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Assessment of left ventricular function using serum cardiac troponin I measurements following myocardial infarction
F S Apple1, S W Sharkey, A Falahati
1Department of Laboratory Medicine and Pathology, Hennepin County Medical Center, The University of Minnesota School of Medicine, Minneapolis 55455, USA. fred.apple@co.hennepin.mn.us
Insights
Cardiac troponin I (cTnI) shows promise for detecting acute myocardial infarction (AMI) and assessing heart function. This study found cTnI to be a more sensitive marker than creatine kinase MB (CK MB) over time, potentially replacing it for AMI diagnosis.
Area of Science:
- Cardiology
- Biomarkers
- Myocardial Infarction
Background:
- Serum creatine kinase (CK) MB levels have been used to assess myocardial injury prognosis.
- Acute myocardial infarction (AMI) diagnosis relies on timely and accurate cardiac biomarker assessment.
Purpose of the Study:
- To compare the diagnostic utility of cardiac troponin I (cTnI) and CK MB mass in patients with AMI.
- To evaluate the correlation between cardiac biomarkers and left ventricular ejection fraction (LVEF).
Main Methods:
- Serial serum samples from 39 AMI patients were analyzed for CK MB mass and cTnI levels over 36 hours.
- Half-life determinations and echocardiography were performed to assess infarct characteristics and left ventricular function.
Main Results:
- cTnI levels remained elevated significantly longer than CK MB levels after 9-12 hours post-chest pain onset.
- Half-life of cTnI differed significantly between non-Q-wave and Q-wave infarcts.
- Elevated peak CK MB and cTnI levels were inversely correlated with LVEF, indicating impaired cardiac function.
Conclusions:
- Cardiac troponin I demonstrates superior sensitivity and duration of elevation compared to CK MB in AMI.
- cTnI is a promising biomarker for assessing infarct size and left ventricular function.
- cTnI may potentially replace CK MB as the preferred cardiac-specific marker for AMI detection.
Abstract:
The prognosis and extent of injury to the myocardium have previously been assessed by increased serum creatine kinase (CK) MB levels. We report findings from 39 consecutive, acute myocardial infarction (AMI) patients presenting 4.5 h (range, 0.7-12.1 h) after the onset of chest pain. We compared CK MB mass (upper reference limit, 5.0 ng/ml) and cardiac troponin I (cTnI; upper reference limit, 0.8 ng/ml) (Stratus II, Dade International) in serial serum specimens obtained over 36 h after chest pain from AMI patients; within 6 h after onset of chest pain. While the appearance of the kinetics of CK MB and cTnI were similar during the initial 24 h following the onset of chest pain, cTnI was increased significantly (p < 0.05) over CK MB after 9 to 12 h. Half-life determinations (mean+/-S.D.) in 22 of the 39 AMI patients demonstrated a significantly (p < 0.01) shorter half-life in non-Q-wave infarcts [t1/2 6.8 h (+/-5.6)] vs. Q-wave infarcts [t1/2 20.4 h (+/-10.7)]. Further serial time versus marker (mean+/-S.D.) results were significantly correlated (p < 0.001, r = 0.66). Sixteen of twenty patients assessed by echocardiography had an abnormal left ventricular ejection fraction (LVEF); mean 37.6 (S.D. 15.2)%, ranging from 15.4 to 67.6%. LVEF was significantly and inversely correlated to peak CK MB (r = .50, p = 0.03), as well as to peak cTnI (r = 0.46, p = 0.04). Based on these findings, cTnI shows excellent promise as a useful marker of infarct size, for the assessment of left ventricular function, and may potentially replace CK MB as the cardiac-specific marker for AMI detection.