Diagnosis of myocardial infarction

During myocardial infarction, a significant release of various substances (cardiomarkers) from the necrosis and damage zones is observed. And this release is more significant, the greater the mass of the affected myocardium. Measuring the levels of cardiomarkers accelerates and specifies such an event as diagnostics of myocardial infarction, as well as the ability to predict its further development. The main biochemical markers used in the diagnostics of myocardial infarction are myoglobin, troponin I, troponin T, creatine phosphokinase and lactate dehydrogenase.

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Myoglobin

Myoglobin is an oxygen-binding protein of striated skeletal muscles and myocardium. Its molecule contains iron, is structurally similar to the hemoglobin molecule and is responsible for the transport of O2 in skeletal muscles. Myoglobin is one of the earliest markers of myocardial damage, since an increase in its level in the blood is determined already 2-4 hours after the onset of acute myocardial infarction. The peak concentration is reached within 12 hours, and then within 1-2 days it 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, this marker alone is not enough to accurately diagnose myocardial infarction.

Troponins

The most specific and reliable markers of myocardial necrosis are cardiac troponins T and I (they allow detecting even the most minor myocardial damage).

Troponins are proteins involved in the regulation of muscle contraction. Troponin-I and troponin-T of the myocardium and skeletal muscles have structural differences, which allows for the isolation of their cardiospecific forms using immunoassay methods. Approximately 5% of troponin-I is free in the cytoplasm of cardiomyocytes. It is due to this fraction that troponin-I is detected in the blood plasma as early as 3-6 hours after damage to the heart muscle. The majority of troponin-I in the cell is bound and is released slowly when the myocardium is damaged. 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 14-20 hours after the onset of chest pain. Approximately 95% of patients have an increase in troponin-I concentration 7 hours after the development of acute myocardial infarction.

A slight increase in cardiac troponin-I should be interpreted with considerable caution, as it may be due to various pathological conditions that cause damage to myocardial cells. That is, an increased troponin level alone cannot serve as a basis for diagnosing myocardial infarction.

If a patient with suspected acute coronary syndrome without ST segment elevation has an elevated level of troponin T and/or troponin I, then this condition should be assessed as myocardial infarction and appropriate therapy should be administered.

Troponin measurements can detect myocardial injury in about one-third of patients without elevated CPK-MB. Repeat blood draws and measurements are needed within 6 to 12 hours of admission and after any episode of severe chest pain to detect or exclude myocardial injury.

Creatine phosphokinase (creatine kinase)

Creatine phosphokinase (creatine kinase) is an enzyme contained in the myocardium and skeletal muscles (in small quantities in the smooth muscles of the uterus, gastrointestinal tract and brain). The brain and kidneys contain predominantly the isoenzyme BB (brain), skeletal muscles - MM (muscle) and the heart MB enzyme. Creatine kinase MB has the greatest specificity. There is a high correlation between the level of its activity and the mass of necrosis. When the myocardium and skeletal muscles are damaged, the enzyme is released from the cells, leading to an increase in the activity of creatine kinase in the blood. 2-4 hours after an angina attack, the level of creatine kinase MB in the blood increases significantly, in connection with which the determination 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 (CPK) and its isoenzyme MB CPK are not specific enough, since false-positive results are possible in skeletal muscle injury. 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 oxidation of glucose and the formation of lactic acid. It is found in almost all human organs and tissues. Most of it is found in muscles. Lactate is normally formed in cells during respiration and, with a full supply of oxygen, does not accumulate in the blood. It is destroyed to neutral products, after which it is excreted from the body. In hypoxic conditions, lactate accumulates, causing a feeling of muscle fatigue and disrupting tissue respiration.

More specific is the study of isoenzymes of this enzyme LDH1-5. LDH1 has the greatest specificity. In myocardial infarction, an excess of the ratio of LDH1 and LDH2 by more than 1 is specific (normally LDP/LDH2 < 1). The lactate dehydrogenase norm for adults is 250 U/l.

In myocardial necrosis, the increase in the concentration of these markers in the blood serum does not occur simultaneously. The earliest marker is myoglobin. The increase in the concentration of MB CPK and troponin occurs somewhat later. It should be taken into account that at borderline levels of cardiac markers, the following tendency exists:

• the lower their level, the more false positive diagnoses;
• the higher, the more false negative diagnoses.

Determination of troponin and cardiac markers

Express diagnostics of myocardial infarction is easily performed at any time using various high-quality test systems for determining "Troponin T". The result is determined 15 minutes after applying blood to the test strip. If the test is positive and a second strip appears, then the troponin level 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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Changes in other laboratory parameters

An increase in the AST level is observed in 97-98% of patients with large-focal myocardial infarction. The increase is determined after 6-12 hours, reaching a maximum after 2 days. The indicator usually normalizes on the 4th-7th day from the onset of the disease.

With the development of myocardial infarction, an increase in the number of leukocytes in the blood, an increase in the erythrocyte sedimentation rate (ESR), an increase in the level of gamma globulins, a decrease in the level of albumin, and a positive test for C-reactive protein are observed.

Leukocytosis is observed in approximately 90% of patients. Its severity depends to a certain extent on the extent of the infarction (on average 12-15 x 109/l). Leukocytosis appears several hours after the onset of a pain attack, reaching a maximum on the 2nd-4th day and, in uncomplicated cases, gradually decreasing to normal within a week. Leukocytosis is mainly due to an increase in the number of neutrophils.

In myocardial infarction, ESR begins to increase on the 2nd-3rd day, reaching a maximum on the 2nd week. Return to the initial level occurs within 3-4 weeks. In general, these changes indicate the existence of inflammation or necrosis in the body and are devoid of any organ specificity.

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Echocardiography in myocardial infarction

Echocardiography is a non-invasive method that can provide reliable information about the state of regional and general contractile function of the myocardium, study the movement of blood in the cavities of the heart, and study the structure and functions of its valve apparatus. With the help of echocardiography, it is possible to obtain information about such indicators as cardiac output, end-systolic and end-diastolic volumes of the left ventricle, ejection fraction, etc.

Echocardiography, when applied to the diagnosis of acute coronary syndromes, allows:

• exclude or confirm the diagnosis of acute myocardial infarction;
• identify non-ischemic conditions causing chest pain;
• assess the short-term and long-term prognosis;
• identify complications of acute myocardial infarction.

Myocardial infarction causes disturbances of local contractility of the left ventricle of varying severity. The structure of the tissue in the area with impaired contractility may indicate the duration of the infarction. A sharp demarcation line is often visible at the border with normal segments. The border between akinetic and normal myocardium is sometimes well visualized.

For the development of segmental myocardial contractility impairment, detectable by echocardiography, more than 20% of the ventricular wall thickness must be damaged. The location and extent of myocardial infarction can be determined.

Echocardiography is particularly useful in the early stages. Mitral valve dysfunction, infarction extent, mural thrombus, and mechanical complications of myocardial infarction are easily identified. During an episode of myocardial ischemia, focal hypokinesia or akinesia of the left ventricular wall may be detected. After the disappearance of ischemia, restoration of normal contractility may be observed.

The number of involved segments, derived from the wall motion score, as a measure of residual left ventricular function, has early and late prognostic value in predicting complications and survival. Left ventricular wall thinning indicates previous myocardial infarction. With good visualization, when the entire endocardium is visible, normal left ventricular contractility almost excludes myocardial infarction.

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