Laboratory tests - a way to diagnose chronic heart failure

The onset of myocardial infarction in most cases is difficult to confuse with any other disease other than angina. It is accompanied by obvious symptoms: prolonged attacks of pain, suffocation, excessive sweating, and a feeling of fear of death. Patients who are seen by doctors with coronary artery disease or angina pectoris are susceptible to the disease. However, myocardial infarction can also occur in a person who previously showed virtually no symptoms of cardiovascular disease. At the first signs of an attack, it is important to call an ambulance in a timely manner and trust professional cardiologists.

Clinical biochemical blood test

Blood chemistry

- a laboratory research method that reflects the functional state of organs and systems of the body.

Biochemical blood test indicated

, even if the person has no complaints. By changes in the chemical composition of the blood, it is possible to determine which organ is functioning abnormally, which may indicate the development of the disease and the need for urgent treatment.

Markers of myocardial damage and heart failure:

Myoglobin

- a hemoprotein found in large quantities in skeletal muscle and in small quantities in cardiac muscle. Takes part in tissue respiration. During myocardial infarction, the concentration of myoglobin in the blood increases after 2 hours, but this is a nonspecific marker of myocardial infarction, since the heart muscle contains a small amount of myoglobin. This marker is used in the diagnosis of myocardial infarction in combination with other biochemical tests.

Troponin I

– a protein, a specific marker of damage to the heart muscle, used in the diagnosis of myocardial infarction. An increase in troponin I is observed within 4–6 hours after the attack. This test allows you to diagnose even microscopic areas of myocardial damage.

KFK-MV

– creatine phosphokinase-MB
is an isoenzyme of creatine phosphokinase, characteristic of cardiac muscle tissue.
Determining the activity of CPK-MB- is of great importance in diagnosing myocardial infarction and monitoring the post-infarction state, allowing one to assess the volume of the lesion and the nature of the recovery processes. The diagnosis of acute myocardial infarction is also confirmed by the observation of the characteristic dynamics of the indicator; serial determination of CPK-MB with an interval of 3 hours over a 6-9 hour period with nonspecific ECG changes is more informative than a single measurement. The level of CPK-MB can be measured both in weight terms and in activity units. Currently, for the diagnosis of myocardial infarction, it is preferable to determine not the activity, but the mass of CPK-MB.

To adequately assess the relationship between the concentration of CPK-MB and the total activity of creatine phosphokinase, the calculated relative index RI = CPK-MB (µg/l) / CPK total was introduced. (U/l) x 100 (%). Damage to the heart muscle is characterized by RI > 2.5 - 3%.

Heart failure marker ProBNP

is a precursor of brain natriuretic peptide - BNP (BNP - brain natriuretic peptide).
The name “brain” is due to the fact that it was first identified in the brain of animals. In humans, the main source of ProBNP is the ventricular myocardium and is released in response to stimulation of ventricular cardiomyocytes, such as myocardial distension in heart failure. ProBNP is cleaved into two fragments: the active hormone BNP and N - the terminal inactive peptide NT - proBNP
.
Unlike BNP, NT-proBNP
has a longer half-life, better in vitro stability, less biological variability and higher blood concentrations.
The listed features make this indicator convenient for use as a biochemical marker of chronic heart failure. Determining the level of NT - proBNP
in blood plasma helps to assess the severity of chronic heart failure, predict the further development of the disease, and also evaluate the effect of therapy.

Negative predictive value of the test greater than 95% - that is, normal NT-proBNP

with a high probability allows to exclude heart failure (for example, in cases of shortness of breath due to a sharp exacerbation of chronic obstructive pulmonary disease, or edema not associated with heart failure).
It should be noted that NT-proBNP
should not be used as the sole criterion.

LABORATORY DIAGNOSTICS OF MYOCARDIAL INFARCTION: MODERN REQUIREMENTS D.S.Benevo…

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LABORATORY DIAGNOSTICS OF MYOCARDIAL INFARCTION: MODERN REQUIREMENTS D.S. Benevolensky Representative office (Denmark)

