Myoglobin is an oxygen-binding protein of transverse striated skeletal muscles and myocardium. Its molecule contains iron, structurally similar to the hemoglobin molecule and is responsible for the transport of 02 in skeletal muscles. Myoglobin is one of the earliest markers of myocardial damage, as the increase in its level in the blood is determined already in 2-4 hours after the onset of acute myocardial infarction. The peak concentration is achieved in up to 12 hours, and then within 1-2 days decreases to normal. Due to the fact that the release of free myoglobin into the blood can be caused by a number of other pathological conditions, it is not enough to justify the diagnosis of myocardial infarction with just this marker.
The most specific and reliable markers of myocardial necrosis are cardiac troponins T and I (allow to detect even the most minor damage to the myocardium).
Troponins are proteins involved in the process of regulation of muscle contraction. Troponin-I and troponin-T of the myocardium and skeletal muscles have structural differences, which makes it possible to isolate their cardiospecific forms isolated by methods of immunoassay. Approximately 5% of troponin-I is in free form in the cytoplasm of cardiomyocytes. It is due to this fraction that troponin-I is detected in the blood plasma after 3-6 hours after damage to the heart muscle. The larger part of troponin-I in the cell is in the bound state and when the myocardium is damaged it is released slowly. As a result, the increased concentration of troponin in the blood persists for 1 -2 weeks. Typically, the peak concentration of troponin-I is observed at 14-20 hours after the onset of chest pain. Approximately 95% of patients 7 hours after the development of acute myocardial infarction, an increase in the concentration of troponin-I is determined.
A slight increase in the level of cardiac troponin-I should be interpreted with considerable caution, as this may be due to various pathological conditions that cause damage to myocardial cells. That is, an increased level of troponin alone can not serve as a basis for diagnosing myocardial infarction.
If a patient with suspected acute coronary syndrome without ST segment elevation has elevated troponin T and / or troponin I levels, then this condition should be regarded as a myocardial infarction and appropriate therapy should be performed.
The determination of troponins allows detection of myocardial damage in approximately one-third of patients who do not have an increase in CF-CK. To detect or exclude damage to the myocardium, repeated blood sampling and measurements are necessary within 6-12 hours after admission and after any episode of severe pain in the chest.
Creatine phosphokinase (creatine kinase)
Creatine phosphokinase (creatine kinase) is an enzyme contained in the myocardium and skeletal muscles (in a small amount is contained in the smooth muscles of the uterus, gastrointestinal tract and brain). The brain and kidneys contain primarily isoenzyme BB (brain), in skeletal muscle - MM (muscle) and in the heart of MB enzyme. The most specific is possessed by creatine kinase MB. There is a high correlation between the level of its activity and the mass of necrosis. With damage to the myocardium and skeletal muscles, the enzyme escapes from the cells, leading to an increase in the activity of creatine kinase in the blood. In 2-4 hours after an anginal attack, the level of creatine kinase MB in the blood increases significantly, and therefore the definition of creatine phosphokinase and creatine kinase MB in the blood is widely used in the early diagnosis of myocardial infarction. The normal level of creatine kinase in the blood in men is <190 U / L and <167 U / L in women. The normal content of creatine kinase-MB in the blood is 0-24 U / l. Creatine phosphokinase (CK) and its MB CK isoenzyme are not specific enough, since false-positive results in skeletal muscle injury are possible. In addition, there is a significant overlap between normal and pathological serum concentrations of these enzymes.
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Lactate dehydrogenase (LDH)
Lactate dehydrogenase (LDH) is an enzyme involved in the process of glucose oxidation and the formation of lactic acid. It is contained in virtually all organs and tissues of a person. Most of it is contained in the muscles. Lactate is normally formed in cells in the process of breathing and, with a full supply of oxygen, does not accumulate in the blood. There is its destruction to neutral products, after which it is excreted from the body. Under hypoxic conditions, lactate accumulates, causing a feeling of muscle fatigue and disrupting tissue breathing.
The isoenzymes of this enzyme LDH1-5 are more specific. The most specific is LDG1. With myocardial infarction, the excess of LDH1 and LDH2 ratio is more than 1 (in the norm of LDP / LDH2 <1). The norm of lactate dehydrogenase for adults is 250 U / l.
With necrosis of the myocardium, an increase in the concentration of these markers in the serum does not occur simultaneously. The earliest marker is myoglobin. An increase in the concentration of MB CKK and troponin occurs somewhat later. It should be borne in mind that at boundary levels of cardiomarkers there is the following trend:
- the lower their level, the more false positive diagnoses;
- the higher, the more false-negative diagnoses.
Determination of troponin and cardiomarkers
The rapid diagnosis of myocardial infarction is easily accomplished at any time with the help of various qualitative test systems for the determination of "Troponin T". The result is determined 15 minutes after the application of blood to the test strip. If the test is positive and a second band appears, then the level of troponin exceeds 0.2 ng / ml. Therefore, there is a heart attack. The sensitivity and specificity of this test is more than 90%.
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