Reverse myocardial evaluation method for patient with dilated heart disease

Abstract

The invention discloses a myocardial reversal evaluation method for a patient with dilated heart disease, and relates to the technical field of dilated heart disease. The myocardial reversal evaluation method for the patient with the dilated heart disease comprises the following steps: grading cardiac functions; grading and evaluating the cardiac function of the patient based on the standard cardiac function grading; observing indexes; the plasma of the patient is reserved, and related indexes of the patient about the dilated heart disease are monitored during each re-consultation; follow-up treatment; rechecking the obtained related indexes; statistical processing; statistical analysis of data is completed based on SPSS, and the myocardial reversal effect of the patient before and after treatment is evaluated. By integrating cardiac function grading, cardiac structure, functional indexes, biomarkers, hemodynamics and safety indexes of a patient, pathophysiology omnibearing of myocardial remodeling is covered, limitation of single dependence or symptom scoring is broken through, missed diagnosis or misjudgment is avoided, curative effect difference is visually displayed through a curve graph and an effective rate comparison graph, and the curative effect of myocardial remodeling is improved. And the clinical persuasion is enhanced.

Description

Technical Field

[0001] The present invention relates to the technical field of dilated cardiomyopathy, and in particular to a method for assessing myocardial reversal in patients with dilated cardiomyopathy. Background Art

[0002] Dilated cardiomyopathy (DCM), also known as dilated cardiomyopathy, refers to a heterogeneous group of myocardial diseases characterized by ventricular dilation and decreased myocardial contractility. This group includes a range of cardiomyopathies with dilated cardiomyopathy as a phenotype due to specific etiologies, generally excluding valvular disease, congenital heart disease, or ischemic heart disease. The disease is relatively common, with diverse etiologies, approximately half of which remain unknown. Clinical manifestations include cardiac enlargement, heart failure, arrhythmias, thromboembolism, and sudden death. The pathogenesis of cardiomyopathies characterized by DCM is complex, with multiple causes ranging from hypertension, alcohol, metabolic, endocrine, autoimmune, rheumatic, infiltrative, genetic, infectious, and cardiac toxins.

[0003] In the past, it was believed that the prognosis of this disease was poor, with a five-year survival rate of approximately 50% and a ten-year survival rate of approximately 25%. DCM is usually irreversible once diagnosed. However, with advances in treatment, it has been found clinically that some DCM patients can achieve partial or even complete recovery of cardiac structure and function after guideline-directed drug therapy (GDMT), which is manifested by improved symptoms, improved cardiac function, and even reverse remodeling of myocardial structure. The treatment outcome of this disease is very critical to the patient's mental and psychological stress, treatment expectations, and the choice of future treatment plans. At present, there is still a lack of an effective and complete prognostic risk assessment system for DCM patients with severely impaired myocardial contractile movement in clinical practice, resulting in increasingly unsatisfactory prognosis prediction results, which seriously affects the patient's risk stratification and corresponding treatment strategies, and brings a large health and medical economic burden. Summary of the Invention

[0004] In view of the deficiencies of the prior art, the present invention provides a method for assessing myocardial reversal for patients with dilated cardiomyopathy, which solves the problems raised in the above-mentioned background technology.

[0005] To achieve the above objectives, the present invention is implemented through the following technical solutions: a method for evaluating myocardial reversal in patients with dilated cardiomyopathy, the method comprising the following specific steps:

[0006] S1: Cardiac function classification; assess the patient's cardiac function based on the standard cardiac function classification;

[0007] S2: Observation of indicators: Collect the patient's plasma and monitor the patient's dilated cardiomyopathy-related indicators at each follow-up visit;

[0008] S3: Treatment follow-up: 4 regular follow-up visits are conducted every year to review the relevant indicators obtained in S2;

[0009] S4: Statistical processing: Statistical analysis of S2 and S3 data was completed based on SPSS, and the myocardial reversal effect of patients before and after treatment was evaluated.

[0010] A further improvement of the technical solution of the present invention is that in S1, the graded assessment includes the following specific settings:

[0011] Grade 1: Patients have heart disease but are not restricted in physical activity;

[0012] Level 2: The patient has heart disease, which results in slight limitation of physical activity;

[0013] Level 3: The patient has heart disease, which significantly limits physical activity;

[0014] Level 4: The patient has heart disease and has symptoms of heart failure or angina pectoris even at rest. Any physical activity will increase the discomfort.

[0015] A further improvement of the technical solution of the present invention is that in S2, the related indicators of dilated cardiomyopathy include:

[0016] Cardiac function grade, left ventricular end-diastolic anteroposterior diameter or left-right diameter, left ventricular ejection fraction, NT-proBNP, pulmonary artery pressure, blood potassium, blood creatinine, urea nitrogen, AST, ALT and blood pressure.

[0017] A further improvement of the technical solution of the present invention is that the measurement of blood creatinine index includes the following specific steps:

[0018] Take 225 μL of mixed reagent A and add it to 6 μL of the patient's sample. After shaking evenly, incubate at a constant temperature of 37°C for 5 minutes. After reading the absorbance AO, add mixed reagent B. After shaking evenly, incubate at 37°C for 5 minutes. After reading the absorbance A1, calculate ΔA = A1-A0.

[0019] The components of mixed reagent A include creatinase, sarcosine oxidase, peroxidase, and N-ethyl-N-3-methylaniline, with final concentrations of 2000 U / L, 6000 U / L, 5000 U / L, and 0.4 mmol / L, respectively;

[0020] Component B of the mixed reagent includes creatinase and 4-aminothiazine, with final concentrations of 250,000 U / L and 1.0 mmol / L, respectively.

[0021] The reference range of ΔA is 44-97umol / L for adult males and 35-80umol / L for adult females.

[0022] A further improvement of the technical solution of the present invention is that the measurement of urea nitrogen includes the following specific steps:

[0023] Take 2.5uL of the patient's sample, add 200uL of mixed reagent C, incubate at 37°C for 3-5 minutes, read the absorbance AO, and after incubation, add 100uL of mixed reagent D. After mixing, incubate at 37°C for 60 seconds, continuously monitor for 1-3 minutes, read the absorbance A1, and calculate ΔA = A1-A0;

[0024] The components of mixed reagent C include urease, glutamate dehydrogenase, adenosine diphosphate, and tris buffer, with final concentrations of 8000 U / L, 500 U / L, 1.5 mol / L, and 100 mmol / L, respectively;

[0025] The components of the mixed reagent D include reduced coenzyme I and α-ketoglutaric acid, with final concentrations of 0.3 mmol / L and 13.0 mmol / L, respectively.

[0026] The reference range of ΔA is 1.43-7.14 mmol / L.