Summary : Laboratory methods today play a key role in the diagnosis of myocardial infarction.
However, all currently existing biomarkers of cardiomyocyte necrosis are not ideal. Troponins I and T are the most sensitive and specific. Myoglobin is the least specific, but it appears in the blood more quickly after a heart attack. The third recommended biomarker, creatine kinase MB, has intermediate characteristics. To accurately determine the upper limit of normal for biomarkers, the analytical method must have high sensitivity and specificity. As a result of manufacturers using different sets of antibodies in immunochemical reactions and the lack of clear standardization, biomarker concentrations measured on different analyzers often do not match. Each analyzer has its own reference ranges. This applies primarily to troponin. In cardiology, speed of diagnosis is very important, so testing directly at the patient’s bedside is becoming increasingly important. Some modern analyzers, such as the Radiometer AQT90 FLEX , make it very easy to obtain high-quality biomarker measurement results.
Key words : myocardial infarction, diagnosis, troponin, myoglobin, creatine kinase
MB.
Today, biochemical markers play a key role in the accurate diagnosis of myocardial infarction, and, very importantly, in assessing the risk of an unfavorable outcome and choosing the most adequate treatment method. For the first time, a laboratory method for diagnosing myocardial infarction (measuring the activity of aspartate aminotransferase in the blood) was used more than 50 years ago [5]. Since then, the role of laboratory methods in cardiology has constantly increased. There has been a significant shift from measuring aspartate aminotransferase and lactate dehydrogenase activity to the three biomarkers commonly used today: myoglobin, creatine kinase MB (CK-MB), and troponins I and T. Initially, laboratory results were considered only as an adjunct to the clinical examination and ECG. But in 2000 and then in 2007, the most authoritative American, European and international heart associations decided that the diagnosis of myocardial infarction was directly related to an increase in the level of biomarkers (preferably troponin) in the blood [12]. All other methods of clinical and functional examination are intended only to confirm the ischemic nature of the observed myocardial necrosis. The published document emphasizes the key role of biomarkers in diagnosis: “The term myocardial infarction should be used when there is evidence of myocardial necrosis in the presence of a clinical picture consistent with myocardial ischemia.” Moreover, data on myocardial necrosis is understood as “detection of an increase and/or decrease in the level of cardiac biomarkers (preferably troponin) with at least one value exceeding the upper reference limit,” and at least one of the following is considered sufficient evidence of ischemia: • The presence of symptoms ischemia; • ECG changes indicating the appearance of ischemia (the appearance of ST-T changes or the appearance of a left bundle branch block); • Development of a pathological Q wave on the ECG; • Radiation findings indicating loss of viable myocardium or the appearance of local wall motion abnormalities. Why has the measurement of troponin levels taken center stage in laboratory diagnostics? Table 1 summarizes the properties of an ideal biomarker for myocardial infarction.

Table 1. Properties of an ideal biomarker for myocardial necrosis [3].

