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Cardiac troponin I release correlates with myocardial infarction size
1Institut für Medizinische Chemie & Biochemie, Universität Innsbruck, Austria.
Insights
Cardiac troponin I levels correlate with myocardial infarct size in patients receiving thrombolytic therapy. Troponin I remains elevated longer than creatine kinase MB, offering a more prolonged indicator of cardiac damage.
Area of Science:
- Cardiology
- Biomarker Research
- Nuclear Medicine
Background:
- Acute myocardial infarction (AMI) diagnosis relies on cardiac biomarkers.
- Cardiac troponin I (cTnI) and creatine kinase MB (CK-MB) are key markers.
- Assessing infarct size is crucial for patient prognosis.
Purpose of the Study:
- To compare cTnI and CK-MB levels with infarct size estimates.
- To evaluate the correlation between cTnI release and myocardial scar.
- To determine the diagnostic utility of cTnI in Q-wave AMI.
Main Methods:
- Serial blood sampling for cTnI, CK, and CK-MB in 15 AMI patients.
- Thrombolytic therapy administered to all patients.
- Myocardial scar quantified using SPECT with Tc-sestamibi, compared with cTnI and CK-MB levels.
Main Results:
- cTnI and CK-MB peaked in parallel, with strong correlation (r=0.76).
- cTnI remained elevated longer than CK-MB, detectable up to day 4.
- Significant correlations found between Tc-sestamibi defect size and cTnI (r=0.53) and CK-MB (r=0.64).
Conclusions:
- Cardiac troponin I release is correlated with infarct size in AMI.
- cTnI offers a more sustained biomarker profile compared to CK-MB.
- SPECT Tc-sestamibi defect size is a reliable indicator of infarct size, correlating with cTnI release.
Abstract:
Cardiac troponin I, creatine kinase, and creatine kinase MB activity were tested in serial blood samples from 15 patients with first-time Q wave acute myocardial infarction (2 anterior and 13 inferior wall infarctions). All patients received intravenous thrombolytic therapy. Cardiac troponin I and creatine kinase MB activity were compared with scintigraphic estimates of myocardial scar (single photon emission computed tomography [SPECT] with 99mTechnetium-isonitrile [Tc-sestamibi]) on late images at rest about 5 weeks after myocardial infarction. Scintigraphic defect sizes ranged from 3.2 to 41.2% (median: 27.3%) of left ventricle. Cardiac troponin I increased and peaked in parallel with creatine kinase MB activity, and the peak values correlated with each other (r = 0.76, p = 0.002). Troponin I stayed increased for several days longer than creatine kinase and creatine kinase MB activity. It could be detected at least until the 4th day after admission. Significant correlation coefficients were found between 99mTc-isonitrile defect sizes and areas under cardiac troponin I curves (r = 0.53, p = 0.042) and between 99mTc-isonitrile defect sizes and cumulative creatine kinase MB activity release (r = 0.64, p = 0.01). Animal studies have already shown a very close correlation between histologic infarct size and SPECT 99mTc-isonitrile defect size. Therefore, our results indicate that cardiac troponin I release in patients with acute myocardial infarction is also correlated with infarct size.