[0027] A further improvement of the technical solution of the present invention is that the measurement of alanine aminotransferase includes the following specific steps:

[0028] Take 200 μL of mixed reagent E and add it to 15 μL of patient sample, shake evenly, incubate at 37°C for 3 minutes, read the absorbance AO, then add 100 μL of mixed reagent F and incubate at 37°C for 60 seconds. Monitor continuously for 1-3 minutes, read the absorbance A1, and calculate ΔA = A1-A0;

[0029] The reference range of ΔA is 9-50U / L for adult males and 7-40U / L for adult females.

[0030] A further improvement of the technical solution of the present invention is that the measurement of aspartate aminotransferase includes the following specific steps:

[0031] Take 200uL of mixed reagent G and add it to 15uL of patient sample, shake evenly, incubate at 37℃ for 3min, read the absorbance AO, then add 100uL of mixed reagent H and incubate at 37℃ for 60s. Monitor continuously for 1-3min, read the absorbance A1, and calculate ΔA=A1-A0;

[0032] The reference range of ΔA is 15-40 U / L for adult males and 13-35 U / L for adult females.

[0033] A further improvement of the technical solution of the present invention is that the detection of NT-proBNP includes the following specific steps:

[0034] Turn on the immunofluorescence dry-well quantitative analyzer, return the test card and buffer to room temperature, pipette 75 μL of the patient sample into the buffer, mix thoroughly for 1 minute, then pipette 75 μL of the mixed solution into the sample well of the test card to complete the test. The reference range for NT-proBNP is <300 pg / ml for patients under 75 years of age and <450 pg / ml for patients 75 years of age or older.

[0035] A further improvement of the technical solution of the present invention is that the statistical analysis of the S2 and S3 data in S4 includes: comparison of cardiac function classification, left ventricular end-diastolic anteroposterior diameter or left-right diameter, left ventricular ejection fraction, NT-proBNP, pulmonary artery pressure and adverse reactions, as well as sample rate comparison using t-test, mean comparison using one-way analysis of variance, and pairwise comparison using LSD method.

[0036] Beneficial effects

[0037] Compared with existing technologies, the present invention has the following advantages: integrating the patient's cardiac function classification, cardiac structure, functional indicators, biomarkers, hemodynamics, and safety indicators, covering the full range of myocardial remodeling pathophysiology, breaking through the limitations of single reliance or symptom scoring, avoiding missed diagnoses or misdiagnoses, and visually demonstrating the difference in therapeutic efficacy through curve graphs and efficacy comparison charts, thereby enhancing clinical persuasiveness;

[0038] Through multi-parameter dynamic monitoring, quantitative threshold determination and safety integration, a comprehensive evaluation of the reversal effect of myocardial remodeling in patients with dilated cardiomyopathy is achieved, providing a reliable evaluation method for clinical precision treatment and prognosis management. BRIEF DESCRIPTION OF THE DRAWINGS

[0039] Figure 1 It is a schematic diagram of the process of the present invention;

[0040] Figure 2 This is a line graph comparing the changes in center function classification in the embodiment;

[0041] Figure 3 A bar graph showing the comparison of the anteroposterior diameter or left-right diameter of the left ventricular end-diastole in the embodiment;

[0042] Figure 4 It is a bar graph showing the comparison of left ventricular ejection fraction in the embodiment. DETAILED DESCRIPTION

[0043] Various exemplary embodiments, features, and aspects of the present application will be described in detail below with reference to the accompanying drawings. The same reference numerals in the accompanying drawings represent elements with the same or similar functions. Although various aspects of the embodiments are shown in the accompanying drawings, the drawings are not necessarily drawn to scale unless otherwise indicated.

[0044] The word “exemplary” is used exclusively herein to mean “serving as an example, example, or illustration.” Any embodiment described herein as “exemplary” is not necessarily to be construed as preferred or advantageous over other embodiments.

[0045] In addition, numerous specific details are provided in the following specific examples to better illustrate the present application. Those skilled in the art will appreciate that the present application can be practiced without certain specific details. In some instances, methods, means, and components well known to those skilled in the art are not described in detail in order to highlight the main purpose of the present application.

[0046] The present invention provides a method for evaluating myocardial reversal for patients with dilated cardiomyopathy, the method comprising the following specific steps:

[0047] S1: Cardiac function classification; assess the patient's cardiac function based on the standard cardiac function classification;

[0048] S2: Observation of indicators: Collect the patient's plasma and monitor the patient's dilated cardiomyopathy-related indicators at each follow-up visit;

[0049] S3: Treatment follow-up: 4 regular follow-up visits are conducted every year to review the relevant indicators obtained in S2;

[0050] S4: Statistical processing: Statistical analysis of S2 and S3 data was completed based on SPSS, and the myocardial reversal effect of patients before and after treatment was evaluated.

[0051] In S1, the grading assessment includes the following specific settings:

[0052] Grade 1: Patients have heart disease but are not restricted in physical activity;

[0053] Level 2: The patient has heart disease, which results in slight limitation of physical activity;

[0054] Level 3: The patient has heart disease, which significantly limits physical activity;

[0055] Level 4: The patient has heart disease and has symptoms of heart failure or angina pectoris even at rest. Any physical activity will increase the discomfort.

[0056] In S2, indicators related to dilated cardiomyopathy include:

[0057] Cardiac function grade, left ventricular end-diastolic anteroposterior diameter or left-right diameter, left ventricular ejection fraction, NT-proBNP, pulmonary artery pressure, blood potassium, blood creatinine, urea nitrogen, AST, ALT and blood pressure.

[0058] The measurement of blood creatinine includes the following specific steps:

[0059] Take 225 μL of mixed reagent A and add it to 6 μL of the patient's sample. After shaking evenly, incubate at a constant temperature of 37°C for 5 minutes. After reading the absorbance AO, add mixed reagent B. After shaking evenly, incubate at 37°C for 5 minutes. After reading the absorbance A1, calculate ΔA = A1-A0.

[0060] The components of mixed reagent A include creatinase, sarcosine oxidase, peroxidase, and N-ethyl-N-3-methylaniline, with final concentrations of 2000 U / L, 6000 U / L, 5000 U / L, and 0.4 mmol / L, respectively;

[0061] Components of the mixed reagent B include creatinase and 4-aminothiazine, with final concentrations of 250,000 U / L and 1.0 mmol / L, respectively.

[0062] The reference range of ΔA is 44-97umol / L for adult males and 35-80umol / L for adult females.

[0063] The measurement of urea nitrogen includes the following specific steps:

[0064] Take 2.5uL of the patient's sample, add 200uL of mixed reagent C, incubate at 37°C for 3-5 minutes, read the absorbance AO, and after incubation, add 100uL of mixed reagent D. After mixing, incubate at 37°C for 60 seconds, continuously monitor for 1-3 minutes, read the absorbance A1, and calculate ΔA = A1-A0;

[0065] The components of mixed reagent C include urease, glutamate dehydrogenase, adenosine diphosphate, and tris buffer, with final concentrations of 8000 U / L, 500 U / L, 1.5 mol / L, and 100 mmol / L, respectively;

[0066] The components of the mixed reagent D include reduced coenzyme I and α-ketoglutaric acid, with final concentrations of 0.3 mmol / L and 13.0 mmol / L, respectively.

