RU2166758C1 - Method for predicting cardiac insufficiency occurrence - Google Patents

Abstract

FIELD: medicine. SUBSTANCE: method involves carrying out biochemical examination of blood. Lactate quantity and myeloperoxidase activity level values are determined in plasma. Myeloperoxidase activity level being increased from 115.0 mcM/g of protein per 1 min to 200.0 mcM/g of protein per 1 min and lactate quantity from 6.0 mcM/ml to 10.0 mcM/ml, cardiac insufficiency is to be predicted. EFFECT: high accuracy of prognosis.

Description

 The invention relates to medicine, more specifically to cardiology, and may find application in clinical practice for the timely detection of heart failure.

 Progressive heart failure firmly occupies one of the leading places among the causes of death in patients with diseases of the cardiovascular system. After the onset of clinical signs of heart failure, after 5 years, against the background of traditional therapy, about 50% of patients die, the annual mortality rate in patients with severe heart failure reaches 40-50%, and the 3-year mortality rate is approximately 73%. All patients with cardiovascular pathology and coronary heart disease receive appropriate therapy, which changes the clinical picture of the course of heart failure. Given this, the possibility of timely detection of signs of heart failure, indicating its progression and the search for effective treatment methods, is of great importance.

 Currently, it is rarely possible to trace the natural clinical course of heart failure due to the widespread use of angiotensin-converting enzyme inhibitors and diuretics in patients with both asymptomatic left ventricular dysfunction and congestive heart failure.

 As a result, the clinical manifestations of heart failure in patients with their own compensatory mechanisms, as well as those who are in a state of drug compensation, are difficult to distinguish.

 Given the fact that the clinical severity of symptoms of heart failure does not fully reflect the degree of left ventricular dysfunction, the most accurate method for assessing the structural and functional disorders of the left ventricle is the instrumental one using expensive equipment.

 In this regard, there is a need to search for available laboratory methods to objectify the degree and severity of left ventricular dysfunction in patients with clinical manifestations of heart failure. Laboratory research methods can provide an answer in a short time to assess the adequacy of the functioning of cardiac mechanisms for compensating for heart failure. Conducted research on the medical-scientific and patent literature revealed various methods for the diagnosis of heart failure. So, copyright certificate N 1314269 05/30/1987 bull. N 20, I.I. Saharchuk is protected by the "Method for the diagnosis of heart failure in the preclinical stage", which includes the determination of pyruvate in the blood and an additional determination of the content of oxaloacetate. The ratio of the first to the second - 2.1-2.6 is an indicator for the diagnosis of the preclinical stage of heart failure. However, the disadvantage of this method is the inability to assess the state of compensatory mechanisms in order to timely determine the severity of left ventricular dysfunction and to determine heart failure. The method for diagnosing heart failure is protected by copyright (Shepotinovsky V.I., Mikashinovich Z.I., Firsova I.V. A.S. N 858785, USSR. Bull. N 32. 1981). This method suggests that a decrease in hemoglobin output during hemolysis of erythrocytes destroyed by ultrasound by 40% or more, compared with the control (control is the blood of practically healthy people), indicates the presence of latent circulatory failure 1A.

 At hemoglobin levels of 10.7 g /% or lower, 40% of the control values, a diagnosis of heart failure with circulatory disorders in stage 1A is made. This method is non-specific and reflects the early diagnosis of heart failure.

 However, the course and development of chronic heart failure is determined by the reactivity of the body and its adaptive-compensatory potential, which is not possible to evaluate using this method.

The closest in technical essence and the achieved result and taken as a prototype is "A method for predicting heart failure with myocardial infarction" (Shlyk S.V., Mikashinovich Z.I., Shepotinovsky V.I., Terentyev V.P. RF patent N 1811606, Bull. N 15, 1993). It consists in determining the concentration of intra-erythrocytic 2,3 - DPG and the level of P ₅₀ in response to a reduction in cardiac output.

 Changes in the modulation mechanism of hypoxia compensation appear already in the II Functional class of heart failure until a statistically significant decrease in the main parameters of central hemodynamics appears. However, this method does not allow to assess the state of the compensatory capabilities of the body, which is necessary for the timely prevention of severe heart failure.

