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Effect of acute phase response on cumulative troponin T release
J H Diris1, J A Kragten, A H Kleine
1Department of Clinical Chemistry, Academic Hospital, Maastricht, The Netherlands.
Insights
The acute phase response after myocardial infarction influences troponin T release, particularly in patients not receiving thrombolytic therapy. This suggests the inflammatory response impacts cardiac marker kinetics post-heart attack.
Area of Science:
- Cardiology
- Biochemistry
- Immunology
Background:
- Acute myocardial infarction triggers an acute phase response.
- Cardiac markers like troponin T and hydroxybutyrate dehydrogenase are released into circulation.
- The relationship between the acute phase response and troponin T release requires further investigation.
Purpose of the Study:
- To investigate the effect of the acute phase response extent on cumulative troponin T release after acute myocardial infarction.
- To compare the influence of the acute phase response on troponin T versus hydroxybutyrate dehydrogenase release.
- To assess if thrombolytic therapy modifies the relationship between acute phase response and cardiac marker release.
Main Methods:
- Quantified the acute phase response by measuring cumulative plasma C-reactive protein.
- Related cumulative C-reactive protein to cumulative plasma release of hydroxybutyrate dehydrogenase and troponin T.
- Analyzed data from patients receiving and not receiving thrombolytic therapy.
- Utilized a two-compartment model for calculating cumulative protein release.
Main Results:
- Cumulative plasma C-reactive protein was significantly higher in patients not receiving thrombolytic therapy.
- Cumulative troponin T release was significantly related to cumulative C-reactive protein, especially in patients not receiving thrombolytic therapy.
- The intensity of the acute phase response did not affect the relative proportions of troponin T and hydroxybutyrate dehydrogenase released.
Conclusions:
- The extent of the acute phase response influences troponin T release post-myocardial infarction.
- Thrombolytic therapy appears to modulate the relationship between inflammation and cardiac marker kinetics.
- Findings highlight the complex interplay between inflammatory response and myocardial injury markers.
Unlabelled:
We studied a possible effect of the extent of the acute phase response after acute myocardial infarction on the cumulative release of troponin T. The height of the acute phase response might influence the cumulative release of troponin T, bound to the myofibrillar structures of the heart, in a different way compared to the free cytoplasmic cardiac marker hydroxybutyrate dehydrogenase (EC 1.1.1.27). To investigate this, the cumulative amount of C-reactive protein in plasma, i.e. the quantified acute phase response, was related to the cumulative plasma release of hydroxybutyrate dehydrogenase (an established method for infarct sizing) on the one hand and to that of troponin T on the other hand. The study was performed in patients receiving (n=16) and in patients not receiving (n=6) thrombolytic therapy. Cumulative protein release was calculated using a two-compartment model for circulating proteins.
Conclusions:
The cumulative amount of plasma C-reactive protein is significantly higher in the patients not receiving thrombolytic therapy, as is in accordance with earlier studies. The cumulative amount of troponin T released is significantly related to the cumulated concentration of C-reactive protein, especially in patients not receiving thrombolytic therapy. The intensity of the acute phase response, estimated from cumulative plasma C-reactive protein response, has no effect on the relative proportions of troponin T and hydroxybutyrate dehydrogenase released into plasma.