[0067] The reference range of ΔA is 1.43-7.14 mmol / L.

[0068] The measurement of alanine aminotransferase involves the following specific steps:

[0069] Take 200 μL of mixed reagent E and add it to 15 μL of patient sample, shake evenly, incubate at 37°C for 3 minutes, read the absorbance AO, then add 100 μL of mixed reagent F and incubate at 37°C for 60 seconds. Monitor continuously for 1-3 minutes, read the absorbance A1, and calculate ΔA = A1-A0;

[0070] The reference range of ΔA is 9-50U / L for adult males and 7-40U / L for adult females.

[0071] The measurement of aspartate aminotransferase involves the following specific steps:

[0072] Take 200uL of mixed reagent G and add it to 15uL of patient sample, shake evenly, incubate at 37℃ for 3min, read the absorbance AO, then add 100uL of mixed reagent H and incubate at 37℃ for 60s. Monitor continuously for 1-3min, read the absorbance A1, and calculate ΔA=A1-A0;

[0073] The reference range for ΔA is 15-40 U / L for adult males and 13-35 U / L for adult females. NT-proBNP testing involves the following steps:

[0074] Turn on the immunofluorescence dry-well quantitative analyzer, return the test card and buffer to room temperature, pipette 75 μL of the patient sample into the buffer, mix thoroughly for 1 minute, then pipette 75 μL of the mixed solution into the sample well of the test card to complete the test. The reference range for NT-proBNP is <300 pg / ml for patients under 75 years of age and <450 pg / ml for patients 75 years of age or older.

[0075] Statistical analysis of the data in S2 and S3 in S4 included comparison of cardiac function classification, left ventricular end-diastolic anteroposterior or left-right diameter, left ventricular ejection fraction, NT-proBNP, pulmonary artery pressure, and adverse reactions, as well as comparison of sample rates using t-test, comparison of means using one-way analysis of variance, and pairwise comparison using the LSD method.

[0076] Example 1: This example analyzes the above evaluation method in detail based on specific circumstances:

[0077] S1: Cardiac function classification; assess the patient's cardiac function based on the standard cardiac function classification;

[0078] In this example, 195 patients admitted to the hospital for inpatient and outpatient treatment were selected and divided into a treatment group (110) and a control group (85) according to whether they could tolerate high-dose drug treatment. The treatment group had 81 males and 29 females with an average age of 54.31±14.28 years; 15 patients had grade II heart function, 74 had grade III heart function, and 21 had grade IV heart function. The control group had 52 males and 33 females with an average age of 56.35±11.83 years; 14 patients had grade II heart function, 60 had grade III heart function, and 11 had grade IV heart function.

[0079] Before intervention, there were no statistically significant differences in systolic blood pressure, diastolic blood pressure, New York Heart Association cardiac function class, blood potassium and blood creatinine levels, plasma brain natriuretic peptide level, left ventricular end-diastolic anteroposterior or left-right diameter, and left ventricular ejection fraction between the two groups (P>0.05), indicating that the two groups were comparable.

[0080] This application discloses the inclusion criteria in detail. According to the WHO / ISEC diagnostic criteria, patients diagnosed with dilated cardiomyopathy have the following characteristics:

[0081] ① Slow onset, but may worsen acutely, including manifestations of acute and chronic congestive heart failure;

[0082] ② Imaging examinations show leftward dilatation of the heart border or total enlargement of the heart, which may repeatedly induce various arrhythmias;

[0083] ③X-ray, CT, and myocardial radionuclide scanning showed enlargement of the cardiac border;

[0084] ④ Electrocardiogram or dynamic electrocardiogram shows arrhythmia;

[0085] ⑤ Echocardiography can clearly measure the extent of ventricular and atrial enlargement, accompanied by widespread weakening of ventricular wall motion and a left ventricular ejection fraction (EF) as low as 50 or less;

[0086] ⑥ Cardiac electromechanical examination shows a shortened left ventricular ejection time (LEVT) and a prolonged late ejection phase (PEP), which increases the PEP / LEVT ratio.

[0087] ⑦Exclude rheumatic, hypertensive, congenital, and coronary artery sclerosis heart diseases, etc.

[0088] The criteria for cure of patients excluded from this application include the following specific characteristics:

[0089] ① Patients with severe liver and kidney function damage;

[0090] ② The patient has a clear allergy to ACEI, ARB, beta-blockers, diuretics, digitalis, etc.

[0091] or contraindications;

[0092] ③Excluding intracranial tumors, aortic dissection, active bleeding risks, etc.;

[0093] ④ Those with malignant arrhythmia and no pacemaker installed or other related treatments.

[0094] In this example, the above indicators were measured for all patients before drug intervention. The control group patients were all unable to tolerate high-dose ARBs and / or low-dose ACEIs due to factors such as low blood pressure, severe liver and kidney damage, advanced age, and comorbidities with other systemic diseases, and therefore had to receive conventional clinical drug treatment or discontinue treatment. Both the treatment and control groups received routine basic treatment, including bed rest, low-flow oxygen inhalation, diuretics, and digitalis. The minimum initial dose of metoprolol succinate (AstraZeneca Pharmaceuticals Co., Ltd.) was 11.875 mg / d, taken orally. Depending on the patient's condition, the dose was increased by 23.75-47.5 mg / d every 1-2 weeks to a therapeutic dose of 47.5-95 mg / d. Alternatively, the minimum initial dose of bisoprolol fumarate (Merck KGaA, Darmstadt) was 2.5 mg / d, taken orally. Depending on the patient's condition, the dose was increased by 5-10 mg every 1-2 weeks to a therapeutic dose of 10-15 mg / d. The dose was adjusted based on changes in cardiac function. The patient's heart rate was observed to be around 60-70 beats / min, and the systolic blood pressure was monitored to be no less than 80 mmHg. If the condition progressed and the cardiac function reached grade 3-4, the dose was reduced or digoxin or other cardiotonic treatments were added. The treatment group regimen was formulated as benazepril hydrochloride (produced by Beijing Novartis Pharmaceutical Co., Ltd.) 5-10 mg / d or perindopril (produced by Servier (Tianjin) Pharmaceutical Co., Ltd.) 2-4 mg / d combined with irbesartan (Sanofi Winthrop Industrie) 300 mg-750 mg / night or valsartan (produced by Beijing Novartis Pharmaceutical Co., Ltd.) 160 mg-480 mg / night, with or without metoprolol succinate or bisoprolol fumarate. During follow-up visits, echocardiography was monitored and the anteroposterior or left-right diameter of the left ventricular end-diastolic diameter (LVEDD) was measured to adjust the dose of ACEI and ARB. The dose of metoprolol succinate or bisoprolol fumarate was gradually reduced or even discontinued according to the condition. Charts were made to record the patient's blood pressure, heart rate, and urine volume. If dizziness, lightheadedness, oliguria, or low blood pressure occurred, the patient could seek medical attention at any time.

