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Biomedical subjects

B Maisch

Publications and source records attributed to B Maisch.

At least 19 recordsLinked to original sources
PubMed1992

Cardiac natriuretic peptide hormones during artificial cardiac pacemaker stimulation and left heart catheterization.

Brain natriuretic peptide (BNP) is synthesized and released predominantly in the ventricular myocardium whereas atrial natriuretic peptide (ANP) is produced mainly in the atria. This study evaluated whether artificial pacemaker stimulation or left heart catheterization results in specific changes in BNP and ANP plasma levels. Both BNP and ANP responded sensitively to changes in pacemaker stimulation (single-chamber pacemakers; pacing rates of 72 and 92/min) and during the left heart catheterization procedure. However, whereas higher pacing resulted in a more pronounced increase in plasma BNP levels, a stronger ANP release followed catheterization. This incongruous rise in ANP and BNP plasma concentrations points to at least partly independent mechanisms governing the release of BNP and ANP.

Atrial Natriuretic Factor↗
PubMed1992

Myocardial collagen matrix remodelling in arterial hypertension.

The cardiac interstitium is composed of non-myocyte cells and a structural fibrillar protein network which plays a dominant role in governing the structure, architecture, and mechanical behaviour of the myocardium. Herein we review the fibrillar collagen network, its various components, and the functions they serve in the normal and structurally remodelled myocardium in arterial hypertension. The heterogeneity in myocardial structure, created by the altered behaviour of non-myocyte cells, particularly cardiac fibroblasts, which are responsible for collagen synthesis or degradation and thereby fibrous tissue accumulation, is a major determinant for the appearance of diastolic dysfunction and ultimately systolic myocardial failure. Regulatory mechanisms related to this fibrous tissue response are reviewed to draw attention to the hitherto neglected role of cardiac fibroblasts in mediating adverse structural remodelling of the myocardium and showing how this can be prevented through the use of pharmacological agents that interfere with the regulation of the myocardial collagen matrix. Several lines of evidence suggest that circulating and tissue renin-angiotensin-aldosterone systems (RAAS) are involved in the structural remodelling of the non-myocyte compartment. These include the cardioprotective effects of angiotensin converting enzyme (ACE) inhibition and aldosterone receptor antagonism that were found to prevent myocardial fibrosis in the rat with renovascular hypertension. In the rat with genetic hypertension, established left ventricular hypertrophy and abnormal myocardial diastolic stiffness due to interstitial fibrosis, RAAS inhibition resulted in restoration of myocardial structure and function to normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

A new motion responsive pacemaker: first clinical experience with an acceleration sensor pacemaker.

A new accelerometer-based adaptive rate pacemaker (EXCEL VR) was evaluated to investigate its behavior at nominal settings during treadmill exercise testing and postural changes. Eight patients with sinus rhythm were selected to compare intrinsic heart rate to sensor mediated rate. Throughout exercise treadmill testing, changes in the sensor mediated rate closely paralleled actual physiological changes. The Pearson product moment correlation of pacing rate with sinus frequency, calculated for all patients, was r = 0.82 (P = 0.001). Change in the patient's physical position resulted in immediate change in sensor rate, which corresponded appropriately to the type of position change and activity level. Average (+/- SD) pacing rate was 62.4 +/- 2.7 beats/min supine; 67 +/- 3.8 beats/min sitting; 69.8 +/- 6.4 beats/min standing; 81.6 +/- 8.7 beats/min slow walking; and 96.8 +/- 1.3 beats/min fast walking. After 4 minutes of recovery, the average pacing rate dropped to 65 +/- 3 beats/min. The interaction between the accelerometer and the pulse generator at nominal settings was accurate and infrequently required the use of its many programming options. The accelerometer sensor and pulse generator algorithm in this device during postural change and exercise resulted in physiological-like changes in sensor mediated heart rate.

Acceleration↗
PubMed1992

[Cytomegalovirus associated diseases of the heart].

