RU2697053C1 - Method for prediction of pulmonary edema in patients with myocardial infarction - Google Patents

Abstract

FIELD: medicine.

SUBSTANCE: invention refers to medicine and aims at predicting pulmonary edema in myocardial infarction patients. Venous blood is sampled from the patient, separated into plasma and erythrocyte mass, a set of erythrocyte mass into a dilatometric device, then initial volume of liquid is recorded, dilatometric device is frozen to -10 °C, then using a probe recorded and recorded volume of frozen erythrocyte mass, erythrocyte mass is weighed before and after drying; then content of bound water fraction and K_hydration by formulas. If content of bound water fraction is ≤22.12 %, and K_hydration ≤0.55, developing pulmonary edema within the first day; if content of bound water fraction from 25.8 % to 27.8 %, and K_hydration from 0.68 to 0.74, then uncomplicated myocardial infarction is predicted.

EFFECT: method enables rapid and high-accuracy prediction of developing pulmonary edema in patients with acute myocardial infarction.

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Description

The invention relates to medicine and can be used in cardiology.

A known method for predicting the development of complications in patients with myocardial infarction by counting the leukocyte formula in stained blood smears and the ratio of granulocytes and agranulocytes is used to judge the reactivity of the body. With a ratio of more than 4.0, the development of complications of the course of myocardial infarction is predicted in the form of pulmonary edema, cardiogenic shock, or death. But this method is time-consuming, requires special dyes and time for staining blood cells. In addition, it is non-specific and does not allow the start of preventive treatment to prevent the development of a specific complication. (Reference laboratory methods of research in the clinic. Edited by Professor V.V. Menshikov, Moscow "Medicine" 1987, S. 106-107, 111-112, 124).

A known method for predicting complications in acute myocardial infarction is that blood is taken from a patient on the first day of acute myocardial infarction, then platelets are extracted from it, to which antigen is added from necrotic cardiac tissue, and after the thrombolysis reaction, platelet damage is assessed . If this value is above 14%, then the risk of complications is considered high. However, this method is difficult to use, especially in emergency care: to isolate platelets in their native form, expensive equipment and reagents are needed, this process takes a long time; to obtain antigen from necrotic cardiac tissue, complex equipment, prepared by a specialist, is also required, and standardized conditions and additional time are required to formulate a further thrombolysis reaction. (Patent No. 1388807 of the USSR, IPC G01N 33/49 (Method for predicting complications in acute myocardial infarction) / M.M. Mirrahimov et al .; applicant and patentee of the Kyrgyz Research Institute of Cardiology; application No. 3734043 of 04/27/1984; published 04/15/1988, Bull. No. 14).

It is known that water represents the main component of all systems of living organisms, including humans. All physicochemical metabolic reactions occur only in the aquatic environment. In its structure, it is heterogeneous and emit free and bound water fractions. They are isolated not only because of differences in physicochemical properties, but also because of different physiological functions. (Aksenov S.I. Bound water in disperse systems // State of water in biological systems. - 1980. - No. 57. - P. 46-74 .; Bychkov S.M., Kuzmina S.A .; Effect of proteoglycans on red blood cells in circulating blood // Bulletin of experimental biology and medicine. 1993. - No. 3. S. 240-242. Horizons PD, Belousov OI, Fedotova MI Stress and blood system. M: Medicine, 1983.- 239 p.). The amount of structured water fraction is of great importance for the functioning of biologically active substance molecules, including changing the configuration of proteins and ordering their tertiary and quaternary structures (Zhukovsky A.L., Rovnov N.V., Sorvin S.V., Petrov L.N. , Vuks E.M. Change in protein conformation in aqueous solutions of heterofunctional non-electrolytes // Biophysics. - 1999. - T. 44, issue 3. - P. 407-411).