[0095] S2: Observation of indicators: Collect the patient's plasma and monitor the patient's dilated cardiomyopathy-related indicators at each follow-up visit;

[0096] At each follow-up visit, the same team of color echocardiographers performed color echocardiography on the patients using an ultrasound diagnostic device to measure the internal diameter of the cardiac chambers, changes in myocardial stroke amplitude, and changes in ejection fraction, including LVEDD and LVEF before and after drug intervention. According to the American Society of Echocardiography's recommended standards, the patients were placed in the left lateral decubitus position, and LVEDD was measured on the left ventricular long axis. The LVEF was measured using the Simpsom method in patients with generalized ventricular wall motion disorders. The calculation method for LVEF is LVEF = (left ventricular end-diastolic volume - left ventricular end-systolic volume) / left ventricular end-diastolic volume.

[0097] The cardiac function classification standard adopts the American New York Heart Association cardiac function classification to assess the cardiac function of the selected patients: Grade 1: The patient has heart disease, but physical activity is not restricted. Grade 2: The patient has heart disease, so that physical activity is slightly restricted. Grade 3: The patient has heart disease, so that physical activity is significantly restricted. Grade 4: The patient has heart disease and has symptoms of heart failure or angina pectoris even at rest, and any physical activity will increase discomfort. Efficacy evaluation: ① Effective: Heart function is at level 2-3 after treatment; ② Significantly effective: Heart function improves by more than 2 levels; ③ Ineffective: Heart function has no obvious improvement before and after treatment or may even worsen.

[0098] The plasma collection method is as follows: routine blood collection, the patient is in a semi-recumbent position with an empty stomach, 2 ml of blood is drawn from the elbow vein, placed in an anticoagulant plastic tube, stored at room temperature, and sent for testing within 2 hours.

[0099] S3: Treatment follow-up: 4 regular follow-up visits are conducted every year to review the relevant indicators obtained in S2;

[0100] Both groups of patients were required to undergo four follow-up visits: one month, three months, six months, and one year after treatment. Changes in their condition could be monitored at irregular intervals during these visits. During the follow-up period, blood biochemistry parameters, NT-proBNP, and echocardiographic changes were required to be reviewed.

[0101] The evaluation criteria for adverse reactions are: observing whether the two groups of patients have adverse reactions such as decreased blood potassium, abnormal liver function, abnormal renal function and hypotension.

[0102] S4: Statistical processing: Statistical analysis of S2 and S3 data was completed based on SPSS, and the myocardial reversal effect of patients before and after treatment was evaluated.

[0103] Data were statistically analyzed using SPSS 16.0 software. Continuous data were expressed as mean ± standard deviation (SD). Cardiac functional class, left ventricular end-diastolic anteroposterior or left-right diameter, left ventricular ejection fraction, NT-proBNP, pulmonary artery pressure, and adverse reactions were recorded before treatment and at 1 month, 3 months, 6 months, and 1 year after treatment. Sample rates between two groups were compared using the t-test, and means between multiple groups were compared using one-way analysis of variance (ANOVA). Pairwise comparisons were performed using the LSD method. A P value of less than 0.05 was considered significant.

[0104] In summary, the final result obtained in this embodiment is:

[0105] Comparison of relevant indicators before treatment between the two groups of patients - As shown in Table 1, the difference in cardiac function classification between the treatment group and the control group before treatment was compared using a chi-square test. The results showed that there was no significant difference in cardiac function classification between the two groups before treatment.

[0106] Table 1 Comparison of cardiac function classification between the two groups before treatment

[0107]

[0108]

[0109] χ2=1.441, P=0.487

[0110] Left ventricular end-diastolic anteroposterior or left-right diameters - As shown in Table 2, there was no significant difference in the left ventricular end-diastolic anteroposterior or left-right diameters between the two groups of patients before treatment.

[0111] Table 2 Comparison of left ventricular end-diastolic diameter between the treatment group and the control group before treatment

[0112] Group Number of cases mean Standard deviation Standard error Treatment group 110 74.55 9.59 0.914 control group 85 72.27 7.47 0.810

[0113] t = -1.870, P = 0.063

[0114] Left ventricular ejection fraction. As shown in Table 3, there was no significant difference in left ventricular ejection fraction between the two groups before treatment.

[0115] Table 3 Comparison of left ventricular ejection fraction between the treatment group and the control group before treatment

[0116] Group Number of cases mean Standard deviation Standard error Treatment group 110 33.34 8.73 0.833 control group 85 33.88 9.60 1.041

[0117] t = 0.415, P = 679

[0118] Pulmonary Artery Pressure—As shown in Table 4, there was no significant difference in left pulmonary artery pressure between the two groups before treatment.

[0119] Table 4 Comparison of pulmonary artery pressure between the treatment group and the control group before treatment

[0120] Group Number of cases mean Standard deviation Standard error Treatment group 110 24.97 3.46 0.329 control group 85 25.62 3.14 0.341

[0121] t = 1.356, P = 0.177

[0122] Age.--As shown in Table 5, there was no significant difference in the age of the patients in the two groups before treatment.

[0123] Table 5 Comparison of age of patients in the treatment group and the control group

[0124] Group Number of cases mean Standard deviation Standard error Treatment group 110 54.31 14.28 1.362 control group 85 56.35 11.83 1.283

[0125] t = -1.090, P = 0.277

[0126] Blood Pressure—As shown in Table 6, there was no significant difference in systolic and diastolic blood pressure between the two groups before treatment.

[0127] Table 6 Comparison of blood pressure between the treatment group and the control group

[0128] Group Number of cases Systolic blood pressure (mmHg) Diastolic blood pressure (mmHg) Treatment group 110 120.86±20.76 70.14±9.47 control group 85 124.41±18.72 70.41±9.70 t 1.235 0.199 p <![CDATA[ 0 . 248 ]]> <![CDATA[ 0 . 842 ]]>

[0129] NT-proBNP - As shown in Table 7, there was no statistically significant difference in NT-proBNP between the two groups before treatment.

[0130] Table 7 Comparison of NT-proBNP in the treatment group and the control group

[0131] Group Number of cases Geometric mean Treatment group 110 393.24 control group 85 267.10

[0132] t = -1.680, P = 0.095

[0133] In summary, before treatment, the two groups of patients were comparable in terms of cardiac function grade, left ventricular end-diastolic anteroposterior diameter or left-right diameter, left ventricular ejection fraction, blood pressure, NT-proBNP and age (P>0.05).