To date, none of the existing biomarkers meets all of the above criteria. Troponins I and T are closest to the ideal. Their main advantage is their unique specificity for the myocardium. Troponins are proteins of the muscle contractile apparatus. They are part of the troponin-tropomyosin complex of thin myofibrils. This complex regulates the interaction of the contractile proteins actin and myosin and, thereby, ensures a change in muscle contraction or relaxation. There are three types of troponin - C, I and T. All of them are small proteins with a molecular weight of 20–40 thousand. Troponin T binds the remaining troponins and tropomyosin into a single complex. In relaxed muscle, troponin I prevents the interaction of the myosin head with actin and prevents contraction. Excitation of the cardiomyocyte leads to an increase in the intracellular concentration of Ca2+ ions, which bind to troponin C. The conformation of the entire complex changes, and actin is freed from the inhibitory influence of troponin I - muscle contraction occurs. Troponin C is one of the very conserved proteins. Thus, troponin C from human skeletal muscles differs from troponin C from bovine heart by only one amino acid [10]. In other words, the troponins of the heart and slow skeletal muscles are almost identical. In contrast, the cardiac isoforms of troponins I and T are expressed only in the heart, whereas the isoforms of the analogous fast and slow muscle troponins in skeletal muscle are products of other genes. Being part of the contractile apparatus, troponins I and T are present in high concentrations in myocardial cells. In the blood of healthy people, the concentration of these proteins is extremely low, but in the case of myocardial infarction it increases tenfold (Fig. 1), and the increased concentration persists for several days, in some cases up to one, and for troponin T, even two weeks. According to the general opinion of experts, the concentration of troponins in the blood increases only with irreversible destruction (necrosis) of cardiomyocytes, although the causes of necrosis may be different. Unfortunately, troponins are structural proteins, and they do not appear in the blood immediately, usually 4-6 hours after a heart attack. True, the increasing sensitivity of modern tests is increasingly reducing this time. The kinetics of troponin elimination is ambiguous and depends on renal function. Troponins I and T are contained in the myocardium in equimolar quantities, they are both unique to the heart, and although these are different proteins, from the point of view of diagnosing myocardial infarction, both troponins I and T are completely equivalent, and all international recommendations do not distinguish between them. If it is not possible to measure troponin concentration, then international recommendations suggest as an alternative to measure the level of creatine kinase MB (by mass, not by activity!) [7]. Until recently, this indicator was the “gold” standard in the laboratory diagnosis of myocardial infarction due to its relative specificity for the myocardium. Creatine kinase MB is an enzyme that catalyzes the transfer of high-energy phosphate from creatine phosphate to ATP and is involved in the transport of energy from mitochondria to the contractile apparatus. For intensive and continuous work, the heart needs a constant flow of energy, so this enzyme is contained in large quantities in cardiomyocytes. Creatine kinase consists of two subunits and has a molecular weight of about 42 thousand. Two types of subunits Mi and B are known, and, accordingly, three isoenzymes MM, BB and MB. CPK-MM predominates in skeletal muscle, and CPK-MB accounts for only 1–3%. In the myocardium, the main isoenzyme is also CPK-MM, but approximately 15% is accounted for by CPK-MB. Therefore, an increase in the level of CPK-MB in the blood is specific (but not absolutely!) for myocardial damage. The activity of the gene encoding the B subunit may be increased, for example, in regenerating skeletal muscle, reducing the specificity of this biomarker. Creatine kinase MB is a less sensitive biomarker than troponin. It has been shown that almost 30% of patients admitted with chest pain, without ST-segment elevation on the ECG and without an increase in the level of creatine kinase CPK-MB, actually had myocardial infarction, as shown by measuring troponin levels. For patients admitted within 6 hours of the onset of pain, international recommendations include the determination of an early biomarker of myocardial necrosis in addition to cardiac troponin [7]. Myoglobin is the most studied biomarker for this purpose. It is a small heme-containing soluble protein of skeletal muscle and myocardium (mw 17,500). Its main function is the transport of oxygen in the muscles. Due to its high solubility and small size, myogloblin is quickly released when muscles are damaged and is excreted by the kidneys. The main disadvantage of myoglobin as a biomarker is low specificity. A normal myoglobin level helps exclude the diagnosis of myocardial infarction. But its increase may also be associated with various lesions of skeletal muscles. What are the normal concentrations of biomarkers in the blood, and what is considered a proven increase in their level? According to the recommendations of the National Academy of Clinical Biochemistry (USA) and the International Federation of Clinical Chemistry and Laboratory Diagnostics, for each biomarker it is necessary to establish the upper limit of normal values ​​based on a study of a group of healthy people without a history of heart disease [1,2]. For troponins (T and I) and creatine kinase MB, the threshold value for detecting cardiac damage is the 99th percentile of measurements in a group of healthy people. This means that 99% of healthy people have plasma levels of the relevant analyte below this threshold. On the contrary, exceeding this threshold indicates myocardial damage. Moreover, for creatine kinase MB, studies should be conducted separately for men and women, since in men the 99th percentile value is 2–3 times higher than in women. There are also racial differences. For myoglobin concentration, the 97.5th percentile is taken as the normal limit. Ideally, each laboratory should establish its own reference range, but given the complexity of conducting such a study, it is permissible to rely on the figures provided by the manufacturers. In the above definition of myocardial infarction, the words “rise or fall” in the level of a biomarker are very important. That is, ideally, it is necessary to identify a new peak in the concentration of a biomarker in the blood, corresponding to the clinical picture. To do this, the concentration of the biomarker must be measured at least twice, and measured quantitatively. For most patients, blood sampling is indicated on admission and 6–9 hours later [7]. Once the diagnosis of myocardial infarction is confirmed, subsequent measurements of biomarkers of myocardial damage (approximately once a day) allow us to estimate the size of the infarction and assess the risk of complications for a given patient. Accurate assessment of cardiovascular risk is critical to clinical decision making because the benefits, risks, and costs of different treatments must be weighed to determine the best treatment for each individual patient [4]. Of these biomarkers, the most difficult to measure in the blood is the concentration of troponin, since it is normally extremely low. To accurately determine the upper limit of normal (99th percentile), the analytical sensitivity of the measurement method must be sufficient to determine the concentration of troponin in the blood of, if not all, then at least many healthy people. Figure 2 shows the “true” distribution of troponin I concentration in the blood in healthy people and patients with myocardial infarction. The normal