One of the mechanisms of the body's response to external influences is the phenomenon of adaptive stabilization of structures. This process is based on the mechanism of accumulation of proteins of the HSP70 family, i.e., heat shock proteins. These proteins have the unique ability to disaggregate or renature damaged cellular structures. In the case of prolonged or extremely strong exposure to a damaging factor, the content of stress proteins decreases (Meerson F.Z. “Protection of the heart from ischemic injuries: the role of stress-limiting systems and stabilization of myocardial structures”, Russian Journal of Cardiology, 2001, No. 5 (31 ), p. 49-59). Changes in the ratios of free and bound water fractions in the blood components are a reflection of the processes occurring in the cells of organs and the intercellular medium as a result of a pathological process.

The method is based on the property of water to increase in volume during freezing (crystallization) and various properties of free and bound water fractions in this process. The free fraction of water crystallizes at a temperature slightly below 0 ° C, and the fraction of water associated with biomacromolecules begins to crystallize at a temperature below -20 ° C.

The technical result of the invention consists in predicting the development of pulmonary edema in patients with myocardial infarction.

The essence of the proposed method lies in the fact that by determining the content of bound water in the erythrocyte mass of the patient’s blood and calculating the erythrocyte mass hydration, the development of pulmonary edema in patients with acute myocardial infarction is predicted.

The method is as follows.

In the erythrocyte mass, the content of free and bound water is determined by the dilatometric method in the modification of N.F. Farashchuk (ed. St. No. 1544381). The basis of this method is the property of crystallization of water, which is accompanied by an increase in its volume. In biological fluids, water is represented by free and bound fractions. During freezing, the free fraction transforms into a crystalline state at a temperature slightly below 0 ° C, while the bound fraction crystallizes at a temperature below -20 ° C. This property allows you to calculate and evaluate the volume of each of the water fractions. To implement the method, the following set of equipment is required: a centrifuge, a freezer, an oven, an analytical balance, a medical training microscope MIKMED-5U, a dilatometric device for measuring fluid volume before and after freezing, a device for sampling liquid tissues described in patent No. 1710000 .

In patients with acute myocardial infarction with a suspicion of developing pulmonary edema, 4 ml of venous blood are collected in a dry glass tube with 2 drops of heparin solution upon admission. The resulting blood is centrifuged until the erythrocyte mass plasma is separated. After that, using an automated pipette, the separated plasma from the erythrocyte mass is removed, which is collected into the capillary using a device for sampling biological fluids. As a result of the reciprocating movement of the roller along the elastic tube fixed in the bottom of the casing, the red blood cell fills the capillary. The Panchenko capillary is used because its divisions after 1 mm coincide with those in the reference scale of the microscope, which allows the volume of liquid to be recorded with an accuracy of 0.05 mm. The erythrocyte mass is collected up to a column height of 90-92 mm so that the volume of liquid increased during crystallization of the water remains within the scale. A capillary with samples of blood components is fixed in a metal holder and clamped with a screw on the upper platform. After that, a metal probe having a strictly transverse lower section is passed through the hole in the screw, not reaching the level of biological fluids. Using the microscope of the medical training MIKMED-5U, the initial volume of fluid is recorded. After that, the dilatometric device is assembled immersed in a freezer with a constant temperature of -10 ° C for 20 minutes. Then the device is removed and with the help of a metal probe, pushing into the capillary until it stops, the volume of red blood cells is fixed after freezing (crystallization) of the free fraction of water and it is recorded using the microscope of the medical training MIKMED-5U. A piece of metal foil measuring 3 cm * 3 cm is weighed. After this, the probe is removed from the capillary, which is released from the holder, and the erythrocyte mass is poured onto a previously weighed piece of metal foil, weighed on any analytical balance to the nearest 0.0001 g and dried in a drying oven cabinet at 100 ° C for 40 minutes, followed by registration of the mass of solids.

The total water content is calculated by the formula:

m _{f + Er.mass} is the mass of a weighed piece of metal foil and erythrocyte mass,

^m _{F +} dry residue - the weight of the suspended piece of metal foil and dry residue,

m _f - the weight of the suspended piece of metal foil.