[0134] Example 2: In view of the above test, this example combines the relevant indicators of dilated cardiomyopathy to evaluate the clinical efficacy, as shown in Table 8:

[0135] Table 8 Comparison of cardiac function classification between the treatment group and the control group one month after treatment

[0136]

[0137] χ2=6.326, P=0.097

[0138] As shown in Table 8, the cardiac function classification in the treatment group was as follows: 4 cases of grade I, an increase of 4 cases compared with before treatment; 41 cases of grade II, an increase of 26 cases compared with before treatment; 62 cases of grade III, a decrease of 12 cases compared with before treatment; and 3 cases of grade IV, a decrease of 18 cases compared with before treatment. The cardiac function classification in the control group was as follows: 3 cases of grade I, an increase of 3 cases compared with before treatment; 38 cases of grade II, an increase of 24 cases compared with before treatment; 36 cases of grade III, a decrease of 24 cases compared with before treatment; and 41 cases of grade IV, a decrease of 3 cases compared with before treatment.

[0139] After one month of treatment, the effective rates of cardiac function classification in the two groups were 40.91% and 48.24%, respectively, with no statistically significant difference (χ 2 =6.326, P=0.097>0.05), it can be considered that there was no significant difference in the cardiac function classification between the two groups one month after treatment.

[0140] Furthermore, this example compares the changes in cardiac function classification between the two groups after 3 months of treatment:

[0141] Table 9 Comparison of cardiac function classification between the treatment group and the control group 3 months after treatment

[0142]

[0143] χ2=56.451,P=0.000

[0144] As shown in Table 9, the cardiac function classification in the treatment group was as follows: 26 cases of Class I, an increase of 22 cases compared to one month after treatment; 77 cases of Class II, an increase of 36 cases compared to one month after treatment; 7 cases of Class III, a decrease of 55 cases compared to one month after treatment; and 3 cases of Class IV compared to one month after treatment. The cardiac function classification in the control group was as follows: 3 cases of Class I, no change compared to one month after treatment; 38 cases of Class II, no change compared to one month after treatment; 3 cases of Class III, a decrease of 3 cases; and 3 cases of Class IV compared to one month after treatment.

[0145] After 3 months of treatment, the effective rates of cardiac function classification in the two groups were 93.64% and 48.24%, respectively, with statistically significant differences (χ 2 =56.451, P=0.000<0.05), indicating that there was a significant difference in cardiac function classification between the two groups 3 months after treatment.

[0146] Furthermore, this example compares the changes in cardiac function classification between the two groups after 6 months of treatment:

[0147] Table 10 Comparison of cardiac function classification between the treatment group and the control group 6 months after treatment

[0148]

[0149] χ2=107.498, P=0.000

[0150] As shown in Table 10, the cardiac function classification of the treatment group was: 83 cases of grade I, an increase of 57 cases compared with 3 months after treatment.

[0151] There were 27 cases of grade II, a decrease of 50 cases compared with 3 months after treatment, and 7 cases of grade III compared with 3 months after treatment. The cardiac function classification of the control group was as follows: 3 cases of grade I, no change compared with 3 months after treatment, 60 cases of grade II, an increase of 22 cases compared with 3 months after treatment, 17 cases of grade III compared with 3 months after treatment, and 5 cases of grade IV compared with 3 months after treatment.

[0152] After 6 months of treatment, the effective rates of cardiac function classification in the two groups were 100.00% and 74.12%, respectively, with statistically significant differences (χ 2 =101.498, P=0.000<0.05), it can be considered that there was a significant difference in the cardiac function classification between the two groups 6 months after treatment.

[0153] Furthermore, this example compares the changes in cardiac function classification between the two groups after one year of treatment: Table 11 Comparison of cardiac function classification between the treatment group and the control group one year after treatment:

[0154]

[0155] χ2=147.051,P=0.000

[0156] As shown in Table 11, the cardiac function classification in the treatment group was as follows: 109 cases of Class I, an increase of 26 cases compared to 6 months after treatment; 1 case of Class II, a decrease of 26 cases compared to 6 months after treatment. The cardiac function classification in the control group was as follows: 12 cases of Class I, an increase of 9 cases compared to 6 months after treatment; 50 cases of Class II, a decrease of 10 cases compared to 6 months after treatment; and 23 cases of Class III, an increase of 1 case compared to 6 months after treatment.

[0157] After 1 year of treatment, the effective rates of cardiac function classification in the two groups were 100.00% and 75.29%, respectively, with statistically significant differences (χ 2 =147.051, P = 0.000 < 0.05), it can be considered that there was a significant difference in the cardiac function classification between the two groups one year after treatment

[0158] Furthermore, this example compares the changes in cardiac function classification between the two groups after treatment:

[0159] Table 12 Changes in the effective rate of cardiac function in the two groups after treatment:

[0160]

[0161]

[0162] And refer to the attached Figure 2 The changes in the effective rate of cardiac function remission in the two groups after treatment were found. The effective rate of cardiac function remission in the treatment group was higher than that in the control group starting from 3 months after treatment, and the effective rate of remission in the treatment group was 100.00% starting from 6 months after treatment.

[0163] The comparison of the anteroposterior or left-right diameters at the end of left diastole in the two groups is shown in the following table: Table 13 Changes of the anteroposterior or left-right diameters at the end of left diastole in the two groups before and after treatment:

[0164]

[0165] As shown in Table 13 and Figure 3 As shown, the average anteroposterior or left-right diameter of the left ventricular end-diastole before treatment was 74.55±9.59 in the treatment group and 72.27±7.47 in the control group. The test results showed that there was no statistical significance in the anteroposterior or left-right diameter of the left ventricular end-diastole between the two groups before treatment (P>0.05).

[0166] The AV or left-right end-diastolic diameters of the treatment group were 68.65±10.19, 64.87±10.02, 62.46±10.44, and 61.08±10.87 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. The differences in AV or left-right end-diastolic diameters among these four time periods were statistically significant (F=30.902, P=0.000<0.05). In the control group, the AV or left-right end-diastolic diameters were 69.68±7.46, 68.64±7.66, 68.27±7.42, and 66.69±7.51 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. The differences in AV or left-right end-diastolic diameters among these four time periods were statistically significant (F=6.450, P=0.000<0.05). One month after treatment, there was no statistically significant difference in the anteroposterior or left-right end-diastolic diameter between the two groups (P>0.05). Three months, six months, and one year after treatment, there was a statistically significant difference in the anteroposterior or left-right end-diastolic diameter between the two groups (P<0.05).

[0167] As shown in Table 14, the anteroposterior or left-right diameter of the left ventricular end-diastolic of the treatment group at 1 month, 3 months, 6 months and 1 year after treatment were statistically significant compared with those before treatment, the anteroposterior or left-right diameter of the left ventricular end-diastolic at 3 months, 6 months and 1 year after treatment were statistically significant compared with those at 1 month after treatment, the anteroposterior or left-right diameter of the left ventricular end-diastolic at 6 months after treatment was not statistically significant compared with that at 3 months after treatment, the anteroposterior or left-right diameter of the left ventricular end-diastolic at 1 year after treatment was statistically significant compared with that at 3 months after treatment, and the anteroposterior or left-right diameter of the left ventricular end-diastolic at 1 year after treatment was not statistically significant compared with that at 6 months after treatment.

