Clinical Significance of Three Rapid Detection of Myocardial Infarction
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Three rapid diagnostic tests for myocardial infarction refer to: troponin (CTnI), creatine kinase isoenzyme (CKMB), and myoglobin (Myo).
Myoglobin (Myo): It is a myocardial protein marker that abnormally increases early after myocardial injury. Serum Myo begins to increase 2 hours after the onset of acute myocardial infarction (AMI), and reaches a peak at 4-6 hours. Since Myo is not myocardial specific, myoglobin negativity helps to rule out the diagnosis of AMI; the strategy for using this marker is to take advantage of its high negative predictive value and sensitivity to rule out AMI
Troponin I (CTn I): is currently recognized as a reliable indicator for the diagnosis of myocardial infarction with high specificity and long duration. Cardiac troponin generally increases gradually in peripheral blood 4-8 hours after myocardial injury, and the high value appears at 12-24 hours. Elevated cardiac troponin was still detectable in peripheral blood 7-10 days after myocardial injury. The concentration of cTnI in the blood of patients with acute myocardial infarction can be as high as 100-300ng/ml. It is mainly used for the diagnosis of myocardial injury-especially minor injury, and can also be used as a reliable indicator of myocardial ischemia during cardiac surgery, and can be used to evaluate myocardial protective measures. Indicator of thrombolytic therapy after acute myocardial infarction; to judge the effect of reperfusion.
CK-MB: It is currently the "gold standard" for AMI detection trusted by clinicians, with high specificity.
Relevant markers should be detected simultaneously during the detection of myocardial injury markers. The release times of the three markers Myo, cTnI, and CK-MB are different. Rapid determination of the three markers at the same time is more convenient and faster than separate determination. Make fast and accurate diagnosis.
Troponin is a complex composed of three proteins: troponin T, troponin C, and troponin I. The main role of troponin is to inhibit the interaction between striated muscle actin and myosin. In addition, troponin is an inhibitor of actin myosin ATPase. There are three isomeric forms of troponin, and troponin I is only present in cardiac tissue. The specific detection of cTnI can be achieved by the application of anti-cTnI monoclonal antibody, so cTnI has been used as a standard diagnostic method for acute myocardial infarction.
It has been reported that the detection of cTnI concentration is very effective in the diagnosis of myocardial-specific disorders in patients with AMI, cardiac contusion, and unstable stenosis. When an acute myocardial infarction occurs, cTnI is released into the blood within 4 to 8 hours due to the disturbance of the myocardium, so its concentration is out of the concentration range of a healthy person. Typically, cTnI concentrations peaked 12-18 hours after the onset of AMI and were maintained for 5-10 days. For AMI patients, the increase or decrease of cTnI concentration during treatment was similar to that of CKMBmass. However, recent studies have found that cTnI is more effective than CK-MB in detecting myocardial disorders, especially skeletal muscle disorders.
Myoglobin MYO mainly exists in the cardiac muscle and skeletal muscle. When skeletal muscle and cardiac muscle are damaged (acute myocardial infarction), excessive exercise and muscle disease, myoglobin is released into the blood. In acute myocardial infarction, due to myocardial tissue disorder The concentration of myoglobin in serum deviates from the normal value within 2-3 hours in the initial stage of heartache, reaches the highest value in 6-9 hours, and returns to normal value in about 24 hours. The concentration of myoglobin in blood is effective for monitoring the diagnosis and treatment of acute myocardial infarction In addition, it can also be used as an indicator of coronary re-dredging in thrombolytic therapy. The myoglobin concentration reaches the highest level after 30 minutes to 2 hours of dredging. The myoglobin concentration can be used as an early diagnosis indicator of myocardial infarction.
CKMB mainly exists in the myocardium and is a very effective indicator in the diagnosis of acute myocardial infarction. AMI should be considered if the patient has a sequential change in CK-MB activity that increases and decreases, and the peak value exceeds the upper limit of the reference value by 2 times, and there is no other reason to explain it. When CKMB mass (CK-MB mass) is used for the diagnosis of myocardial infarction, the recommended diagnostic cutoff is the 99% quantile of the upper limit of the reference value for normal people. CK-MB mass has a positive rate of 50% in the diagnosis of AMI 3 hours after the onset of chest pain. The diagnostic positive rate at 6 hours can reach 80%. If thrombolytic therapy is not performed after the onset of AMI, CK-MB usually increases within 3 to 8 hours, peaks at 9 to 30 hours after the onset, and returns to normal levels within 48 to 72 hours. Compared with the determination of total CK, the peak time of CK-MB was slightly earlier and disappeared faster. Due to the narrow diagnostic window, the diagnosis of AMI with a longer duration of onset cannot be made. This can also be used clinically to diagnose reinfarction. During thrombolytic therapy, the early increase of CK-MB and the peak in a short time are the signs of AMI. CK-MB increased by more than 2.2 times after 2 hours of treatment for inferior wall AMI, and more than 2.5 times after treatment for anterior wall AMI, both of which indicated myocardial reperfusion. The sensitivity of the above criteria was 85% and the sensitivity was 100%. .