The content of the free fraction of water is calculated by the formula:

V1 is the initial volume of liquid;

V2 is the volume of liquid after crystallization of the free fraction of water;

K is the compression coefficient of the erythrocyte mass upon cooling from room temperature to the crystallization temperature (0 ° C), established experimentally.

The content of the bound water fraction is calculated by the formula;

- содержание общей воды,

- total water content,

- содержание свободной фракции воды.

- the content of the free fraction of water.

The coefficient of hydration of the erythrocyte mass is calculated according to the following formula:

, где С1 - содержание связанной фракции воды, С2 - содержание свободной фракции воды.

where C1 is the content of the bound fraction of water, C2 is the content of the free fraction of water.

And they conclude: if in patients with acute myocardial infarction the content of the bound fraction of water is ≤22.12%, and Hydration is ≤0.55, then the development of pulmonary edema is predicted during the first day; if in patients with myocardial infarction the content of the bound fraction of water is determined from 25.8% to 27.8%, and hydration from 0.68 to 0.74, then an uncomplicated course of myocardial infarction is predicted.

The proposed method is illustrated by the following examples.

Example 1

Patient S., 68 years old, was admitted to the clinic on July 17, 2018 with complaints of intense pain in the heart region with radiation to the left shoulder, neck, feeling of lack of air, aggravated in the supine position, expressed general weakness.

History: arterial hypertension, constantly takes losartan 50 mg 2 times a day, bisoprolol 2.5 mg in the morning and cardiomagnyl 75 mg at night. The above complaints did not bother before and arose about 14 hours ago, independently took NSAIDs, Corvalol, Validol, Glycine - without improvement, caused an SMP. Medical assistance was provided and the patient was taken to the clinic.

Objectively: Height: 168 cm, weight: 74 kg, BMI = 26.22 kg / m ² . HELL = 135/80 mm Hg. Art., heart rate = 84 per minute, NPV = 18-20 per minute. SpO2 = 98-99%. Skin integument, moderate humidity. Peripheral edema was not detected. Breathing over the entire surface of the lungs is vesicular, slightly weakened in the lower parts, no wheezing. Heart sounds are rhythmic, muffled. The abdomen is soft, painless on palpation. Stool and diuresis are normal.

Changes in the general analysis of blood and the general analysis of urine are not revealed.

Biochemical blood test: ALT = 62 U / L, AST = 108 U / L, LDH = 800, KFK = 2418 U / L, KFK-MV = 132 U / L, cholesterol = 9.2 mmol / L, creatinine = 87 μmol / L, urea = 5.2 mmol / L, total protein = 73 g / L, blood glucose = 7.1 mmol / L.

Chest x-ray - no visible infiltration. The roots of the lungs are slightly widened.

Electrocardiogram: sinus rhythm, heart rate = 80 per minute, e.o.s. not rejected. Dynamics of the course of acute antero-lateral myocardial infarction of the left ventricle with ST segment elevation. Pathological tooth Q _V2-V5 .

The patient received venous blood for examination. The following changes were identified:

The data obtained are regarded as a criterion for a high risk of developing acute left ventricular failure in the form of pulmonary edema.

Within 1.5 hours of hospital stay, the patient developed alveolar pulmonary edema, which was stopped. Against the background of the therapy, the patient's condition improved and she was discharged for further outpatient monitoring.

Example 2

Patient T., 54 years old, was admitted to the clinic on September 4, 2018 with complaints of intense pain behind the sternum with radiation to the epigastric region, a feeling of lack of air, and pronounced general weakness.

In the anamnesis: occasionally noted an increase in blood pressure to 160/90 mm RT. Art. against the background of emotional and physical stress, he took captopril (usual blood pressure 135-140 / 85 mm Hg). The above complaints arose about 10 hours ago, I took validol on my own, externally - diclofenac - without improvement, caused an SMP. Medical assistance was provided. The patient is delivered to the clinic.

