Diagnosis of myocardial infarction

With myocardial infarction, there is a significant output of various substances (cardiomarkers) from necrosis and damage zones. And this yield is all the more significant, the more the mass of the affected myocardium. Measurement of cardiomarker levels speeds up and specifies such an event as the diagnosis of myocardial infarction, as well as the ability to predict its further development. The main biochemical markers, which uses the diagnosis of myocardial infarction - myoglobin, troponin I, troponin T, creatine-phosphokinase and lactate dehydrogenase.

[1], [2], [3], [4], [5], [6],

Myoglobin

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.

Troponins

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.

[7], [8], [9], [10], [11], [12], [13], [14]

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%.

[15], [16], [17], [18], [19], [20]

Changes in other laboratory indicators

The increase in the level of ASA is noted 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 to 4-7 days from the onset of the disease.

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

Leukocytosis occurs 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 a few hours after the onset of a pain attack, peaking at 2-4 days and, in uncomplicated cases, gradually dropping to normal within a week. Leukocytosis is mainly due to an increase in the number of neutrophils.

With myocardial infarction, the ESR starts to increase on the 2-3rd day, reaching a maximum at the 2nd week. Return to baseline 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.

[21], [22], [23]

Echocardiography with myocardial infarction

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

Echocardiography, with reference to the diagnosis of acute coronary syndromes, allows:

• to exclude or confirm the diagnosis of acute myocardial infarction;
• identify non-ischemic conditions that cause pain in the chest;
• estimate short-term and long-term forecast;
• Identify the complications of an acute myocardial infarction.

Myocardial infarction causes violations of local contractility of the left ventricle of varying degrees of severity. The tissue structure in the area with impaired contractility may indicate the duration of the infarction. Often, a sharp demarcation line is visible on the border with normal segments. The boundary between the akinetic and normal myocardium is sometimes well visualized.

For the appearance of a segmental violation of myocardial contractility, determined by echocardiography, more than 20% of the ventricular wall thickness is damaged. Localization and prevalence of myocardial infarction can be determined.

Echocardiography is especially useful in early periods. Mitral valve dysfunction, extent of myocardial infarction, parietal thrombus and mechanical complications of myocardial infarction are easily identified. During an episode of myocardial ischemia, local hypokinesia or akinesia of the left ventricular wall can be detected. After the disappearance of ischemia, restoration of normal contractility can be noted.

The number of segments involved, obtained in assessing the contractility of the heart wall, as a measure of residual left ventricular function has an early and late prognostic value in predicting the possibility of complications and survival. Thinning of the wall of the left ventricle indicates a previous myocardial infarction. With good visualization, when the entire endocardium is seen, the normal contractility of the left ventricle almost eliminates myocardial infarction.

[24], [25], [26], [27], [28], [29], [30], [31], [32]