 The aim of the invention is to simplify the method and improve the accuracy of predicting the occurrence of heart failure in post-infarction patients.

 This goal is achieved by the fact that lactate is determined in the blood plasma of patients, and myeloperoxidase activity in leukocytes. With an increase in myeloperoxidase activity from 115.0 μM / g protein per min to 200.0 μM / g protein per min and, accordingly, the lactate level from 6.0 μM / ml to 10.0 μM / ml, heart failure is predicted.

 The method is as follows: 3 ml of blood is taken from a patient from a vein. Blood cells (red blood cells and white blood cells) are obtained from venous blood stabilized with heparin (1 ml of blood 20 units of heparin).

 To study the activity of enzymes and protein content, a hemolysate with distilled water is prepared (dilution 1:20, 1.9 ml of distilled water + 0.1 ml of red blood cells).

The determination of the concentration of lactate in red blood cells is carried out according to the method of Barker and Summerson in the description of Prokhorova M.I. and Tushkova Z.N. (1965). 0.5 ml of 20% CuSO ₄ and 4 ml of H ₂ O are added to 0.5 ml of hemolysate. Then 250 mg of CaO are added to precipitate carbohydrates and left in the refrigerator for 20 minutes. The precipitate was centrifuged for 10 minutes at 3000 rpm and filtered. To 0.5 ml of faltrate add 1-2 drops of 4% CuSO ₄ and 3 ml of H ₂ SO ₄ - Saval samples, boil for 5 minutes in a water bath. After boiling, 2-3 drops of paraoxydiphenyl are added to the filtrate and incubated for 30 minutes at 37 ^° C. Then, they are boiled for 90 seconds in a bath, cooled and colorimetric on FEK at λ = 590 nm against the H ₂ SO ₄ - Saval sample. The results are expressed in μmol / ml solid erythrocyte sediment.

The activity of myelopyroxidase in leukocytes is determined according to the Klebanoff method described by M. Shafran, S. N. Lyzlova. (1975). The reaction is started by adding a leukocyte suspension containing 300-400 g protein to a medium comprising: 0.1 M phosphate buffer - pH = 6.0; 0.01 M H ₂ O ₂ ; 0.02 M orthodianisidine in methanol. Estimated spectrophotometrically at 460 nm. The enzyme activity is determined in the first minute of the reaction, taking the unit of enzyme activity as a change in extinction at 0.001 per minute. Results are expressed in μM / mg protein per minute.

 The protein content in the blood is determined by the Lowry method. The method is based on the formation of a complex, which in the presence of phenol gives a characteristic blue color proportional to the amount of protein. The intensity is measured at 680 nm. The results are expressed in mg / ml of hemolysate.

 With myeloperoxidase activity from 115.0 μM / g protein per minute to 200.0 μM / g protein per minute and lactate levels from 6.0 μM / ml to 10.0 μM / ml, heart failure is predicted.

 Clinical example 1.

 Patient K. Medical history N ____.

 47 years old. I turned to the OKD with complaints of shortness of breath during exertion, weakness, chest pains when walking at a distance of up to 100 m, asthma attacks at night. In March 1998, he suffered MI. According to a clinical examination, objective signs of decompensation were not detected. Heart sounds are muffled, heart rate = 94 beats / min, blood pressure = 130/80. In the lungs, vesicular breathing, no wheezing. No peripheral edema. on an ECG: cicatricial changes in the posterior wall of the left ventricle, left ventricular hypertrophy with overload.

 The diagnosis was established: coronary heart disease, functional class III angina, post-infarction cardiosclerosis (MI in 1998). The results of biochemical blood tests, the lactate content of 8.54 μm / ml; MPO activity - 174.0 μM / g protein per min. Such indicators indicate the failure of compensatory mechanisms and the progression of heart failure.