Latent cytomegalovirus (CMV) infection is not uncommon in the juvenile and adult population. The full blown disease is mostly restricted to immunosuppressed and immunodeficient patients, but may also occur in healthy individuals. The acute CMV-myocarditis often takes a mild course with only transient changes of left ventricular hemodynamics or a pericardial effusion as assessed by echocardiography. In our patient population it was characterized by the presence of anti-interfibrillary antibodies. In acute myocarditis the virus genome can be detected by in-situ hybridization in 42% (40% in the myocytes, 21% in the interstitial cells and 41% in endothelial cells). In patients with perimyocarditis CMV-DNA is found in 24% of patients in the myocytes, in 24% of patients in the interstitial cells and in 50% of patients in the endothelium. In healthy controls CMV-DNA could be assessed only in interstitial and endothelial cells (70% and of the infected 30% of positive cases) but not in the myocytes. In dilated cardiomyopathy (DC) CMV-DNA can be found in 48%. Particularly in myocytes in 45% of cases, in interstitial cells in 50% and in the endothelium of small vessels in 68%. An induction of the disease by a chronic local stimulation of the immune system is a likely pathogenetic explanation of the immuno phenomena observed in parallel to the viral persistence. Additive damage by chronic CMV infection can be caused by the infection of the endothelium and smooth muscle cells of the intima of coronary arteries. There are some reports of CMV-DNA detection in the arterial walls or atherosclerotic plaques of patients with atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1992

Cytolytic anticardiac membrane antibodies in the pathogenesis of myopericarditis.

Antisarcolemmal (ASAs) and antimyolemmal antibodies (AMLAs) are serological hallmarks of inflammatory heart muscle disease. They occur in a similar incidence in postcardiac injury syndromes, sarcoid heart disease or in dilated and hypertrophic cardiomyopathy. Rarely but still notably they are found with increasing age or in coronary artery disease. We therefore examined whether they are truly pathogenetic or whether they also possess properties of 'natural antibodies'. AMLAs and ASAs, like natural antibodies, have specificity for preserved structures on the membrane; they possess cross-reactivity and increase with age. In contrast to natural antibodies, however, they occur frequently after viral stimulation or other forms of trauma, are more often of the IgG and IgA than of the IgM isotype and fix complement in the acute stage of the disease. They also possess cytolytic and cytotoxic properties when incubated in vitro with isolated heart muscle cells. Antigenic mimicry has been demonstrated to be operative, since they are cross-reactive to viral proteins.

Adult↗
PubMed1992

Anticardiac antibodies in hypertrophic cardiomyopathy as a marker of severity.

Twenty-three patients (mean age 27 years, 15 male, 8 female) with hypertrophic cardiomyopathy (10 'obstructive', 13 'non-obstructive') mostly of the sporadic type were examined for anticardiac antibodies circulating in the peripheral blood or bound in the endomyocardial biopsy. Immunoglobulin deposition in the biopsies was found in 41% of cases of the IgG isotype. IgM and complement fixation occurred less frequently. Predominant findings in the patients sera were antimyolemmal (78%) and antifibril antibodies (43%). The patients' sera were not cytolytic except for one case indicating that neither a toxic serum factor nor antibody-mediated cardiocytolysis were operative to a significant degree in hypertrophic cardiomyopathy. The patient's lymphocytes did not demonstrate a cytotoxic effect either alone or in the presence of the autologous serum.

Adult↗
PubMed1992

[Indium-111 or Tc-99m-HMPAO marked granulocytes as specific markers of florid stage endocarditis--results comparing clinical, histological and scintigraphic findings in 30 patients with suspected endocarditis].

Thirty patients with clinically suspected infective endocarditis were scanned with Indium-111- or Tc-99m-HM-PAO-labeled granulocytes. The scans were correlated with the clinical course, and in 20 cases with the results from histologic examination of the valves. In six cases the scintigraphic examination gave correct positive results, in three cases false negative, in one case a false positive, and in 20 cases correct negative results. If we limit the analysis to only the histologically proven cases, our data suggest a specificity of the method of 86% and a sensitivity of about 67%.

Abscess↗
PubMed1992

Myocarditis and pericarditis--old questions and new answers.

Old questions in diagnosis, pathophysiology, aetiology, pathogenesis and treatment of inflammatory heart diseases are manyfold. However, with the availability of the new techniques and tools from molecular biology, immunology and virology many of the basic questions should be revisited e.g.: 1. Which is the role of the aetiopathogenetic agent, most probably a cardiotropic virus, in the initiation of myocarditis? 2. Which is the role of DNA-viruses and cytomegalovirus in particular in the initiation and progression of myocardial disease? Are there connections to small vessel alterations or myocarditis? 3. What is the role in the chronic state, when it can no longer be recovered as an active viral particle from myocardial tissue but may be still detectable by in situ-hybridization possibly as a defective virus or mutant? 4. Is autoreactive heart muscle disease still an attractive hypothesis by which one can explain the development of dilated heart muscle disease as its end-stage manifestation? Which role can be attributed to T cells, granulocytes and macrophages that we detect by monoclonal antibodies in the endomyocardial or epicardial biopsies of patients with suspected myocarditis or perimyocarditis? Which role can be attributed to autoreactive anticardiac antibodies, whose cytotoxic or cytolytic properties we can assess in vitro? 5. Are there new investigative tools available apart from those listed above to permit a better classification of pericardial disease in particular? 6. Should our therapeutic repertoire not be supplemented by drugs, that interfere directly with the pathogenetic inflammatory mechanisms, that we can identify today, apart from conventional antiphlogistic therapy or steroid treatment? Today to all these questions a positive answer can be given.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoantibodies↗
PubMed1992

[Pericardioscopy--a new window to the heart in inflammatory heart diseases].

