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Biomedical subjects

B Maisch

Publications and source records attributed to B Maisch.

At least 289 records · Page 16Linked to original sources
PubMed1986

Antibodies to human sinus node in sick sinus syndrome.

The incidence of autoantibodies against human conducting tissue was studied in 45 pacemaker patients with sick sinus syndrome (SSS), in 17 patients with bradyarrhythmia, and five patients with hypersensitive carotid sinus syndrome. Antibodies against the human sinus node were demonstrated in 29% of patients with SSS and in 24% of patients with bradyarrhythmia; a tenfold risk of SSS could be calculated in patients with this antibody as compared to age-matched controls. At least two subtypes of anti-sinus node antibodies were demonstrated: an antibody absorbable and another one not absorbable with ventricular myocardium. Patients with SSS and prior myocarditis of rheumatic fever have a threefold incidence of that antibody, demonstrating that anti-conducting tissue antibodies are etiologic indicators for former inflammatory heart disease. These antibodies may play a role in the secondary immunopathogenesis of sick sinus syndrome. This hypothesis emerges as an interesting new pathogenetic concept.

Aged↗
PubMed1986

[Clinical experiences with 3 different rate-adaptive pacemaker systems].

Physiological stimulation can be achieved by either bifocal or rate responsive pacing. The latter pacemakers adapt the heart rate to physical activity by biological signals. Of many possible approaches only three pacemaker systems for rate responsive pacing are available: the QT pacemaker (Tx or Quintech), the respiratory Biorate pacemaker and the activity detecting Activitrax. First our own experiences (8 QT, 6 Biorate, 8 Activitrax pacemakers) and a survey of 95 QT- and 37 Biorate pacemakers from 11 centers are reported. The Biorate pacemaker functions without any problems, its present disadvantage is limited programmability. With the Tx pacemaker failing frequency adaptation (26%) was found more often in the early series, mostly due to voltage polarisation at the tip of the electrode. The Activitrax pacemaker gives satisfactory frequency adaptation, largely depending on the activity of the muscles of the shoulder and pectoral region.

Adult↗
PubMed1985

Surface antigens of adult heart cells and their use in diagnosis.

The mapping of immunologically relevant epitopes of the myolemma, sarcolemma and endothelium are prerequisites for the analysis of humoral and cellular effector mechanisms. Mapping was carried out by monospecific anticollagen and anticytoskeleton antibodies, monoclonal antibodies against the surface of white blood cells and by lectins which bind to specific sugars on membranes. Characteristic differences between myolemma, sarcolemma and endothelium could be defined. In patients with perimyocarditis and postmyocarditic cardiomyopathy antibodies directed against the myolemma were detected. They are cytolytic in the presence of complement and cross-reactive to the causative viral agents. Furthermore lymphocytotoxic effector mechanisms could be demonstrated in vitro in one third of patients with AMLA-negative primary dilated cardiomyopathy.

Animals↗
PubMed1985

Cardiomyopathy and myocarditis--a review of new aspects in research in West Germany.

New aspects in the research of myocarditis and dilated cardiomyopathy in West Germany have evolved from molecular biology, immunobiology of the mitochondrion, immunoserology, and immunohistology. Coxsackie B3 virus inoculated into fetal human myocytes induced myocytolysis in the absence of immunologic effector mechanisms. By pretreatment with beta-interferon, the virus yield from the myocytes was reduced significantly. In myocarditis and dilated cardiomyopathy, antibodies against an organ-specific autoantigen of cardiac mitochondria, the adenine nucleotide translocator, were demonstrated. Antibody titers roughly correlated with the ejection fraction using the Elisa technique. It could also be shown that in 13% of cases in myocarditis and 31% in dilated cardiomyopathy heart-associated antimitochondrial antibodies are found, called anti-M7. Most of the patients had an interfibrillary staining pattern in the immunofluorescence test. No correlation with the severity of heart disease could be established. In dilated cardiomyopathy and myocarditis, there has recently been controversy over low suppressor T-cell activity. Whereas other groups have demonstrated a low concanavaldin-A-induced suppressor T-cell activity in both diseases, we have not been able to confirm reduced Con-A-induced or spontaneous T-suppressor cell activity in the different indicator systems used in analysis.

Animals↗
PubMed1985

Four years of experience in endomyocardial biopsy--an immunohistologic approach.