Echocardiography results: akinesia of the posterior and lateral walls of the left ventricle, MJP hypokinesia, local contractility of the uninfected myocardium in the MJP region Δ T _MJP - 13.8%, CSF = 67.3 mm; KDR = 73 mm; PV = 18.56%; SI = 2.0 l / min / m ² . EchoC data indicate the loss of compensatory capabilities by the cardiac mechanism of left ventricular dilatation: with the same CRC as in the previous case, the SV and myocardial contractility were significantly lower; reserve capacities of uninfected myocardium were also lost.

 The patient was prescribed therapy: Prestarium at a dose of 4 mg / day, Digoxin 0.25 mg / day, Verpiron 25 mg / day. Despite the regular intake of drugs, the patient was admitted to the cardiology department of the OKB with congestive heart failure. An objective examination revealed moist wheezing in the lungs, an enlarged liver, and peripheral edema. Thus, the biochemical parameters of blood, an increase in the activity of myeloperoxidase and the level of lactate adequately reflected the “disruption” of compensatory cardiac adaptive mechanisms, which allows them to be used as a prognostic marker for the progression of heart failure, when the clinical manifestations of the disease are still not symptomatic or are leveled out by the active use of medications.

 Clinical example 2.

 Patient I., medical history N __, age 47 years. I contacted the Regional Cardiology Dispensary for the purpose of preventive examination. In 1996, he suffered a large focal myocardial infarction. At the time of the examination, he complained of shortness of breath during physical exertion, rapid fatigue, palpitations, chest pains while walking to a distance of 100 m. According to an objective study: the borders of the heart are expanded to the left by 1.0-1.5 cm, heart sounds are deaf , rhythmic, heart rate = 80 beats, blood pressure = 110/80. In the lungs, vesicular breathing, no wheezing. The liver is not enlarged. No peripheral edema. On the ECG: cicatricial changes in the anterior septal apical region with a transition to the side wall. ECG - signs of chronic post-infarction aneurysm. Left ventricular hypertrophy with overload. The diagnosis was established: coronary heart disease, angina of a functional class III disorder, post-infarction cardiosclerosis (MI in 1996), post-infarction aneurysm N. 1 tbsp. According to biochemical blood tests, the lactate content in erythrocytes was 6.6 μm / ml; MPO activity in leukocytes is 105.0 μM / g protein per min, which indicates the stabilization of the state of cardiac mechanisms of hypoxia compensation.

Echocardiography results: DAC = 60 mm; KDR = 73 mm; LVEF = 35%; SI (cardiac index) = 3.65 L / min / m ² ; ATzs (local contractility of the posterior wall of the left ventricle) = 48.7%. The akinesia of the entire cerebrospinal fluid, apex, aneurysm of the septal apical region, thus the results of the EchoCS testify to the viability of the Franky-Starling mechanism, which maintains the volume of cardiac output at a level comparable to healthy individuals, despite the decrease in the global contractility of the left ventricular myocardium.

 The maintenance of the state of compensation is also carried out thanks to the adequate functioning of the posterior wall of the left ventricle not involved in the cicatricial zone of the myocardium. During the observation, the patient's condition remained stable, signs of progression of heart failure were not detected. The biochemical parameters of blood, reflecting the activity of myeloperoxidase and the level of lactate, were unchanged. Thus, a blood test has prognostic value and allows you to adequately assess the state of the cardiovascular system.

 Studies and analysis of indicators suggest that the proposed method has convincing significance and can be used to predict heart failure in patients taking angiotensin-converting enzyme inhibitors and diuretics, as well as in patients with severe congestive heart failure. The proposed method can be used in practical public health to predict the course of heart failure in post-infarction patients.

 Thus, the proposed method allows timely prediction of heart failure and take urgent measures for subsequent surgery. The method is simple, available at any medical institution. The advantage of the method is its information content and specificity. To diagnose using the proposed method requires 60 minutes and 3 ml of blood.

Claims (1)

 A method for predicting the occurrence of heart failure in post-infarction patients by biochemical blood testing, characterized in that in patients in plasma lactate and myeloperoxidase activity are determined, with an increase in myeloperoxidase activity from 115.0 μM / g protein per minute to 200.0 μM / g protein min and, accordingly, lactate levels from 6.0 μM / ml to 10.0 μM / ml predict heart failure.