limit at the level of the 99th percentile of the distribution of troponin I concentration in healthy people best allows us to distinguish patients from healthy people [2]. If the analysis method has a detection limit (1), then this threshold can be set quite accurately. A method with a detection limit (2) will certainly identify the majority of patients with myocardial infarction, but the true limit of normal remains unknown, and therefore in some patients myocardial damage remains undiagnosed. According to the recommendation of the International Federation of Clinical Chemistry and Laboratory Medicine (IFCC), to reduce the influence of nonspecific factors, analytical sensitivity should be approximately 5 times lower than the clinically significant threshold level [9]. In addition, the measurement error at the threshold level should be quite low [1]. The error is determined by the value of the coefficient of variation (CV), which is equal to: CV = SD/M*100%, where M is the arithmetic mean of the results of measuring a given concentration, and SD is the standard deviation. At the level of the upper limit of the norm, the error should be no more than 10%, otherwise the test will give many false-positive and false-negative results. Unfortunately, the recommendations outlined are not always followed in real life. The official website of the International Federation of Clinical Chemistry and Laboratory Medicine [https://www.ifcc.org/PDF/IFCC_Troponin_Web_Page_Table_of_Assays_Oct_2008.pdf] provides analytical characteristics for 19 tests for troponins I and T from different manufacturers (data as of October 2008). Only 12 of them had a detection limit less than the upper limit of normal, that is, for the remaining tests, the upper limit of normal (99th percentile) was actually not established. With measurement accuracy, the situation is even worse. Even at a level twice the normal limit, the coefficient of variation does not exceed 10% in only eight tests. Thus, analytical quality is a very important and not fully resolved topic that deserves close attention. All currently available methods for determining the concentration of troponin are based on an immunochemical reaction, the so-called “sandwich” analysis. The quality of the result obtained depends on the correct choice of antibodies. The triple complex of troponins I, T and C, entering the blood from destroyed cardiomyocytes, breaks down into free troponin T and a double complex of troponins I and C. These are the main forms of troponins in the blood. In the blood, under the influence of proteases, the cleavage of the terminal fragments of troponin molecules begins (Fig. 3). Therefore, the antibodies used for analysis must interact with the central, most stable part of the troponin molecule. In addition, troponin I can be in phosphorylated/dephosphorylated, as well as oxidized/reduced forms. The binding of the antibodies selected for analysis should not be affected by chemical modification of the troponin I molecule. In addition, the central part of the troponin I molecule is the object of interaction with autoantibodies, which, by blocking the binding of test antibodies, can lead to false-negative test results. The presence of autoantibodies to troponin I is quite common. They were found in 5.5% of people without signs of cardiovascular disease and in 21% of patients with acute coronary syndrome [6]. Attempts by manufacturers to overcome these difficulties and select the best combination of antibodies for analysis lead to the use of antibodies to different epitopes. As a result of manufacturers using different sets of antibodies in immunochemical reactions and the lack of clear standardization, biomarker concentrations measured on different analyzers often do not match. With almost perfect correlation of values ​​obtained by the best measurement methods, the absolute value of concentration can differ by an order of magnitude. Therefore, direct comparison of absolute values ​​is not possible, and normal limits must be determined separately for each analyzer. Although the clinical interpretation of the results, taking into account the relevant reference ranges, is generally consistent for all tests, this situation creates an obvious inconvenience. Here, a thoughtful clinical and laboratory council is needed to develop general rules for assessing the results obtained, for example, on portable analyzers at the patient’s bedside and in the central laboratory, for each specific hospital. Time plays a critical role in the diagnosis and treatment of myocardial infarction. Reperfusion initiated within the first hour after the onset of myocardial infarction was associated with a 1% mortality rate, whereas the same treatment initiated after 6 hours or more resulted in a 10% mortality rate [11]. According to the general opinion of clinicians and laboratory doctors, the time before receiving a response from the laboratory about the concentration of cardiac biomarkers in a blood sample should not exceed 60 minutes [7]. In reality, few places provide such a speed of analysis around the clock. Therefore, the National Academy of Clinical Biochemistry (USA) has given the following clear recommendations [8]: · The laboratory should measure cardiac biomarkers within 1 hour, preferably in 30 minutes or less. The time is calculated from sample collection to reporting of the result. · Institutions unable to consistently provide cardiac biomarker results within approximately 1 hour should use bedside analyzers. Bringing analyzers closer to the patient, that is, moving them from the laboratory to clinical departments, brings with it new problems. First of all, it is necessary to ensure maximum ease of operation with a minimum need for maintenance. The analyzer will be used by clinical department personnel who do not have special laboratory training. Personnel turnover, which often prevents timely additional training of personnel, should also be taken into account. At the same time, it is necessary to ensure laboratory quality of the analysis (high sensitivity and accuracy of measurement) and sufficient productivity. The optimal scheme is to maintain control of laboratory specialists over all instruments located in the departments. Connecting the analyzer to an in-hospital information system that allows remote access from a laboratory computer terminal greatly facilitates such control. An example of an analyzer that most fully meets all these requirements is the new immunofluorescence analyzer AQT90FLEX manufactured (Denmark), shown on the cover of this magazine. This is a fairly compact benchtop device capable of measuring all of the specified biomarkers of myocardial necrosis (troponin I, creatine kinase MB, myoglobin). TroponinT will join them next year. In addition, biomarkers of heart failure (NT-proBNP), coagulation system activation (D-dimer), inflammation (CRP) and pregnancy (β-subunit of human gonadotropin) can be measured. The operator can freely select the necessary parameters, which are measured in parallel. It is important that no pre-treatment of the blood sample is required. To measure, you just need to insert a closed standard vacuum tube with a sample into the analyzer, select parameters and get the result and the closed tube. Contact with blood or waste during the analysis is excluded. All processes are as automated as possible; it is possible to connect the analyzer to information systems. All this makes it easy to use the analyzer for express diagnostics directly in the department. At the same time, the measurement result meets the highest laboratory standards. Doctors will no longer have to clarify the diagnosis by sending a sample to a central laboratory. Table 2 provides data on the analytical quality of measurements of the main biomarkers of myocardial necrosis. Table 2. Analytical measurement quality of the AQT90FLEX analyzer.