[0168] As shown in Table 15, the anteroposterior or left-right diameter of the left ventricular end-diastole in the control group at 1 month, 3 months, 6 months and 1 year after treatment were statistically significant compared with those before treatment, the anteroposterior or left-right diameter of the left ventricular end-diastole at 3 months and 6 months after treatment were not statistically significant compared with those at 1 month after treatment, the anteroposterior or left-right diameter of the left ventricular end-diastole at 1 year after treatment was statistically significant compared with that at 1 month after treatment, the anteroposterior or left-right diameter of the left ventricular end-diastole at 6 months and 1 year after treatment were not statistically significant compared with those at 3 months after treatment, and the anteroposterior or left-right diameter of the left ventricular end-diastole at 1 year after treatment was not statistically significant compared with that at 6 months after treatment.

[0169] Table 14 Pairwise comparison of left ventricular end-diastolic anteroposterior diameter or left-right diameter in treatment groups

[0170]

[0171]

[0172] Table 15 Pairwise comparison of left ventricular end-diastolic anteroposterior diameter or left-right diameter in the control group

[0173] Classification Before treatment 1 month after treatment 3 months after treatment 6 months after treatment 1 year after treatment Before treatment 0.025 0.002 0.001 0.000 1 month after treatment - 0.367 0.221 0.010 3 months after treatment - - 0.748 0.091 6 months after treatment - - - 0.171 1 year after treatment - - - -

[0174] Please refer to Figure 3 , we can know the changes in the anteroposterior or left-right diameter of the left ventricle at end diastole in the two groups in the four stages after treatment.

[0175] Furthermore, this embodiment compares the left ventricular ejection fraction of the two groups:

[0176]

[0177]

[0178] As shown in Table 16 and Figure 4 As shown, the average left ventricular ejection fraction in the treatment group before treatment was 33.34±8.73, and the average left ventricular ejection fraction in the control group was 33.88±9.60. The test results showed that there was no statistically significant difference in the left ventricular ejection fraction between the two groups before treatment (P>0.05).

[0179] The left ventricular ejection fraction (LVEF) in the treatment group was 38.91±9.18, 41.31±10.06, 45.23±10.11, and 50.60±11.09 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. The differences in LVEF among these four time periods were statistically significant (F=47.822, P=0.000<0.05). The LVEF in the control group was 36.62±11.26, 38.24±10.74, 37.16±11.14, and 37.35±11.10 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. The differences in LVEF among these four time periods were not statistically significant (F=2.001, P=0.094>0.05). There was no statistically significant difference in left ventricular ejection fraction between the two groups at 1 month after treatment (P>0.05). However, there was a statistically significant difference in left ventricular ejection fraction between the two groups at 3 months, 6 months, and 1 year after treatment (P<0.05).

[0180] As shown in Table 17, the left ventricular ejection fraction of the treatment group at 1 month, 3 months, 6 months and 1 year after treatment was statistically significant compared with that before treatment, the left ventricular ejection fraction at 3 months after treatment was not statistically significant compared with that at 1 month after treatment, the left ventricular ejection fraction at 6 months and 1 year after treatment was statistically significant compared with that at 3 months after treatment, and the left ventricular ejection fraction at 1 year after treatment was statistically significant compared with that at 6 months after treatment.

[0181] As shown in Table 18, the left ventricular ejection fraction of the control group one month after treatment was not statistically significant compared with that before treatment, the left ventricular ejection fractions three months, six months and one year after treatment were statistically significant compared with those before treatment, the left ventricular ejection fractions three months, six months and one year after treatment were not statistically significant compared with that one month after treatment, the left ventricular ejection fractions six months and one year after treatment were not statistically significant compared with that three months after treatment, and the left ventricular ejection fraction one year after treatment was not statistically significant compared with that six months after treatment.

[0182] Table 17 Pairwise comparison of left ventricular ejection fraction in treatment groups

[0183] Classification Before treatment 1 month after treatment 3 months after treatment 6 months after treatment 1 year after treatment Before treatment 0.000 0.000 0.000 0.000 1 month after treatment - 0.072 0.000 0.000 3 months after treatment - - 0.003 0.000 6 months after treatment - - - 0.000 1 year after treatment - - - -

[0184] Table 18 Pairwise comparison of left ventricular ejection fraction in the control group

[0185]

[0186]

[0187] The left ventricular ejection fraction (LVEF) in the treatment group was 38.91±9.18, 41.31±10.06, 45.23±10.11, and 50.60±11.09 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. Significant differences were observed in these four time periods (F=47.822, P=0.000<0.05). In the control group, the LVEF was 36.62±11.26, 38.24±10.74, 37.16±11.14, and 37.35±11.10 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. No significant differences were observed in these four time periods (F=2.001, P=0.094>0.05). No significant differences were observed in LVEF between the two groups at 1 month after treatment.

[0188] Furthermore, this example compares two groups of NT-proBNP:

[0189] Table 19 Changes of NT-proBNP before and after treatment in the two groups

[0190]

[0191] As shown in Table 19, the average NT-proBNP before treatment was 393.24 in the treatment group and 267.10 in the control group. The test results showed that there was no statistical significance in the NT-proBNP between the two groups before treatment (P>0.05).

[0192] The NT-proBNP levels in the treatment group were 292.74, 357.49, 182.41, and 136.46 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. The differences in NT-proBNP across these four time periods were statistically significant (F = 10.411, P = 0.000 < 0.05). In the control group, the NT-proBNP levels were 267.10, 238.00, 153.79, 174.35, and 207.16 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. There was no statistically significant difference in NT-proBNP levels between the two groups at 1 month and 6 months after treatment (P > 0.05). However, there was a statistically significant difference in NT-proBNP levels between the two groups at 3 months and 1 year after treatment (P < 0.05).

[0193] As shown in Table 20, the NT-proBNP levels of the treatment group 1 month and 3 months after treatment were not statistically significant compared with those before treatment, the NT-proBNP levels of the treatment group 6 months and 1 year after treatment were statistically significant compared with those before treatment, the NT-proBNP levels 6 months and 1 year after treatment were statistically significant compared with those 1 month after treatment, the NT-proBNP levels 3 months after treatment were not statistically significant compared with those 1 month after treatment, the NT-proBNP levels 6 months and 1 year after treatment were statistically significant compared with those 3 months after treatment, and the NT-proBNP levels 1 year after treatment were not statistically significant compared with those 6 months after treatment.

[0194] As shown in Table 21, the NT-proBNP levels of the control group 1 month, 6 months, and 1 year after treatment were not statistically significant compared with those before treatment. The NT-proBNP levels of the treatment group 3 months after treatment were statistically significant compared with those before treatment, the NT-proBNP levels 6 months and 1 year after treatment were not statistically significant compared with those at 1 month after treatment, the NT-proBNP levels 3 months after treatment were statistically significant compared with those at 1 month after treatment, the NT-proBNP levels 6 months and 1 year after treatment were not statistically significant compared with those at 3 months after treatment, and the NT-proBNP levels 1 year after treatment were not statistically significant compared with those at 6 months after treatment.

