure,
humoral indicators like altered lipid fractions in the peripheral blood,
as well as cellular indicators like monocyte/makrophage lipid
receptors indicate the risk for myocardial infarction on a statistical
but not on an individual person level.
- The appearence of thrombocyte activation antigens like CD62, CD63 or thrombospondin on the thrombocyte surface membrane is the consequence of accelerated blood flow through arteriosclerotically narrowed coronary arteries. Myocardial infarction is ultimately caused by thrombocyte aggregates obstructing such arteries. It seems of interest to determine thrombocyte activation antigen patterns for individual patient risk assessment of myocardial infarction. A blood test would be substantially easier, with lower risk and less costly than coronary angiography from a cathether.
- The average expression of the above antigens on thrombocytes of angiographically verified myocardial infarction risk patients is increased in a statistically significant way. The specificity and sensitivity of each of these parameters alone is, however, too low to identify individual risk patients.
2. Goal:
Identification of myocardial infarction risk patients from peripheral
blood thrombocyte activation antigen expression (CD62, CD63, thrombospondin,
IgG binding). The activation antigen expression is flow cytometrically
determined on thrombocytes in platelet rich plasma.
3. CLASSIF1 Data Pattern Classification:
The classification of the learning set of normal individuals,
angiographically verified myocardial risk as well as of diabetic patients
(type II) provides correct recognition of
> 95%
of normal and infarction risk patients, while diabetic patients are only
recognized in around 50% of the cases.
4. Conclusion:
- The
standardized
and automated evaluation of flow cytometrically
determined CD62, CD63 and thrombospondin
thrombocyte activation antigens permits a > 95%
correct identification of individual myocardial
infarction risk patients from thrombocyte activation
antigen measurements.
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