The results of troponin measurements on the AQT90 FLEX correlate almost perfectly with the results of the TnI-Ultra ADVIA Centaur laboratory analyzer (Siemens) and the correlation coefficient R2 = 0.984. Thus, modern requirements for laboratory diagnosis of myocardial infarction are reduced to the rapid and accurate determination of biomarkers (preferably troponin). For this, in addition to laboratory ones, non-laboratory analyzers are also needed, which would be easy to use and would give quantitative results comparable in accuracy to laboratory data. The use of such analyzers directly in emergency departments and intensive care units will improve the quality of medical care in emergency situations. References 1. Apple FS, Jesse RL, Newby LK, Wu AH, Christenson RH. National Academy of Clinical Biochemistry and IFCC Committee for Standardization of Markers of Cardiac Damage Laboratory Medicine Practice Guidelines: Analytical issues for biochemical markers of acute coronary syndromes. Circulation. 2007 Apr 3;115(13): e352-5. 2. Apple FS, Quist HE, Doyle PJ, Otto AP, Murakami MM. Plasma 99th percentile reference limits for cardiac troponin and creatine kinase MB mass for use with European Society of Cardiology/American College of Cardiology consensus recommendations. Clin Chem. 2003 Aug;49(8): 1331-6. 3. Cardiovascular biomarkers: pathophysiology and disease management (edited by David A. Morrow). 2006 Humana Press Inc. p.6. 4. Criteria for Evaluation of Novel Markers of Cardiovascular Risk. A Scientific Statement From the American Heart Association. Circulation. 2009; 119: 2408-2416. 5. Karmen A, Wroblewski F, LaDue JS. Transaminase activity in human blood. J Clin Invest 1954;34:126–133. 6. Kim Pettersson, Susann Eriksson, Saara Wittfooth, Emilia Engström, Markku Nieminen and Juha Sinisalo. Autoantibodies to Cardiac Troponin Associate with Higher Initial Concentrations and Longer Release of Troponin I in Acute Coronary Syndrome Patients. Clinical Chemistry. 2009;55:938-945. 7. Morrow DA, Cannon CP, Jesse RL, Newby LK, Ravkilde J, Storrow AB, Wu AH, Christenson RH, Apple FS, Francis G, Tang W. National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical characteristics and utilization of biochemical markers in acute coronary syndromes. Clin Chem. 2007 Apr; 53(4): 552-74. 8. National Academy of Clinical Biochemistry: Laboratory Medicine Practice Guidelines: Evidence-Based Practice for Point-of-Care Testing. (Editor James H. Nichols) AACCPress. 2006. 9. Panteghini M, Gerhardt W, Apple FS, Dati F, Ravkilde J, Wu AH. Quality specifications for cardiac troponin assays. Clin Chem Lab Med. 2001 Feb;39(2):175-9. 10. Romero-Herrera, A. E.; Castillo, O.; Lehmann, H. : Human skeletal muscle proteins: the primary structure of troponin CJ Molec. Evol. 8: 251-270, 1976. 11. Rosalki SB, Roberts R, Katus HA, Giannitsis E, Ladenson JH, Apple FS. Cardiac biomarkers for detection of myocardial infarction: perspectives from past to present. Clin Chem. 2004 Nov;50(11): 2205-13. 12. Thygesen K, Alpert JS, White HD on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. Circulation. 2007 Nov 27; 116(22): 2634-53.