[0195] Table 20 Pairwise comparison of NT-proBNP in treatment groups

[0196] Classification Before treatment 1 month after treatment 3 months after treatment 6 months after treatment 1 year after treatment Before treatment 0.138 0.632 0.000 0.000 1 month after treatment - 0.315 0.018 0.000 3 months after treatment - - 0.001 0.000 6 months after treatment - - - 0.145 1 year after treatment - - - -

[0197] Table 21 Pairwise comparison of NT-proBNP in the control group

[0198]

[0199] Furthermore, this embodiment compares the two groups of pulmonary artery pressures:

[0200] Table 22 Changes in pulmonary artery pressure before and after treatment in the two groups

[0201]

[0202]

[0203] As shown in Table 22, before treatment, the average pulmonary artery pressures of the treatment group and the control group were 24.97±3.46 and 25.62±3.14, respectively. The test results showed that there was no statistical significance in the pulmonary artery pressures of the two groups before treatment (P>0.05).

[0204] The pulmonary artery pressures in the treatment group were 25.42±4.52, 25.52±3.45, 24.16±2.92, and 24.50±2.82 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. The differences in pulmonary artery pressures among these four time periods were statistically significant (F=3.091, P=0.016<0.05). The pulmonary artery pressures in the control group were 25.11±3.11, 25.58±3.01, 25.06±2.96, and 26.94±2.56 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. The differences in pulmonary artery pressures among these four time periods were statistically significant (F=5.587, P=0.000<0.05). There was no statistically significant difference in pulmonary artery pressure levels between the two groups at 1 month and 3 months after treatment (P>0.05). However, there was a statistically significant difference in pulmonary artery pressure levels between the two groups at 6 months and 1 year after treatment (P<0.05).

[0205] As shown in Table 23, the pulmonary artery pressure of the treatment group 1 month, 3 months, 6 months and 1 year after treatment was not statistically significant compared with that before treatment, the pulmonary artery pressure 3 months and 1 year after treatment was statistically significant compared with that at 1 month after treatment, the pulmonary artery pressure 6 months after treatment was not statistically significant compared with that at 1 month after treatment, the pulmonary artery pressure 6 months after treatment was statistically significant compared with that at 3 months after treatment, the pulmonary artery pressure 1 year after treatment was not statistically significant compared with that at 3 months after treatment, and the pulmonary artery pressure 1 year after treatment was not statistically significant compared with that at 6 months after treatment.

[0206] As shown in Table 24, the pulmonary artery pressure of the control group at 1 month, 3 months, 6 months and 1 year after treatment was not statistically significant compared with that before treatment, the pulmonary artery pressure 1 year after treatment was statistically significant compared with that before treatment, the pulmonary artery pressure 3 months and 6 months after treatment was not statistically significant compared with that at 1 month after treatment, the pulmonary artery pressure 1 year after treatment was statistically significant compared with that at 1 month after treatment, the pulmonary artery pressure 6 months after treatment was not statistically significant compared with that at 3 months after treatment, the pulmonary artery pressure 1 year after treatment was statistically significant compared with that at 3 months after treatment, and the pulmonary artery pressure 1 year after treatment was statistically significant compared with that at 6 months after treatment.

[0207] Table 23 Pairwise comparison of pulmonary artery pressure in treatment groups

[0208] Classification Before treatment 1 month after treatment 3 months after treatment 6 months after treatment 1 year after treatment Before treatment - 0.339 0.243 0.085 0.318 1 month after treatment - - 0.832 0.008 0.051 3 months after treatment - - - 0.004 0.060 6 months after treatment - - - - 0.470 1 year after treatment - - - - -

[0209] Table 24 Pairwise comparison of pulmonary artery pressure in the control group

[0210]

[0211]

[0212] Therefore, based on the description in Example 1 and Example 2, the present application uses a low-dose angiotensin-converting enzyme inhibitor (ACEI) combined with a high-dose angiotensin II receptor (ARB) and a beta-blocker to treat dilated cardiomyopathy, and compares the effects of the two treatments on cardiac function classification, left ventricular end-diastolic diameter, left ventricular ejection fraction, NT-proBNP and pulmonary artery pressure, as well as adverse reactions;

[0213] The method used was the same as that disclosed in this application. Patients were divided into two groups based on their ability to tolerate high-dose drug therapy. The treatment group (110 patients) received a low-dose ACEI combined with a high-dose ARB and conventional treatment for DCM, while the control group received a beta-blocker and conventional treatment for DCM. Cardiac function classification, left ventricular end-diastolic anteroposterior or left-right diameter, left ventricular ejection fraction, NT-proBNP, pulmonary artery pressure, serum potassium, serum creatinine, blood urea nitrogen, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and blood pressure were recorded before treatment and one month, three months, six months, and one year after treatment.

[0214] The results showed that there were no statistically significant differences in cardiac function classification, left ventricular end-diastolic diameter, left ventricular ejection fraction, blood pressure, NT-proBNP, and age between the treatment group and the control group before treatment (P>0.05).

[0215] The treatment group achieved a cardiac function remission rate of 40.91%, 93.64%, 100.00%, and 100.00% at one month, three months, six months, and one year after treatment. The control group achieved a cardiac function remission rate of 48.24%, 48.24%, 74.12%, and 75.29% at one month, three months, six months, and one year after treatment. Except for one month after treatment, the cardiac function remission rate in both groups remained statistically significant.

[0216] The AV or left-right end-diastolic diameters of the treatment group were 68.65±10.19, 64.87±10.02, 62.46±10.44, and 61.08±10.87 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. The differences in AV or left-right end-diastolic diameters among these four time periods were statistically significant (F=30.902, P=0.000<0.05). In the control group, the AV or left-right end-diastolic diameters were 69.68±7.46, 68.64±7.66, 68.27±7.42, and 66.69±7.51 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. The differences in AV or left-right end-diastolic diameters among these four time periods were statistically significant (F=6.450, P=0.000<0.05). One month after treatment, there was no statistically significant difference in the anteroposterior or left-right end-diastolic diameter between the two groups (P>0.05). Three months, six months, and one year after treatment, there was a statistically significant difference in the anteroposterior or left-right end-diastolic diameter between the two groups (P<0.05).

[0217] The left ventricular ejection fraction (LVEF) in the treatment group was 38.91±9.18, 41.31±10.06, 45.23±10.11, and 50.60±11.09 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. The differences in LVEF among these four time periods were statistically significant (F=47.822, P=0.000<0.05). The LVEF in the control group was 36.62±11.26, 38.24±10.74, 37.16±11.14, and 37.35±11.10 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. The differences in LVEF among these four time periods were not statistically significant (F=2.001, P=0.094>0.05). There was no statistically significant difference in left ventricular ejection fraction between the two groups at 1 month after treatment (P>0.05). However, there was a statistically significant difference in left ventricular ejection fraction between the two groups at 3 months, 6 months, and 1 year after treatment (P<0.05).

