Diagnostics Of Myocardial Infarction: Troponin Test, Ecg, Blood Test

2024 Author: Rachel Wainwright | [email protected]. Last modified: 2024-01-15 19:51

Diagnosis of myocardial infarction: troponin test, other laboratory and instrumental methods

The content of the article:

Laboratory diagnostics
1. Creatine phosphokinase
2. Lactate dehydrogenase
3. ALT, AST and de Ritis coefficient
4. Troponin
5. Myoglobin
6. General blood analysis
Instrumental diagnostics
Differential diagnosis
Video

Diagnosis of myocardial infarction - a dangerous cardiac disease, in which necrosis of the heart muscle area develops against the background of impaired blood flow in the coronary arteries, is based on the recommendations of the World Health Organization.

The diagnosis is made if at least two of the three diagnostic criteria are present:

characteristic clinical picture;
typical changes on the electrocardiogram;
hyperenzymemia.

A preliminary diagnosis is made on the basis of characteristic symptoms, primarily anginal pain, however, the diagnosis of a heart attack can be difficult with the development of atypical forms of pathology, low-symptom or asymptomatic (typical for patients with diabetes mellitus) course. Atypical forms of heart attack are more common in women.

In case of acute sudden pain in the heart, myocardial infarction should be suspected and an ambulance should be called

Since it is impossible to reliably establish a diagnosis without examination, if you suspect a myocardial infarction, you should immediately call an ambulance and hospitalize the patient to the clinic. Only after a series of laboratory and instrumental studies can the diagnosis be finally confirmed.

The name of this or that test, and when it is most informative in time, is described below.

Laboratory diagnostics

Laboratory diagnostics of myocardial infarction is based on the detection of markers of myocardial infarction in the patient's blood - indicators of the inflammatory process and tissue necrosis.

The destruction of the muscle cells of the heart (cardiomyocytes) and the release of the released cellular enzymes into the blood leads to hyperenzymemia in patients with myocardial infarction.

Of greatest importance for the diagnosis of heart attack is the determination of the concentration of creatine phosphokinase (MB fraction), aspartate aminotransferase, lactate dehydrogenase (and its isoenzyme 1), as well as the level of troponin and myoglobin.

Creatine phosphokinase

An increase in the activity of creatine phosphokinase (MB-fraction), which is found mainly in the heart muscle, is specific for a heart attack. This fraction does not respond to damage to skeletal muscles, brain, thyroid gland.

3-4 hours after the infarction, the activity of the CF-fraction of creatine phosphokinase begins to increase, after 10-12 hours the indicator reaches its maximum figures, after 2 days it returns to its original values. By the end of the first day, the concentration of creatine phosphokinase exceeds the norm by 3–20 times. The degree of increase in this fraction of the enzyme correlates with the size of the lesion of the heart muscle - the larger the volume of myocardial damage, the higher the activity of this indicator. It should be borne in mind that a short-term increase in the level of the CF fraction of creatine phosphokinase can be observed after any surgical interventions performed in cardiology (including electrical pulse therapy, coronary angiography, catheterization of cardiac cavities, etc.).

Sometimes, with extensive myocardial damage, the release of enzymes into the blood is slowed down; in such cases, the absolute value of the activity of the MB fraction of creatine phosphokinase and the rate of its achievement may be less than with ordinary leaching of the enzyme.

A study for creatine phosphokinase is indicated for all patients who were hospitalized on the first day after the onset of the attack. Normal values of creatine phosphokinase (and its MB-fraction), which were obtained in a single study at the time of admission of the patient to the hospital, are not sufficient grounds for excluding the diagnosis of myocardial infarction. In this case, the analysis is recommended to be repeated after 12 and 24 hours.

When a patient is admitted to the hospital 1-14 days after the onset of the disease, biochemical studies are carried out to determine the concentration of lactate dehydrogenase, alanine and aspartate aminotransferase with the calculation of the de Ritis coefficient.

Lactate dehydrogenase

The activity of lactate dehydrogenase in myocardial infarction increases more slowly than creatine phosphokinase, and remains elevated longer. The peak of this enzyme activity occurs 2-3 days after the onset of the disease. The return to the initial values is noted after 8-14 days. It should be borne in mind that the level of lactate dehydrogenase also increases with congestive heart failure, pulmonary embolism, myocarditis, liver pathologies, shock, megaloblastic anemia, hemolysis, as well as after excessive physical exertion.

ALT, AST and de Ritis coefficient

The concentration of aspartate aminotransferase (AST) increases after 1-1.5 days from the onset of the disease and returns to the initial values after 4-7 days. The change in AST activity for myocardial infarction is nonspecific; it also occurs in liver diseases and some other pathologies.

In the case of liver disorders, the activity of alanine aminotransferase (ALT) increases to a greater extent, and in heart disease - AST. With myocardial infarction, the de Ritis coefficient (the ratio of AST to ALT) is higher than 1.33, and with liver disorders, it is lower.

Troponin

The troponin complex consists of three components - troponin C, I, and T. Troponin I and T exist in cardiac muscle-specific isoforms that differ from those in skeletal muscles, which is the reason for the absolute cardiospecificity of the indicator. 4-5 hours after the death of cardiomyocytes in myocardial infarction, troponin enters the peripheral blood. The peak concentration is reached 0.5-1 days after the onset of myocardial infarction. Troponin I is detected in the blood within 5-7 days, troponin T - within 2 weeks. Determination of troponin in the blood, as a rule, is carried out using the method of immunoassay diagnostics using specific antibodies.