Pericardioscopy is a new diagnostic tool to visualize macroscopically alterations of both the epicardium and pericardium. For the first time the macropathology of the epicarditis and pericarditis can be observed in vivo by the cardiologist in viral, bacterial, uremic and autoimmune cardiac processes. It enables us also to get an insight into neoplastic and metastatic processes affecting the heart and the pericardium. The prerequisite is the documentation of a larger pericardial (greater than 150 ml by the cubic model) effusion with an echocardiographically documented effusion of type C (Figure 1b), which must have at least 5 mm separation of the epicardial and pericardial layer in diastole at the anterior side of the heart when echocardiographic imaging is performed from the subxyphoidal or third intercostal space (Figure 1a). The first experience in 30 patients is reported. After puncture of the pericardial effusion a 9F sheath was introduced by use of a guide wire under echocardiographic and/or x-ray control (Figure 3). The fluid was removed by aspiration and 100 to 150 ml of body warm saline were infused in the pericardial sack. A flexible 8F fiber glass instrument (Vantec, Baxter or Storz) and a rigid 110 degrees 8F endoscope (Storz) were used for visualization of peri- and epicardium and for video documentation (Figure 2). After endoscopic inspection of the macropathology fibrinous strands (Figure 4) or increased vascular injection (Figure 5) can be observed in viral, autoimmune or idiopathic pericarditis or perimyocarditis. In the latter three forms of pericardial effusion only inflammatory cells (Figure 6) can be observed when the pericardial fluid is analyzed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Humoral and cellular immune reactions to the myocardium in myocarditis.

Myocarditis is characterized by an infiltration of poly- and mononuclear leucocytes next to necrosis of myofibers in the heart. Various viruses induce this cardiac disorder in most cases, either by their direct cytotoxic action on the cardiocytes or by humoral and cellular immune reactions to the myocardium arising after the infection. Epidemiological and experimental and serological studies suggest, that viral myocarditis may lead to dilated heart muscle disease. Therapy consists of reducing cardiac stress by physical inactivity and drugs decreasing cardiac pre- and afterload. Immunosuppression is beneficial in some but not all patients with myocarditis.

Adult↗
PubMed1991

Local cardiac responses--alternative methods of control.

Much attention has been paid to the influence of the beta-adrenoceptor system on cardiac function in heart failure. Full agonists and partial agonists acting on cardiac beta 1 receptors have been widely investigated, as has the density of these receptors in the failing heart. However, other cardiac control mechanisms may play important roles in the normal heart as well as in heart failure. The Frank-Starling mechanism of enhanced cardiac contraction produced by mechanical stretching of the ventricular myofibrils is well known. When treating patients with heart failure with diuretics, vasodilators and other drugs that influence preload, it is important to consider their overall effects in relation to the Starling curves. Atrial stretching also produces compensatory responses which are currently being intensively studied. Reflex release of atrial natriuretic factor after stimulation of atrial receptors has important physiologic effects in heart failure. The atria, but not the ventricles, are innervated by the vagus; the influence of the parasympathetic nervous system on the heart and circulation is often overlooked. The initial increase in heart rate during exercise is primarily due to withdrawal of vagal influence. Besides acetylcholine, the parasympathetic transmitter, many other local hormones may affect cardiac function; these include prostaglandins, 5-hydroxytryptamine and histamine. Although the activity of the sympathetic nervous system is mediated primarily through beta 1 adrenoceptors, both beta 2 and alpha receptors are also found in the heart. Myocardial alpha 1 receptors, which mediate a positive inotropic effect, have been identified, and prejunctional alpha 2 receptors may mediate inhibition of norepinephrine release from sympathetic nerves.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1991

Are antisarcolemmal (ASAs) and antimyolemmal antibodies (AMLAs) "natural" antibodies?

Antisarcolemmal (ASAs) and in particular antimyolemmal antibodies (AMLAs) are a serologic hallmark of inflammatory heart muscle disease and its sequelae. Since they may also occur to a much lesser incidence with increasing age, it was examined whether they also possess properties of "natural antibodies". As natural antibodies, AMLAs and ASAs have specificity for conserved structures on the membrane. They possess cross-reactivity and increase with age. In contrast to natural antibodies, however, they occur most frequently after viral stimulation, and are more often of the IgG- and IgA- than of the IgM-isotype and fix complement in the acute stage of the disease. They also exhibit cytolytic and cytotoxic properties when incubated in vitro with isolated heart muscle cells. In addition, antigenic mimicry has been demonstrated to be operative, since they are cross-reactive to viral proteins.