Left ventricular biopsies from 376 patients (including 78 patients undergoing bypass surgery) were analyzed by light microscopy (necrosis, infiltration with or without fibrosis) and by immunohistology (bound antibodies). Circulating antisarcolemmal antibodies (ASA) were determined at the time of biopsy using a double-sandwich technique. Circulating antimyolemmal antibodies were assessed in intact rat and human cardiocytes. Histologic findings, heart catheterization, and echocardiography together with the patient's history established the diagnosis of perimyocarditis, myocarditis, postmyocarditic dilated cardiomyopathy, healed myocarditis, and healed perimyocarditis. Both bound and circulating ASA were found in up to 100% of cases in acute inflammatory heart disease and postmyocarditic cardiomyopathy, indicating a secondary immunopathogenesis of the myocardial disease. Analysis of immunoglobulin subclasses revealed: IgG-binding does not discriminate between acute/healing/healed carditis and postmyocarditic dilated heart disease (61.1%-91.7% positive); IgM binding is diagnostic for acute or healing perimyocarditis but has a relatively low incidence (33.3%); IgA binding occurs in acute or healing myocarditis (45.5%), perimyocarditis (33.3%), and in postmyocarditic heart disease (39.4%), but not in controls; complement fixation was never seen in controls, but was seen in acute myocarditis (45.4%), perimyocarditis (25%), and postmyocarditic heart disease (46%). Pretreatment of cryostat sections with collagenase to avoid "nonspecific" binding of antibodies to collagen considerably reduced the sensitivity but increased the specificity. Thus, endomyocardial biopsy proved a safe and valuable method for the further analysis of patients with carditis and myocardial disease of unknown origin.

Acute Disease↗
PubMed1985

Immunologic regulator and effector mechanisms in myocarditis and perimyocarditis.

The diagnosis and etiology of myocarditis and perimyocarditis are often difficult to ascertain. We therefore investigated regulator and humoral and cellular effector mechanisms in patients with viral heart disease (Coxsackie B3, influenza, EBV, mumps). In acute carditis, OKIA1-positive cells were increased and no significant alteration in suppressor cell activity was observed in our patients in contrast to others reports. The characteristic immunofluorescent pattern is the presence of antimyolemmal antibodies (AMLA) with rat and human collagenase-pretreated intact cardiocytes (in titers of 1:40-1:320) as antigens. The pattern is indistinguishable on cardiocytes from antibodies against cytoskeletal antigens (microtubules, intermediate filaments--tubulin/vemitin) when associated with antibodies directed against the Z-bands. In contrast, only anti-interfibrillary antibodies are present in cytomegalovirus myocarditis. The antimyolemmal fluorescence can be absorbed with the respective causative virus, indicating that the antibodies are cross-reactive. AMLA-positive sera induce cytolysis of vital rat cardiocytes in vitro, indicating that the antibodies are of pathogenetic relevance. Cytolytic serum activity could be absorbed out with the respective virus. Immunohistologic specimens obtained from patients with carditis demonstrate the fixation of IgG-type antibodies to the sarcolemma that also fix complement. In the acute phase of carditis, circulating immune complexes were also measured, thus monitoring immunoreactivity. Cellular effector mechanisms against vital cardiocytes were maintained or even slightly enhanced; in vitro NK-cell activity against K 562, however, was decreased. This is compatible with a more target-specific cytotoxicity in carditis but reduced NK-cell activity in peripheral blood cells.

Acute Disease↗
PubMed1985

Extraction of a chronically infected endocardial screw-in pacemaker lead by pigtail catheter and wire loop via the femoral vein.

A 71-year-old woman was admitted after partial removal of an infected pacemaker system. Septicemia and subclavian vein thrombosis were present. With combined use of a pigtail catheter and a wire loop originally developed for endoscopic polypectomy, the infected catheter was pulled into the inferior vena cava. Counterclockwise rotation of the pigtail catheter following its fixation to the electrode by the wire loop allowed removal of the tip of the endocardial screw-in electrode from the myocardium and its extraction. Open heart surgery was avoided and the source of chronic infection was removed.

Aged↗
PubMed1985

Immunological cellular regulator and effector mechanisms in myocarditis.

The diagnosis, pathogenesis and etiology of myocarditis are often difficult to establish with certainty. Consequently, we investigated cellular regulator and effector mechanisms in patients with viral heart disease (Coxsackie B3, influenza, EBV, mumps) as well as other inflammatory heart diseases which could not be classified etiologically. In acute myocarditis there was an elevation of B- and activated T-lymphocytes (OKIa 1-positive) but, in contrast, no significant changes in the activity of peripheral suppressor T-cells (OKT 8-positive). The activity of cell-specific lymphocytic effector mechanisms against vital cardiocytes was unchanged or slightly elevated in myocarditis, while the activity of the less target cell specific natural killer cells, which were measured in vitro against K562 tumor cells, was diminished. These findings are indicative of increased activity of target specific cytotoxic effector mechanisms and a reduction in the activity of nonspecific cellular effector mechanisms in peripheral blood.