Myocardial infarction markers found on a biochemical blood test to confirm the diagnosis

The troponin test for myocardial infarction does not apply to early diagnosis of the disease. If the test result is negative in patients with suspected acute coronary syndrome (exacerbation of ischemic heart disease, clinically manifested by the development of unstable angina pectoris or myocardial infarction without / with ST segment elevation), a second study is performed 6–12 hours after the attack. At the same time, even a slight increase in the indicator indicates a risk for the patient due to the correlation between the level of troponin increase in the peripheral blood and the volume of myocardial damage.

Myoglobin

The specificity of myoglobin for the diagnosis of cardiac infarction roughly corresponds to that of creatine phosphokinase. An increase in myoglobin level by 10 times or more is considered diagnostically significant. With myocardial infarction, the increase in the concentration of myoglobin in the blood begins earlier than creatine phosphokinase.

Myoglobin in the blood rises to a diagnostically significant level 4-6 hours after the onset of an attack and remains high only for several hours. Therefore, it is advisable to perform an analysis for myoglobin no later than 6-8 hours after the onset of a heart attack.

General blood analysis

A general blood test according to the instructions should be carried out when the patient is admitted to the hospital, and then weekly in order to timely detect the development of infectious or autoimmune complications of myocardial infarction.

In a general blood test, leukocytosis is usually found not exceeding 15 × 10 ⁹ / l, the absence of eosinophils in the peripheral blood, a slight shift in the leukocyte formula to the left, an increase in the erythrocyte sedimentation rate. An adequate interpretation of these indicators is possible only when compared with the existing clinical manifestations and electrocardiographic data. Prolonged (more than 1 week) persistence of leukocytosis and / or moderate fever in patients with myocardial infarction may indicate the development of complications (pericarditis, pleurisy, thromboembolism of small branches of the pulmonary artery, pneumonia).

Instrumental diagnostics

One of the most important methods for diagnosing heart infarction is electrocardiography (ECG), which allows not only to determine the disease, but also shows the localization and depth of the lesion, makes it possible to diagnose the developed complications (heart aneurysm, arrhythmias, etc.).

For topical diagnosis of heart attack (localization of myocardial infarction by ECG), an electrocardiogram is usually recorded in 12 conventional leads.

The table shows the leads in which pathological changes are found depending on one or another localization of the necrosis focus.

Localization of myocardial infarction	Leads
Anterior septal	V1-V3
Anterior apical	V3, V4
Front side	V5, V6, I, aVL
Front high	V2 / 4-V2 / 6 and / or V3 / 4-V4 / 6
Anterior spread	V1-V6, I, aVL
Posterior diaphragmatic (lower)	II, III, aVF
Posterior basal	V7-V9
Posterolateral	V5, V6, III, aVF
Posterior common	V5, V6, V7-V9, II, III, aVF

The method of precordial electrocardiographic mapping of the heart is used to indirectly determine the size of the necrosis focus and the area of ischemic damage in acute heart attack of the anterior and anterolateral walls of the left ventricle. To do this, after registering the electrocardiogram, a cartogram is built, which consists of 35 squares in leads. The size of the necrosis focus is conventionally determined by the number of leads in which signs of transmural necrosis were detected. Cartographic indicators are used to monitor the dynamics of the necrosis focus and peri-infarction zone during treatment of patients with acute myocardial infarction, as well as for prognosis.

Two-dimensional echocardiography (echocardiography, ultrasound of the heart) may be required to confirm or rule out myocardial infarction. The absence of a violation of local contractility makes it possible to exclude myocardial infarction. Also, using this method, it is possible to differentiate an infarction with hypertrophic cardiomyopathy, pericarditis, aortic dissection and rupture, massive pulmonary embolism, which are also characterized by intense chest pain.

Perfusion scintigraphy in the diagnosis of heart attack is rarely used. A normal scytigram of the heart muscle with 99Th at rest excludes macrofocal myocardial infarction. However, an abnormal scintigram is not an indicator of acute myocardial infarction, more research is required.

Electrocardiography is the main method for diagnosing myocardial infarction

Coronary angiography is important in assessing the criticality of the plaque occluding the blood vessel if subsequent revascularization is expected.

Magnetic resonance imaging is not a routine method for imaging coronary vessels, but provides information on the perfusion and viability of the heart muscle, as well as on regional contractility. In addition, the method is effective for the differential diagnosis of cardiac infarction with pericarditis, myocarditis, pulmonary embolism, dissecting aortic aneurysm.

In some cases, the use of computed tomography and some other additional research methods may be required.

Differential diagnosis

If myocardial infarction is suspected, differentiation with other pathologies is necessary, especially with an atypical clinical picture.

In some cases, differential diagnosis of heart attack is carried out with infectious-toxic and allergic shock, which are also characterized by a decrease in blood pressure and shortness of breath, and chest pain may occur. With these pathologies, there is no QS complex and a deep Q wave on the electrocardiogram, which distinguishes them from a typical heart attack.

Pericarditis can mimic the clinical picture of a heart attack, in which the subepicardial layers of the heart muscle are affected and pain occurs in the precordial region. Unlike a heart attack with pericarditis, the Q wave is not detected on the electrocardiogram.

In addition, differential diagnosis of heart attack is carried out with the following pathologies:

osteochondrosis of the thoracic spine;
bronchial asthma;
chest contusion;
dissecting aortic aneurysm;
left-sided pneumonia;
shingles;
perforated stomach ulcer;
food toxicoinfection;
acute cholecystopancreatitis;
spontaneous pneumothorax;
neoplasms of the heart;
cancer of the cardiac stomach;
non-coronary necrosis of the myocardium in leukemia, anemia, thyrotoxicosis, systemic vasculitis.