Adult↗
PubMed1991

Expression of MHC class I and II antigens and the Il-2 receptor in rejection, myocarditis and dilated cardiomyopathy.

In myocarditis and dilated cardiomyopathy a secondary immunopathogenesis is likely, since alterations to the humoral and cellular immune system have been repeatedly demonstrated. In rejection after heart transplantation activation of the immune system has been clearly seen. This may be comparable to myocarditis and thus could be a model for inflammatory heart disease. This study was set up to investigate whether an increased expression of antigens of the major histocompatibility complex and of the Il2 receptor in endomyocardial biopsies of patients after cardiac transplantation, myocarditis and dilated cardiomyopathy takes place. Cryostat sections were investigated immunohistologically by the immunoperoxidase test. There was an expression of class II antigens (HLA-DR, HLA-DP, HLA-DQ) in acute rejection and in myocarditis and in some patients with dilated cardiomyopathy on endothelial cells, interstitial cells but not on the myocytes. The results for class I (HLA-A, B, C) are similar, but in addition an expression on myocytes was observed in myocarditis and rejection. A second immunopathogenesis is most likely in some patients with dilated cardiomyopathy. The expression of the Il2 receptor on interstitial cells as a specific marker of cell activation was only seen in acute rejection and in some cases of myocarditis.

Adult↗
PubMed1991

Immune response to the endothelium in myocarditis, dilated cardiomyopathy and rejection after heart transplantation.

The role of endothelial cells in inflammatory heart disease and rejection after heart transplantation is only partly understood. To determine whether an immune reaction against endothelial cells occurs we examined endomyocardial biopsies from patients with myocarditis (n = 13), dilated cardiomyopathy (n = 23), no clinical rejection (n = 10) and moderate to severe rejection after heart transplantation (n = 10). These were compared to 'normal' donor hearts with monoclonal endothelial-specific antibodies EN4, Pal-E and F VIII-related antigen. Nearly all endothelial cells were stained positively with EN4. There were no significant changes in the binding of the antibodies except in rejection when Pal-E and F VIII-related antigen were significantly increased. It is concluded that apart from their possible role as antigen-presenting cells, endothelial cells are important targets in rejection after heart transplantation. Damage or cytolysis of endothelial cells may cause both altered transendothelial permeability and functional decrease in antigen presentation.

Antibodies, Monoclonal↗
PubMed1991

Pericardioscopy--a new diagnostic tool in inflammatory diseases of the pericardium.

Pericardioscopy is a new diagnostic tool to visualize macroscopically alterations in both the epicardium and pericardium. The first experience in 30 patients is reported, after pilot investigations were carried out in experimental animals. After puncture of the pericardial effusion a 9F sheath was introduced under echocardiographic and/or x-ray control. The fluid was removed by aspiration and 100-150 ml of body warm saline were infused in the pericardial sack. A flexible 8F fiberglass instrument (Vantec, Baxter or Storz) and a rigid 110 degree 8F endoscope (Storz) were used for visualization of peri- and epicardium and for video documentation. Complementary to visualization, optically-guided and controlled epicardial and pericardial biopsies were performed and analysed further. Specific diagnosis of pericardial effusion is thus greatly facilitated by the triad, pericardioscopy, cytology and epicardial as well as pericardial biopsy.

Animals↗
PubMed1991

Treatment of experimental murine Coxsackie B3 myocarditis.

Using the murine model of coxsackievirus B3-induced myocarditis we studied the effects of various immunosuppressive agents on the course and outcome of the disease in genetically different strains of mice. The response to drug treatment varied greatly among the strains of inbred mice, which suggests different immune pathomechanisms operative in mediating myocarditis.

Animals↗
PubMed1991

Impaired myocyte function in vitro incubated with sera from patients with myocarditis.

Sera positive for antimyolemmal antibodies (AMLAs) from patients with acute biopsy-proven myocarditis exerted a cytotoxic effect on cardiocytes stimulated in vitro. Using an edge-detecting system, contraction amplitude and contraction velocity were altered after the addition of AMLA-positive sera when compared to sera from healthy controls. Antibodies alone did not change the functional parameters. Only the presence of complement and heart-reactive antibodies mediated the detrimental effects. This suggests that a complement-mediated antibody-dependent immune mechanism is operative in human myocarditis.

Animals↗