Figure 1. Increase in the level of markers in the blood during myocardial infarction [7].

Figure 2. Detection limit of a good (1) and insufficiently sensitive test (2) in relation to the true normal limit for troponin I concentration.

Figure 3. Factors influencing the choice of antibodies for troponin I detection.

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Diagnostic methods

Physical examination

The primary diagnosis of myocardial infarction, which will be carried out by the arriving doctors, consists, first of all, of examining the patient and asking about health complaints. This disease can be confused with an attack of angina, especially if it appears for the first time. The nature of the pain is similar - they spread from the sternum to the left arm (including fingers), shoulder, shoulder blade, neck, jaw. The difference between a heart attack is more severe and acute pain, which is not relieved by taking nitroglycerin.

Pain syndrome during myocardial infarction can last about a day, accompanied by weakness, a drop in blood pressure, and vomiting. The patient is in emotional arousal, in contrast to an attack of angina, when patients, on the contrary, try to move as little as possible.

The doctor measures pressure (most often it decreases by 10-15 mm) and pulse, checks for possible dysfunction of the left ventricle and myocardium, listening to heart sounds.

Lab tests

At the hospital stage, the diagnosis of a heart attack consists of conducting biochemical and general blood tests. With this disease, noticeable changes occur in the composition of the blood:

• the level of leukocytes, ALT, AST, cholesterol, fibrinogen levels increase;
• the erythrocyte sedimentation rate and albumin indicator decrease.

These are indicators of necrosis, scarring of cardiac muscle tissue and the presence of inflammation. The patient has polymorphic cell leukocytosis.

The laboratory method for diagnosing myocardial infarction also checks the level of serum enzymes. Markers appear in it indicating myocardial necrosis, in particular the contractile protein troponin, which is not found in a healthy person. Markers also include CPK and myoglobin, which appear in the blood serum in the first hours after the onset of the disease.

A number of biochemical reactions in the blood are not specific to a heart attack, so it is extremely important to entrust the diagnosis to highly qualified doctors and a clinic with extensive technical capabilities.

Electrocardiography

ECG for myocardial infarction is one of the most effective, objective and informative diagnostic methods. If possible, seek emergency help from the doctors of the cardiology team - their car must be equipped with a portable electrocardiograph, which will allow you to diagnose the disease as soon as possible.

ECG equipment picks up the electrical impulses generated by the heart muscle and records them on paper. Based on the analysis of the cardiogram, a qualified doctor can determine:

• localization of necrosis (posterior, anterior or lateral wall, septum, basal wall, etc.);
• the size and depth of the lesion;
• process stage;
• complications that have arisen.

The doctor pays attention to the nature of the electrocardiogram waves and analyzes the increase in the level of individual segments. In particular, large-focal transmural myocardial infarction is characterized by the appearance of a pathological Q wave.

The examination takes about 10 minutes and does not cause any discomfort. During a heart attack, an ECG may be performed every half hour to provide continuous data updates.

Echocardiography

The more common name for echocardiography among patients is cardiac ultrasound. This is an extremely effective tool for diagnosing acute myocardial infarction and other types of this pathology.

The examination is not associated with painful sensations and takes 20-25 minutes. The doctor lubricates the patient’s chest with a special gel and moves an ultrasonic sensor over it. The echocardiograph reads the data obtained on the state of the myocardium, pericardium, large vessels, and valves, and the doctor immediately analyzes them. The advantage of the method is the ability to visually assess the functionality of the organ in the shortest possible time and diagnose regional contractility disorders.

The Doppler mode in which modern ultrasound machines operate makes it possible to assess the quality of blood flow in the heart and determine the presence of blood clots. The sound signals of the heart are also analyzed, the pressure in the organ cavities is measured, and complications are studied.

Radiography

To objectively predict the development of complications during myocardial infarction, a chest x-ray is performed as part of the diagnosis.

Among the dangerous complications, this method most often diagnoses pulmonary edema, which is one of the clear signs of acute left ventricular failure. The image shows impaired blood flow in the upper parts of the lungs, pulmonary artery, blurry pattern of blood vessels, etc. Also, with a heart attack, dissection of the aorta and other changes in the thoracic part are likely. Radiography allows you to diagnose disorders of the blood supply to organs located in close proximity to the heart.

Among the radiological methods used in cardiology to determine a heart attack, coronary angiography and multislice computed tomography of the heart are also common. With their help, the location and nature of the narrowing of the coronary artery is determined.

Blood tests that determine the risk of heart attack and stroke

The blood tests below help determine the risk of developing coronary heart disease, stroke , peripheral vascular disease and, if necessary, prescribe treatment.

Lipoprotein A ( Lp (a)) is a blood protein whose levels indicate an increased risk of heart attack and stroke.

Normal value:

Desired level for adults: no more than 30 mg/dl.

Preparing for the analysis:

Blood is taken for analysis after a 12-hour fast (except for drinking water). To get more accurate results, you should refrain from taking the test for at least two months after a heart attack, surgery, infection, injury, or pregnancy.

Lipoprotein A is a low-density lipoprotein (LDL) that has a protein called apo attached to it. Currently, it is not fully known what function lipoprotein A performs in the body, but it is known that blood levels of lipoprotein A higher than 30 mg/dl increase the risk of developing myocardial infarction and stroke. In addition, high levels of lipoprotein A can lead to the development of fat embolism and increases the risk of developing blood clots.