Animals↗
PubMed1985

[Humoral and cellular immunity in perimyocarditis and congestive cardiomyopathy].

In coxsackie B-, influenza and mumps-induced perimyocarditis the characteristic immunological features were cross-reacting cytolytic antimyolemmal antibodies, circulating immune complexes and no NK- or K-cell activity. Cytolytic antimyolemmal antibodies are markers of a secondary immunopathogenesis in perimyocarditis. In cytomegalovirus myocarditis antiinterfibrillary antibodies could be found and immune complexes were rarely observed. Postmyocarditic cardiomyopathy could be identified by circulating antimyolemmal and antisarcolemmal antibodies which also bind to the endomyocardial autopsy specimens. In these patients circulating immune complexes are more frequent than in normals and in dilated cardiomyopathy. In dilated cardiomyopathy antifibrillary and antiinterfibrillary antibodies were observed, the incidence of which correlated with the severity (NYHA) of the disease. A group of patients with dilated cardiomyopathy could be distinguished who demonstrated regardless of the severity lymphocytotoxic reactions against vital cardiocytes.

Antigen-Antibody Complex↗
PubMed1984

[Secondary immunopathogenesis of cardiac diseases].

Antimyolemmal antibodies can be demonstrated in sera of patients with coxsackie B, influenza, mumps and Q-fever perimyocarditis, in sera of patients with postpericardiotomy and postinfarction syndromes, in part of the sera of patients with endocarditis and in some patients with dilated heart disease most likely due to secondary immunopathogenesis after perimyocarditis. Antimyolemmal antibodies in titres greater than 1: 40 are complement fixing and cytolytic when added to cultures of vital myocytes. In vitro cardiocytolysis indicates that humoral effector mechanisms could also play a pathogenetic role in vivo. In vitro antibody dependent and independent cellular cytotoxicity of patients lymphocytes against isolated cardiocytes could not be observed in perimyocarditis and postmyocarditic cardiomyopathy. It could be demonstrated, however, in patients with postpericardiotomy syndrome and in some patients with dilated cardiomyopathies. Immunological investigations are therefore not only of diagnostic significance but have widened our knowledge of the etiology and pathogenesis of perimyocardial diseases. Furthermore they are helpful in the follow-up and prognosis of patients with protracted perimyocardial affections.

Antigen-Antibody Complex↗
PubMed1984

[Effect of nifedipine and nitroglycerin on epicardial vessels in coronary heart disease].

The effect of nifedipine and nitroglycerin on the diameter of epicardial coronary arteries, the stenosis diameter, as well as arterial blood pressure and heart rate were recorded in 20 patients with coronary-heart disease. Nifedipine (20 mg sublingually) caused a significant fall in arterial pressure and a significant rise in heart rate. Additional administration of nitroglycerin (0.8 mg sublingually) caused a further fall in arterial pressure while heart rate remained constant. A definite relaxation (vasodilatation) of the epicardial vessels was demonstrated after nifedipine and a further increase after nitroglycerin. While nifedipine on average led to a significant increase in the diameter at the site of stenosis, response of individual stenoses was highly variable. In one patient with subtotal stenosis of the anterior interventricular branch a complete, transitory occlusion at the site of the stenosis occurred during nifedipine medication. This paradoxical reaction was not noted after nitroglycerin. Relaxation of the epicardial coronary arteries by nifedipine with suppression of phasic tone thus seems to be the major part of its anti-anginal effect. This effect is potentiated by nitroglycerin so that the combination of nitrate and calcium-antagonist appears to be therapeutically reasonable. In individual patients, however, there may be a paradoxical reaction to nifedipine.

Adult↗
PubMed1984

Demonstration of organ specific antibodies against heart mitochondria (anti-M7) in sera from patients with some forms of heart diseases.