Objectively: Height: 189 cm, weight: 106 kg, BMI = 29.67 kg / m ² . HELL = 145/90 mm Hg. Art., heart rate = 58 per minute, NPV = 18-20 per minute. SpO2 = 98%. Skin integument, moderate humidity. Peripheral edema was not detected. Breathing over the entire surface of the lungs is vesicular, weakened in the lower parts, no wheezing. Heart sounds are rhythmic, muffled. The abdomen is soft, painless on palpation. Stool and diuresis are normal.

Changes in the general analysis of blood and the general analysis of urine are not revealed.

Biochemical analysis of blood: ALT = 56 IU / l, AST = 112 IU / l, LDH = 643, KFK = 2128 IU / l, KFK-MV = 116 IU / l, cholesterol = 8.7 mmol / l, creatinine = 82 μmol / L, urea = 5.8 mmol / L, total protein = 84 g / L, blood glucose = 6.9 mmol / L.

Chest x-ray - no visible infiltration. The roots of the lungs are dilated. The shadow of the heart is expanded to the left.

Electrocardiogram: sinus bradycardia, heart rate = 56-58 per min, e.s. rejected to the left. The dynamics of the course of acute lower left myocardial infarction. Pathological Q wave in III and aVF.

The patient received venous blood for examination. The following changes were identified:

The data obtained are regarded as a criterion for a high risk of developing acute left ventricular failure in the form of pulmonary edema.

After 11 hours and 45 minutes of hospital stay, the patient developed alveolar pulmonary edema, which was successfully stopped. Against the background of the therapy, the patient's condition improved and he was discharged under the supervision of a cardiologist at the place of residence.

Example 3

Patient M., 59 years old, was admitted to the clinic on 02.09.2018 with complaints of intense pressing pain behind the sternum with radiation to the neck, lower jaw, feeling of lack of air, aggravated in the supine position, expressed general weakness.

In the anamnesis: arterial hypertension, periodically with high blood pressure takes capoten, lisinopril. I did not seek medical help.

On the eve of the patient notes intense physical labor ("digging potatoes"). The above complaints did not bother before and arose about 17 hours ago, independently took validol, tincture of valerian, motherwort, hawthorn - without significant improvement, relatives called the ambulance. Medical assistance was provided and the patient was taken to the clinic.

Objectively: Height: 179 cm, weight: 94 kg, BMI = 29.34 kg / m ² . HELL = 150/90 mm RT. Art., heart rate = 96 per minute, NPV = 18-20 per minute. SpO2 = 98-99%. Skin integument, moderate humidity. Peripheral edema was not detected. Breathing over the entire surface of the lungs is vesicular, no wheezing. Heart sounds are rhythmic, muffled. The abdomen is soft, painless on palpation. Stool and diuresis are normal.

Changes in the general analysis of blood and the general analysis of urine are not revealed.

Blood biochemical analysis: ALT = 56 IU / L, AST = 102 IU / L, LDH = 853, KFK = 2326 IU / L, KFK-MV = 118 IU / L, cholesterol = 7.4 mmol / L, creatinine = 76 μmol / L, urea = 4.2 mmol / L, total protein = 81 g / L, blood glucose = 6.9 mmol / L.

Chest x-ray - no visible infiltration. The roots of the lungs are slightly widened.

Electrocardiogram: sinus tachycardia, heart rate = 96 per minute, e.s. not rejected. Dynamics of the course of acute antero-septal left ventricular myocardial infarction. Pathological tooth Q _V1-V4 .

The patient received venous blood for examination. The following changes were identified:

The data obtained indicate adequate activation of adaptation mechanisms in this patient and a low risk of developing pulmonary edema.

During the 14-day hospital stay on the background of the therapy, the patient's condition improved and he was discharged for further outpatient monitoring.

Example 4

Patient F., 48 years old, was admitted to the clinic on 08/12/2018 with complaints of burning pain behind the sternum without irradiation, a feeling of lack of air, pronounced general weakness, sweating.

History: rarely increased blood pressure to 150/80 mm RT. st. against a background of emotional stress, took no-shpu (normal blood pressure 115-120 / 80 mm RT. Art.).

