Antimyocardial Antibodies Research Articles

Immune reactions in infective endocarditis I. Clinical data and diagnostic relevance of antimyocardial antibodies

Clinical data from 72 patients with infective endocarditis (41 with defined pathogen, 31 with no pathogen isolated) were analyzed with respect to the diagnostic relevance of immunologic parameters. In our patients from a rural area, no significant changes in the epidemiology and pathogenesis of infective endocarditis were observed. Antiendocardial and antisarcolemmal (ASA) antibodies were demonstrated in 60% to 100% of cases. Their frequency depended on the endocarditic pathogen and on the clinical course: in subacute or chronic endocarditis these antibodies were found regularly, in acute lethal cases their occurrence was diminished. Whereas antiendocardial antibodies are diagnostic markers of endocarditis, ASA and antimyolemmal antibodies in particular most likely indicate myocardial involvement in endocarditis. Only complement fixing antimyolemmal antibodies induced cytolysis of vital, adult, heterologous cardiac cells. Our data suggest that antibody-mediated cytolysis in vitro may also play a pathogenetic role in vivo.

Immune reactions in tuberculous and chronic constrictive pericarditis: Clinical data and diagnostic significance of antimyocardial antibodies

Humoral immune reactions were analyzed in 12 patients with exudative tuberculous pericarditis, 10 patients with constrictive pericarditis due to former tuberculosis, 10 patients with viral pericarditis, 20 patients with pulmonary tuberculosis and 98 healthy donors. Pericarditis occurred in 12.5% of the patients with tuberculosis, whereas the incidence of tuberculosis in the 149 patients with pericarditis was 8%. Repeated pericardial puncture and pericardial effusions of greater than 500 ml with impending cardiac tamponade had to be performed in 4 patients. Clinical data indicated probable myocardial involvement in 4 of 12 patients. Antimyolemmal antibodies, which are a muscle-specific subtype of antisarcolemmal antibodies, were found in all patients with exudative tuberculous pericarditis and viral perimyocarditis, in only 1 of 12 patients with constrictive pericarditis and in no patient with pulmonary tuberculosis. Antifibrillary antibodies—primarily of the antimyosin type—were missed in patients with viral heart disease but were demonstrated in 75% of patients with tuberculous pericarditis. Only sera with complement-fixing antimyolemmal antibodies of the IgG type in liters greater than 1:40 induced cytolysis of vital adult heterologous cardiocytes isolated and enriched by silica sol gradient centrifugation. These findings suggest not only that antimyolemmal antibodies are diagnostic indicators of perimyocardial involvement in tuberculous pericarditis, but also that they may play a significant role in its pathogenesis.

Correlation of myocardial deposition of immunoglobulin with circulating antimyocardial antibodies in patients with heart failure

Correlation of myocardial deposition of immunoglobulin with circulating antimyocardial antibodies in patients with heart failure

Reactivity of antistreptococcus hyperimmune sera with human myocardial tissue

Antimyocardial antibodies were determined in hyperimmune rabbit sera against group A streptococci. The detection method was indirect immunofluorescence in human myocardial tissue sections. Positively reacting sera were absorbed with group A streptococcus cell walls and cytoplasmic membranes, the objective being to locate the cross-reacting antigen in the streptococcus cell under the given experimental conditions. Cell walls gave the better absorption results. Whether or not the streptococci possessed the Fc-reacting factor was without influence on the absorption result.

Interaction in vitro between Myocardial Cells and Autologous Lymphocytes and Sera from Patients with Rheumatic Carditis

The cytotoxicity of antimyocardial antibodies and peripheral blood lymphocytes from patients with rheumatic carditis on autologous myocardial cells was investigated. Although sera obtained after open-heart surgery from seven out of eight patients with rheumatic carditis were bound to cultures of autologous myocardial cells, they were not cytotoxic. Peripheral blood leukocytes obtained both before and after surgery from one of these eight patients aggregated around and underwent blast transformation when exposed to autologous myocardial cells in vitro, but not after exposure to autologous skin fibroblasts. Only the postoperative leukocytes from another of these eight patients aggregated around autologous myocardial cells in vitro; however, these lymphocytes were also not cytotoxic to autologous myocardium. To investigate the effect of antimyocardial antibodies on myocardial function, antimyocardial antibodies were added to the culture medium of pulsating cultures of mouse myocardial explants. Although antimyocardial antibody from 27 patients with chronic rheumatic carditis and seven postcardiotomy patients had no effect on the pulsation of the mouse myocardial cultures, serum gamma-globulin from a patient suffering from acute rheumatic fever with myocardial involvement first accelerated and then gradually stopped the pulsation of mouse myocardial explants.

Anti-myocardial antibodies in chronic cor pulmonale; its relation to prognosis

Anti-myocardial antibodies in chronic cor pulmonale; its relation to prognosis

Immunofluorescence Method for Detecting Anti-Myocardial Antibodies, and Its Use in Diagnosing Heart Disease

Demonstration of autoimmune antibodies to myocardial tissue enables one to detect and assess cardiac disease long after abnormalities in serum enzyme activities are no longer measurable. We describe and indirect immunofluorescence procedure in which cryostat sections of rat heart (ventricle) and Evan's Blue counterstaining are used to detect anti-myocardial antibodies. Sena from patients with myocardial infarct or some other cardiac diseases reveal a distinct fluorescent staining of the sarcolemmal membrane. In contrast, sera from patients with systemic lupus erythematosis demonstrate nuclear plus diffuse staining and sera from myasthenia gravis patients show a characteristic striated staining pattern. The role of anti-myocardial antibodies in cardiac disease is discussed briefly.

Antimyocardial antibodies in patients with coronary heart disease

Clinical and monitored data were collected from 173 patients admitted to a Medical Intensive Care Unit for suspected acute myocardial infarction. Infarction was proven in 117, and 56 had coronary insufficiency. Sera obtained on the first, fifth, and fourteenth days of hospitalization were tested for antimyocardial antibodies by the indirect fluorescent antibody and antiglobulin consumption methods. Fifty of the 117 patients with infarcts and 28 of 56 with coronary insufficiency had antibodies. None was found in 11 of 13 patients with non-coronary heart disease and in 15 normal controls. Antimyocardial antibodies were identified in patients with coronary disease whether they had acute myocardial infarction or not. This finding indicates that myocardial damage often accompanies non-infarctive myocardial ischemia. The detection of antimyocardial antibodies in patients without overt evidence of infarction may, therefore, aid in the diagnosis of coronary insufficiency. While antibodies to components of heart muscle are not specific for coronary disease, other conditions in which they occur are relatively rare and can usually be excluded on clinical grounds. Finally, our studies show that many patients with coronary disease already have antimyocardial antibodies in their serum when they arrive at the hospital. Subclinical myocardial damage may thus precede the onset of symptoms. Periodic tests for antimyocardial antibodies could reveal these prodromal events and indicate the need for therapeutic intervention.