[0218] The NT-proBNP levels in the treatment group were 292.74, 357.49, 182.41, and 136.46 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. The differences in NT-proBNP across these four time periods were statistically significant (F = 10.411, P = 0.000 < 0.05). In the control group, NT-proBNP levels were 267.10, 238.00, 153.79, 174.35, and 207.16 at 1 month, 3 months, 6 months, and 1 year after treatment, respectively. There was no statistically significant difference in NT-proBNP levels across these four time periods (F = 2.185, P = 0.070 > 0.05). Statistically significant differences in NT-proBNP levels between the two groups were observed at 3 months and 1 year after treatment (P < 0.05).

[0219] It should be noted that, in this document, relational terms such as first and second, etc., are used only to distinguish one entity or operation from another entity or operation, and do not necessarily require or imply any actual relationship or order between these entities or operations. Moreover, the terms "comprises," "comprising," or any other variations thereof are intended to cover non-exclusive inclusion, such that a process, method, article, or apparatus that includes a list of elements includes not only those elements but also other elements not explicitly listed, or elements inherent to such process, method, article, or apparatus.

[0220] While embodiments of the present invention have been shown and described, it will be appreciated by those skilled in the art that various changes, modifications, substitutions, and variations may be made to these embodiments without departing from the principles and spirit of the invention, and that the scope of the invention is defined by the appended claims and their equivalents.

Claims

1. A method for evaluating myocardial reversal in patients with dilated cardiomyopathy, characterized in that: The evaluation method comprises the following specific steps: S1: Cardiac function classification; assess the patient's cardiac function based on the standard cardiac function classification; S2: Observation of indicators: Collect the patient's plasma and monitor the patient's dilated cardiomyopathy-related indicators at each follow-up visit; S3: Treatment follow-up: 4 regular follow-up visits are conducted every year to review the relevant indicators obtained in S2; S4: Statistical processing: Statistical analysis of S2 and S3 data was completed based on SPSS, and the myocardial reversal effect of patients before and after treatment was evaluated.

2. A method for evaluating myocardial reversal for patients with dilated cardiomyopathy according to claim 1, characterized in that: In S1, the grading assessment includes the following specific settings: Grade 1: Patients have heart disease but are not restricted in physical activity; Level 2: The patient has heart disease, which results in slight limitation of physical activity; Level 3: The patient has heart disease, which significantly limits physical activity; Level 4: The patient has heart disease and has symptoms of heart failure or angina pectoris even at rest. Any physical activity will increase the discomfort.

3. A method for evaluating myocardial reversal for patients with dilated cardiomyopathy according to claim 1, characterized in that: In S2, the related indicators of dilated cardiomyopathy include: Cardiac function grade, left ventricular end-diastolic anteroposterior diameter or left-right diameter, left ventricular ejection fraction, NT-proBNP, pulmonary artery pressure, blood potassium, blood creatinine, urea nitrogen, AST, ALT and blood pressure.

4. A method for evaluating myocardial reversal for patients with dilated cardiomyopathy according to claim 3, characterized in that: The measurement of blood creatinine includes the following specific steps: Take 225 μL of mixed reagent A and add it to 6 μL of the patient's sample. After shaking evenly, incubate at a constant temperature of 37°C for 5 minutes. After reading the absorbance AO, add mixed reagent B. After shaking evenly, incubate at 37°C for 5 minutes. After reading the absorbance A1, calculate ΔA = A1-A0. The components of mixed reagent A include creatinase, sarcosine oxidase, peroxidase, and N-ethyl-N-3-methylaniline, with final concentrations of 2000 U / L, 6000 U / L, 5000 U / L, and 0.4 mmol / L, respectively; Component B of the mixed reagent includes creatinase and 4-aminothiazine, with final concentrations of 250,000 U / L and 1.0 mmol / L, respectively.

5. A method for evaluating myocardial reversal for patients with dilated cardiomyopathy according to claim 3, characterized in that: The measurement of urea nitrogen includes the following specific steps: Take 2.5uL of the patient's sample, add 200uL of mixed reagent C, incubate at 37°C for 3-5 minutes, read the absorbance AO, and after incubation, add 100uL of mixed reagent D. After mixing, incubate at 37°C for 60 seconds, continuously monitor for 1-3 minutes, read the absorbance A1, and calculate ΔA = A1-A0; The components of the mixed reagent C include urease, glutamate dehydrogenase, adenosine diphosphate, and tris-hydroxymethylaminomethane buffer, with final concentrations of 8000 U / L, 500 U / L, 1.5 mol / L, and 100 mmol / L, respectively; The components of the mixed reagent D include reduced coenzyme I and α-ketoglutaric acid, with final concentrations of 0.3 mmol / L and 13.0 mmol / L, respectively.

6. A method for evaluating myocardial reversal for patients with dilated cardiomyopathy according to claim 3, characterized in that: The measurement of alanine aminotransferase involves the following specific steps: Take 200uL of mixed reagent E and add it to 15uL of patient sample, shake evenly, incubate at 37℃ for 3min, read the absorbance AO, then add 100uL of mixed reagent F, incubate at 37℃ for 60s, continuously monitor for 1-3min, read the absorbance A1, and calculate ΔA=A1-A0.

7. A method for evaluating myocardial reversal for patients with dilated cardiomyopathy according to claim 3, characterized in that: The measurement of aspartate aminotransferase involves the following specific steps: Take 200uL of mixed reagent G and add it to 15uL of patient sample, shake evenly, incubate at 37℃ for 3min, read the absorbance AO, then add 100uL of mixed reagent H, incubate at 37℃ for 60s, continuously monitor for 1-3min, read the absorbance A1, and calculate ΔA=A1-A0.

8. A method for evaluating myocardial reversal for patients with dilated cardiomyopathy according to claim 3, characterized in that: The detection of NT-proBNP includes the following specific steps: Turn on the immunofluorescence dry quantitative detector, restore the test card and buffer to room temperature, draw 75uL of patient sample into the buffer, mix thoroughly for 1 minute, draw 75uL from the mixed solution and add it into the sample well of the test card to complete the test. The reference range of NT-proBNP includes: <300pg / ml for patients under 75 years old, and <450pg / ml for patients 75 years old or older.

9. A method for evaluating myocardial reversal for patients with dilated cardiomyopathy according to claim 1, characterized in that: The statistical analysis of the S2 and S3 data in S4 included comparison of cardiac function classification, left ventricular end-diastolic anteroposterior diameter or left-right diameter, left ventricular ejection fraction, NT-proBNP, pulmonary artery pressure and adverse reactions, as well as comparison of sample rates using t-test, comparison of means using one-way analysis of variance, and pairwise comparison using LSD method.

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