The above complaints arose about 18 hours ago, I took no-shpa myself, nitroglycerin - with a short improvement, I contacted the clinic myself.

Objectively: Height: 182 cm, weight: 92 kg, BMI = 27.77 kg / m ² . HELL = 140/85 mm Hg. Art., heart rate = 88 per minute, NPV = 18-20 per minute. SpO2 = 98%. TTela = 36.8 ° C. Skin integument, moist. Peripheral edema was not detected. Breathing over the entire surface of the lungs is vesicular, no wheezing. Heart sounds are rhythmic, muffled. The abdomen is soft, painless on palpation. Stool and diuresis are normal.

Changes in the general analysis of blood and the general analysis of urine are not revealed.

Blood biochemical analysis: ALT = 51 IU / l, AST = 98 IU / l, LDH = 759, KFK = 2054 IU / l, KFK-MV = 83 IU / l, cholesterol = 8.9 mmol / l, creatinine = 76 μmol / L, urea = 5.1 mmol / L, total protein = 77 g / L, blood glucose = 6.2 mmol / L.

Chest x-ray - no visible infiltration.

Electrocardiogram: sinus rhythm, heart rate = 80-88 per min, e.o.s. rejected to the left. The dynamics of the course of acute subendocardial myocardial damage in the region of the anterior wall of the left ventricle.

The patient received venous blood for examination. The following changes were identified:

The data obtained indicate adequate activation of adaptation mechanisms in this patient and a low risk of developing pulmonary edema.

As a result of the therapy, the patient's condition improved and on the 13th day he was discharged under the supervision of a cardiologist at the place of residence.

The presented examples illustrate the ability to predict the development of pulmonary edema in patients with myocardial infarction by changing the content of the bound fraction of water in the erythrocyte mass and Hydration. An increase in the amount of bound water fraction reflects the adaptive stabilization of tissue structures in response to the development of damage to cardiomyocytes and the general stress response of the body during the development of myocardial infarction. At the same time, a significant decrease in the bound fraction of water in patients with developed acute left ventricular failure in the form of pulmonary edema indicates the depletion of the compensatory mechanisms of the body and the need for active intervention to restore them.

The proposed method for the first time allows predicting the development of acute left ventricular failure in the form of pulmonary edema in patients with acute myocardial infarction, it is easy to perform, at the same time it has high accuracy, speed of obtaining results, their reliability, it allows you to start preventive therapy in time to prevent the development of pulmonary edema in patients with myocardial infarction. In addition, to perform this method, elementary laboratory equipment is required, which is used repeatedly; expensive reagents are not required, which is economically viable.

Claims (8)

A method for predicting the development of pulmonary edema in patients with myocardial infarction, including collecting venous blood from a patient, dividing it into plasma and erythrocyte mass by centrifugation, then the erythrocyte mass is collected in a dilatometric device, the initial volume of fluid V1 is recorded with a microscope, the dilatometric device is frozen in freezer with a temperature of -10 ° C for 20 minutes, then using the probe fix the volume of frozen red blood cells, using a microscope register the floor chenny volume V2, is weighed on the balance piece of metal foil, and then it was poured into packed red blood cells from the capillary dilatometric device and weighed again, then dried red cell mass in an oven at 100 ° C for 40 minutes and record weight of dry residue; then calculate the total water content by the formula

calculate the content of the free fraction of water calculated by the formula

calculate the content of the bound fraction of water calculated by the formula

calculate the coefficient of hydration of red blood cells according to the following formula:

where C1 is the content of the bound fraction of water, C2 is the content of the free fraction of water; then they conclude: if in patients with acute myocardial infarction the content of the bound water fraction is ≤22.12%, and the hydration is ≤0.55, then the development of pulmonary edema during the first day is predicted; if in patients with myocardial infarction the content of the bound fraction of water is determined from 25.8% to 27.8%, and hydration from 0.68 to 0.74, then an uncomplicated course of myocardial infarction is predicted.