Product Description
Expected use
For the simultaneous qualitative determination of myoglobin (Myo), creatine kinase MB (CK-MB) and troponin I (cTnI) in human plasma or serum as an aid in the diagnosis of acute myocardial infarction in the emergency room, critical care, point of care - care and hospital measure. The Myo / CK-MB / cTnI test provides a qualitative analytical test result. The qualitative nature of this assay does not provide information on any change, either increase or decrease, in the concentration of cardiac myoglobin, CK-MB and troponin I with a single test.
A quantitative method should be used, if desired, to quantify the concentration of Myo, CK-MB, and cTnI at any given time. Only with serial tests was it possible to conclude a temporary change in the level of Myo, CK-MB and cTnI. Clinical consideration and professional judgment should be applied when interpreting Myo / CK-MB / cTnI test results, especially when using a single test result.
Summary and explanation
Myo, CK-MB, and cTnI are proteins found in heart muscle cells and released into the blood when heart tissue is damaged or dies. Myoglobin is an oxygen-binding heme protein with a molecular weight of 17,800 daltons, normally found in skeletal and cardiac tissue. It makes up about 2% of total muscle protein and is found in the cytoplasm of cells. Creatine kinase is also found in the cytoplasm. CK catalyzes the reversible phosphorylation reaction of creatine with ATP. In humans, CK isozymes have been identified in both the cytosol and mitochondria of cells from a wide variety of tissues.Cytosolic CK exists as a dimeric molecule formed from two types of subunits of a single polypeptide, designated "M" and "B". Each subunit has a molecular weight of approximately 41,000 daltons and different immunological epitopes. These two subunits combine to form three different isozymes of CK: CK-MM, CK-BB, CK-MB. The relative abundance of the particular isozyme depends on the tissue being examined.
The CK-MM isozyme predominates in skeletal muscle tissue, while the CK-MB isozyme is more abundant in cardiac muscle tissue. CTnI is part of the troponin complex that, together with tropomyosin, forms the main component that regulates the Ca ++ -sensitive ATPase activity of actomyosin in skeletal muscle (skeletal and cardiac). The troponin complex consists of three subunits, troponin T (TnT), troponin I (TnI), and troponin C (TnC). Each subunit has a different function with TnC as the Ca ++ binding site, TnT as the tropomyosin binding, and TnI as the inhibitory subunit.There are different isoforms of TnI in skeletal and cardiac muscles (sTnI and cTnI, respectively) with different immunological epitopes that allow the production of heart-specific TnI antibodies.
The cardiac markers myoglobin, CK-MB, and troponin I have been established as useful tools in the diagnosis of acute myocardial infarction (AMI). Since the temporal release patterns of the three markers differ significantly, all three are useful tools in determining the source and timing of chest pain onset. Cell injury by AMI has been shown to result in a blood myoglobin level above the upper limit of normal in approximately 2-3 hours after the onset of chest pain. Peak concentrations are generally observed after 9-12 hours. CK-MB and troponin I are found in the blood at elevated concentrations approximately 4 to 6 hours after the onset of chest pain and peak within 12-24 hours. However, while CK-MB levels return to normal in approximately 72 hours, troponin I levels remain elevated for up to 5-7 days. The use of these three markers is therefore complementary, since they detect cardiac tissue damage over a wide range of times after myocardial infarction.