Using submitochondrial particles (SMP) from beef heart, pig kidney and rat liver in the ELISA, we detected partial organ specific anti-mitochondrial antibodies (AMA) against heart and kidney SMP in sera from patients with different forms of cardiomyopathies. Serum samples from 50 of 159 patients with congestive or hypertrophic cardiomyopathy (31%) and from two of 15 patients with acute myocarditis (13%) were AMA positive. These AMA could be clearly differentiated from other known AMA (anti-M1-M6) and were therefore named anti-M7. Thirteen of the 52 sera (25%) reacted only with heart SMP (type a) and 39 showed a cross-reaction with kidney, lung and pancreas mitochondria (type b). However, using liver SMP, no positive reaction was found. The anti-M7 type a and b activity was abolished completely by absorption with heart SMP. The anti-M7 antibodies were directed against an antigen which co-purified with the inner mitochondrial membrane and had a molecular weight of 67,000-72,000. They seem to be confined to some forms of cardiomyopathies and myocarditis of unknown aetiology and were not detected in sera from patients with other diseases.

Animals↗
PubMed1983

Quantification of antimyosin antibodies in experimental myocarditis by a new solid phase fluorometric assay.

A solid phase fluorometric assay of high sensitivity and specificity for detection of antimyosin antibodies is described. The method consists of 4 basic steps: (1) coating the carrier stiQ with myosin; (2) incubation of the stiQ in the test serum; (3) labeling of the bound antibodies by FITC-anti-immunoglobulin antibodies; and, (4) quantitation of the bound antibodies in a fluorometer (FIAXTM). Using a purified myosin preparation as antigen, the assay was tested in experimental myocarditis of rabbits injected with cardiac proteins. Reproducibility was excellent, standard deviation of intra-assay variance being 7.86%, and inter-assay variance 9.45%. When compared with immunodiffusion, a complement fixation test with myosin and indirect immunofluorescence, the assay described proved superior since it allows simple monitoring of serum concentrations of antimyosin antibodies.

Animals↗
PubMed1983

Diagnostic relevance of humoral and cytotoxic immune reactions in primary and secondary dilated cardiomyopathy.

Circulating muscle-specific antimyolemmal antibodies (AMLAs) were found in 18 of 61 patients with secondary dilated cardiomyopathy (DC). All 18 patients had clinical or histologic evidence of previous perimyocarditis. AMLAs were found both in patients' serum samples and bound to the sarcolemmal sheath of the autologous myocardial biopsy specimen. Only AMLAs in postmyocardiac DC induced cytolysis of vital cardiocytes in the presence of complement, whereas hepatocytes remained unaffected. Titers of AMLAs correlated with the degree of cardiocytolysis. In contrast, antiinterfibrillary antibodies were found in 49% patients with primary DC (n = 79) and in 61% of patients (n = 30) with alcoholic DC. The incidence of antifibrillary antibodies of the antimyosin type was 23 and 24%, respectively. Incidence of both antibodies increased according to the severity assessed by New York Heart Association functional classes. Circulating immune complexes assayed by a new Clq-solid phase fluorometric assay were present in 30% of patients with postmyocarditic DC only. Lymphocyte-mediated cytotoxicity against heterologous cardiac target cells (K-cell activity) was measured in 33% of patients each with primary and secondary alcoholic DC but not postmyocarditic DC. There were no blocking factors in primary but were some in alcoholic heart disease.

Antibodies↗
PubMed1983

Myasthenia gravis: overlap with 'polyendocrine' autoimmunity.

81 patients with spontaneously acquired myasthenia gravis (MG) were investigated for the presence of autoimmune (AI) diseases and their sera were tested for a range of organ-specific autoantibodies. 77 of the patients were HLA-phenotyped. Antibody titres to acetylcholine receptors (AChR) were higher in non-thymomatous patients who possessed HLA-B8 (p less than 0.05) and/or -DR3 (p less than 0.05) as compared to patients lacking these HLA antigens. 3 out of 20 (15%) patients with ocular MG, 7/23 (30%) with generalized MG of early onset, 11/23 (48%) generalized MG of late onset and 5/14 (35%) patients with thymoma had either overt AI diseases or significant titres of organ-specific autoantibodies suggesting subclinical AI disease. In ocular MG, low titres and an infrequent finding of antibodies to AChR (32%) as well as the low prevalence of associated autoantibodies and AI diseases indicate that this subgroup of MG consists of patients with restricted AI reactivity. HLA-B8 and -DR3 were present in all the patients with associated AI disorders in the young onset group but in none of the patients with old age of onset. In the young group, 6 out of 7 patients with associated AI conditions were women whereas the sex ratio was about equal in the older cases in both, patients with and without associated AI diseases or autoantibodies. We conclude from these observations that ageing provides conditions that allow the breakdown of self tolerance. The simultaneous presence of HLA B8, DR3 and female sex provide important additional factors for early expression of MG.

Adult↗