As early as 1937, when studying rheumatic fever, Brokman et al. used heart tissue extracts extracted from saline as antigens to establish a complement-binding assay, and anti-myocardial antibodies were detected in 82% of patients with rheumatic fever. For more than 60 years, research in this area has been uninterrupted. In addition to the classical indirect immunofluorescence test (using human and rat heart tissue as antigenic tablets), colloidal particle agglutination test and anti-ball have been used. Protein consumption test, citrate-treated or hydroformylated erythrocyte agglutination test, and ELISA method and immunoblotting technique adopted in recent years, etc., but since the antigenic component of myocardial tissue is very complicated, the corresponding autoantibodies are also diverse. Previous studies have used four methods: (1) antiserum obtained by immunizing animals with human heart or skeletal muscle tissue extract; (2) immunization of rabbit antiserum with group A streptococcus; (3) rheumatic heart Patients, patients after streptococcal infection, patients after cardiac surgery, serum of patients with myocardial infarction syndrome; (4) study of connective tissue disease (such as polymyositis) patients and sera of patients with myasthenia gravis. turn out. Immunization of antibodies obtained from rabbits with myocardial infusion or group A streptococcal cell wall can cause three immunofluorescence patterns: 1 staining of peripheralsarcoplasmic/sarcolemmal; 2 between myocardium or skeletal muscle myofibrils (intermyofibrillar) staining; 3 less common smooth muscle staining fluorescence. Serum of patients with connective tissue disease (rheumatoid arthritis, systemic lupus erythematosus) and liver disease (primary biliary cirrhosis) can produce diffuse myofibrillar immunofluorescence of myocardium and skeletal muscle, serum of myasthenia gravis patients The skeletal muscle transverse stripes (A band) can be stained with fluorescence. Anti-linear granule antibodies in the serum of patients with primary biliary cirrhosis can also cause strong myofibrillar fluorescence in the myocardium. The above studies indicate that the anti-myocardial antibodies tested in the past lack tissue specificity and disease specificity. In the early 1990s, myocardial cell membrane antigen was extracted from rat myocardium, and immunoblotting technique was used to confirm that anti-cardiac antibodies in serum of patients with viral myocarditis and dilated cardiomyopathy can interact with calcium channel polypeptide and β1 in cardiomyocyte membrane antigen. - Adrenergic receptor response. In 1989, Schulze et al reported that autoantibodies against the myocardial mitochondrial ADP/ATP vector (adenine nucleotide translocator, ANT) were present in the serum of patients with dilated cardiomyopathy. ANT is a protein of the mitochondrial inner membrane that functions to transport ATP to the cytoplasm and to transfer ADP to the mitochondria for rephosphorylation. Anti-ANT antibodies can affect ANT function, making myocardial cell energy supply and demand balance imbalance. Recently, some people in the country have used immunoblotting to find that about 1/4 of children with viral myocarditis have anti-ANT antibodies.

Basic Information

Specialist classification: cardiovascular examination classification: blood examination

Applicable gender: whether men and women apply fasting: fasting

Analysis results:

Below normal:

Normal value:
no

Above normal:

negative:
normal.

Positive:
The prompt is abnormal.

Tips: Do not eat too greasy, high-protein foods the day before the blood draw, avoid heavy drinking. The alcohol content in the blood directly affects the test results. Normal value

Normal people are negative.

Clinical significance

Since the antigen is not purified, the non-specific reaction of the method is high. The anti-myocardial antibodies measured by indirect immunofluorescence are mainly found in active rheumatic fever (positive rate 40% to 80%) and rheumatic heart disease (positive rate 15% to 60%). %), bacterial endocarditis (83%), heart surgery (60% to 100%), myocardial infarction (65%), systemic lupus erythematosus (35%), rheumatoid arthritis (33%) Hyperthyroidism (29%), acute hepatitis (36%), and chronic hepatitis (43%). The anti-porcine cardiomyocyte membrane antibody was determined by immunoblotting. The positive rate of anti-52kD antibody was 57%, anti-87kD antibody 33%, anti-59kD antibody 24%, coronary heart disease, rheumatic heart disease, normal people were negative. . Since these target antigens are involved in calcium channel-gated (52 kD polypeptide), β1-receptor (59 kD polypeptide), they may cause cell death by increasing the permeability of cardiomyocyte membranes to Ca2+ and intracellular calcium overload. It may also directly inhibit myocardial β1-receptor and isoproterenol-stimulated adenylate cyclase activity, reduce myocardial reactivity to β-agonist positive inotropic effects, limit myocardial muscle reserve, and damage myocardial Features. Anti-ANT (adenine nucleic acid translocation enzyme) antibodies are also found in children with viral myocarditis, in addition to dilated cardiomyopathy.

Positive results may be disease: cardiac myxoma, pericarditis after myocardial infarction, dilated cardiomyopathy, left atrial malignant myxoma, pediatric Caschin-Beck disease, pediatric Keshan disease, neonatal myocarditis considerations

Taboo before the test: Do not eat too greasy, high-protein food the day before the blood draw, avoid heavy drinking. The alcohol content in the blood directly affects the test results.

Attention to check: After the blood draw, symptoms such as dizziness, vertigo, fatigue, etc. should be immediately supine, drink a small amount of syrup, and then undergo a physical examination after the symptoms are relieved.

Inspection process

Inspection method: indirect immunofluorescence:

Fluorescein is labeled on the corresponding antibody and reacts directly with the corresponding antigen.

In the first step, an unknown unlabeled antibody (sample to be tested) is added to a known antigen sample, and incubated at 37 ° C for 30 min in a wet box to sufficiently bind the antigen antibody, followed by washing to remove unbound antibody.

In the second step, a fluorescently labeled anti-globulin antibody or an anti-IgG, IgM antibody is added. If an antigen-antibody reaction occurs in the first step, the labeled anti-globulin antibody will further bind to the antigen-bound antibody, thereby identifying an unknown antibody.

Not suitable for the crowd

Not suitable for the crowd: generally no special population.

Adverse reactions and risks

No special complications.