It is especially important to bring the level of LDL (low-density lipoprotein) to normal if the content of lipoprotein A is high. The causes of high levels of lipoprotein A are kidney disease and some familial (genetic) disorders of lipid metabolism. Apolipoprotein A1 (A p o A1) is the main protein of HDL (high density lipoprotein). Low levels of apolipoprotein A1 indicate an increased risk of early cardiovascular disease. Apo 1 is more often reduced in patients suffering from physical inactivity, obesity, or eating a high amount of fat.

Normal value:

Desired level for an adult: more than 123 mg/dl.

Preparing for the analysis:

Blood should be drawn for testing after a 12-hour fast (excluding drinking water). To get more accurate results, you should refrain from taking the test for at least two months after a heart attack, surgery, infection, injury, or pregnancy.

Apolipoprotein B (a p oB) is the main protein found in cholesterol. ApoB is a better overall marker of cardiovascular risk than LDL, a new study suggests.

Normal value:

Less than 100 mg/dL for low/moderate risk individuals. Less than 80 mg/dL for those at high risk, such as those with cardiovascular disease or diabetes.

Preparing for the analysis:

Blood should be drawn for testing after a 12-hour fast (excluding drinking water). To get more accurate results, you should refrain from taking the test for at least two months after a heart attack, surgery, infection, injury, or pregnancy.

Fibrinogen is a protein found in the blood and involved in the blood clotting system. However, high fibrinogen levels may increase the risk of myocardial infarction and vascular disease.

Normal value:

Less than 300 mg/dl.

Preparing for the analysis:

Blood should be drawn for testing after a 12-hour fast (excluding drinking water). To get more accurate results, you should refrain from taking the test for at least two months after a heart attack, surgery, infection, injury, or pregnancy.

Elevated levels of fibrinogen are more often detected in older patients, in patients with high blood pressure, body weight and LDL. On the other hand, lower levels of fibrinogen are detected in patients who drink alcohol and regularly undergo physical activity. An increase in fibrinogen levels occurs with menopause.

High-sensitivity C-reactive protein (protein) (CRP ) is a protein found in the blood that is called an “inflammatory marker,” meaning its presence indicates an inflammatory process in the body. Inflammation is a normal response to many physical conditions, including fever, injury, and infection. But the inflammatory process, localized in the vessel wall, plays an important role in the initiation and progression of cardiovascular diseases. Inflammation (ie, swelling and damage) of the inner wall of the arteries is an important risk factor for the development of cardiovascular diseases such as atherosclerosis, myocardial infarction, sudden death, stroke, blood clots, and peripheral artery disease.

In the Harvard University Health Study, elevated CRP levels were a more accurate marker of coronary heart disease than cholesterol levels. The study assessed twelve different markers of inflammation in healthy postmenopausal women. After three years, C reactive protein was the strongest predictor of risk. Women in the group with the highest CRP levels were more than four times more likely to die from coronary heart disease or suffer a nonfatal heart attack or stroke.

More recently, the JUPITER (Justification for Statins in Primary Prevention) study showed that statins prevent heart disease and reduce the risk of stroke, heart attack, and death in individuals with normal LDL (bad cholesterol) levels but elevated high-sensitivity C-reactive protein (CRP) levels. ).

While elevated levels of cholesterol, LDL and triglycerides and low HDL are independent risk factors for heart disease, high-sensitivity C-reactive protein provides additional information about the inflammatory process in the arteries that cannot be determined by the lipid spectrum.

Normal value:

Less than 1.0 mg/l = low risk of cardiovascular disease; 1.0 - 2.9 mg/l = intermediate risk of developing cardiovascular diseases; more than 3.0 mg/l = high risk of developing cardiovascular diseases.

CRP levels of 50 mg/L or higher are sometimes detected, but usually CRP levels above 10 mg/L are due to another inflammatory process, such as infection, injury, arthritis, etc.

Therefore, testing should not occur during illness or injury. CRP should be studied to assess the risk of developing cardiovascular disease in apparently healthy individuals who have not had a recent infectious disease or other serious illness. Those patients whose CRP level during the study was above 10 mg/l should be examined to identify the source of the inflammatory process.

Preparing for the analysis:

This test can be performed at any time of the day, without any preparation. The only condition is the absence of acute inflammation.

Myeloperoxidase (MPO) is a marker of the inflammatory process in the arteries. As a result of this process, destruction of atherosclerotic deposits in the vessel wall often occurs, leading to thrombosis. A high level of myeloperoxidase, in combination with other risk factors (CRP, LDL, high blood pressure, excess weight) is an accurate criterion for an increased risk of heart attack, myocardial infarction, sudden death, stroke or peripheral vascular disease, including in apparently healthy people .

Normal value:

Less than 400 microns.

Preparing for the analysis:

This test can be done at any time of the day and does not require fasting.

N -terminal pro-brain natriuretic peptide (N-proBNP, NT- proBNT) is a peptide that is produced in the atria and ventricles of the heart in response to increased compliance of cardiomyocytes and increased pressure in the chambers of the heart. By measuring the concentration of NT-proBNP, one can judge the amount of brain natriuretic peptide synthesized. NT-proBNT level correlates closely with left ventricular ejection fraction and pulmonary artery systolic pressure. NT-proBNP levels indicates a high probability of heart failure and the advisability of appropriate examination to confirm the diagnosis.

Normal value:

Less than 125 pg/ml.

Preparing for the analysis:

This test can be done at any time during the day and no fasting is required.

Level of lipoprotein-associated phospholipase (LP-PLA2, PLAC).

High levels of lipoprotein-associated secretory phospholipase a2 (LP-PLA2) indicate an increased risk of developing cardiovascular diseases. However, in some cases, the cause of the elevated levels may not be an arterial cause.

Normal value:

Less than 200 ng/ml - relatively low risk of developing cardiovascular diseases;

Between 200-235 ng/ml - average risk of developing cardiovascular diseases;

More than 235 ng/ml - high risk of developing cardiovascular diseases.

Preparing for the analysis:

Blood should be drawn for testing after a 12-hour fast (excluding drinking water). To get more accurate results, you should refrain from taking the test for at least two months after a heart attack, surgery, infection, injury, or pregnancy.

The ratio of albumin to creatinine in urine. (Ualb/Cr). The appearance of albumin in the urine is a sign of kidney disease, diabetes and cardiovascular complications.

Normal value:

More than 30 mg/g indicates an increased risk of cardiovascular disease and diabetic nephropathy.

More than 300 mg/g indicates clinical nephropathy.

Preparing for the analysis:

A urine test can be done at any time during the day and does not require fasting.

Laboratory tests - a way to diagnose chronic heart failure

Chronic heart failure (CHF) is a disease in which the pumping function of the heart is reduced. It cannot release the required amount of blood, which causes organs and tissues to suffer. To identify the disease, a consultation with a cardiologist is necessary. But first you can take tests that will help a specialist diagnose heart failure. 1. General blood test. With progressive CHF, iron deficiency anemia may develop due to impaired absorption of iron in the intestine or insufficient intake of iron from food.

2. General urine analysis. Proteinuria and cylindruria may appear as markers of impaired renal function in chronic heart failure.

3.Biochemical blood test: • To diagnose possible liver dysfunction - AST, ALT, total protein, bilirubin. AST and ALT are always given in pairs so that the doctor can see and separate lesions in the heart and liver. Their increase, in most cases, indicates problems with the muscle cells of the heart and the occurrence of myocardial infarction. • LDH (lactate dehydrogenase) and CK (creatine phosphokinase) and especially its MB-fraction (MB-CPK) - increase during acute myocardial infarction. • Myoglobin - increases as a result of the breakdown of cardiac or skeletal muscle tissue. • Electrolytes (K, Na, Cl-, Ca2 ions) - an increase in potassium leads to heart rhythm disturbances, the possible development of excitation and ventricular fibrillation; low potassium levels can cause decreased myocardial reflexes; insufficient sodium ions and an increase in chlorides are fraught with the development of cardiovascular failure. • Cholesterol - its excess serves as a risk for the development of atherosclerosis and coronary heart disease. An increase in cholesterol levels (with significant impairment of liver function - hypocholesterolemia), triglycerides, low and very low density lipoproteins, a decrease in high density lipoproteins is possible with coronary heart disease. • C-reactive protein - appears in the body during an inflammatory process or tissue necrosis that has already occurred, since it is contained in minimal levels in the blood serum of a healthy person.

4. Brain natriuretic peptide (BNP) - used as a marker in the diagnosis of heart failure. BNP levels are elevated in patients with left ventricular dysfunction. At the same time, the content of BNP in blood plasma significantly correlates with the functional classes of chronic heart failure. Determining the level of BNP in blood plasma helps to assess the severity of chronic heart failure, predict the further development of the disease, and also evaluate the effect of therapy.

5. Coagulogram - will give an idea of ​​the process of blood clotting, its viscosity, the possibility of blood clots or, conversely, bleeding. May be given in addition to other tests.

You can take the necessary tests at the Federal State Budgetary Institution “National Medical Research Center for TPM” of the Russian Ministry of Health. A comfortable treatment room and a fully equipped laboratory are at your disposal. Most analyzes are completed within 1 business day.

More details at the link