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Biomedical subjects

B Maisch

Publications and source records attributed to B Maisch.

315 records · Page 18Linked to original sources
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[Alterations of cat papillary muscle mechanics induced by changes of preload under variation of physical and chemical parameters (author's transl)].

A rapid change in length of cat papillary muscle induces two reciprocal diastolic and systolic processes: stretching causes a viscoelastic relaxation of the muscle. The opposite behavior is observed after abrupt releases when - subsequent to an increase in resting tension - diastolic force attains its new equilibrium. The stretch-induced process of relaxation is accompanied by a transient decrease in mechanogram amplitudes; a release is accordingly followed by a temporary increase in isometric muscle performance. The mechanograms of the steady state prove to be the function of the degree of stretch or release, whereas muscle contractions in the early phase of stress relaxation depend on the contractile state before the change in length. All interventions which augment developed tension (increased calcium, decreased potassium, increased or decreased sodium concentrations, strontium, postextrasystolic potentiation, sympathicomimetic agents, frequency potentiation) diminish the transient phenomena due to stretch, whereas low frequency or a lesser intensity of electromechanical coupling (Hexobarbital, Iproveratril, Desoxycorticosteron, Ryanodine) increases them. A decrease of bath temperature enhances the transient increase in force due to a release or an initial reduction of isometric tension after a sudden stretch, although the absolute forces increase. No substantial changes could be observed in reserpinized cats with beta-blocking agents or under hypoxia. It is supposed that alterations in the time course of the action potential could be related to post-stretch and post-release systolic phenomena. A final interpretation of mechanical and electrical events after stretch and release is not possible with the methods used in these experiments.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Transthyretin Leu 68 in a form of cardiac amyloidosis.

A form of transthyretin (TTR)-related cardiac amyloidosis was previously described in a German patient. Electrophoretic analysis of plasma TTR showed the presence of an electrically neutral variant. We have now characterized the variant transthyretin by comparative peptide mapping, aminoacid and DNA sequencing procedures. A new mutation in TTR with a substitution of leucine for isoleucine at position 68 of the monomer is described.

Amino Acid Sequence↗
PubMedDate not supplied

Apoptosis in myocarditis and dilated cardiomyopathy: does enterovirus genome persistence protect from apoptosis? An endomyocardial biopsy study.

UNLABELLED: The purpose of this study was to examine the role of apoptosis in myocarditis and dilated cardiomyopathy. Apoptosis is an active energy-consuming mechanism of cell death in several cardiac diseases in different quality and quantity. METHODS: Endomyocardial biopsies from 81 patients with active (1) and chronic myocarditis (10), dilated cardiomyopathy with inflammation (DCMi; 10) and without inflammation (DCM; 20), with borderline myocarditis and positive PCR for cytomegalovirus-DNA (6), adenovirus-DNA, or enterovirus-RNA (7), and controls (17) were analysed. Apoptosis was detected by using the TUNEL method. The highest rate of apoptotic cardiocytes was found in active and chronic myocarditis. One patient with severe active myocarditis demonstrated 6.15% of apoptotic cardiocytes. Mean percentage of apoptotic cardiocytes in chronic myocarditis was significantly increased (0.61+/-1.25%) when compared to controls (0.01+/-0.04%, P<.05). Particularly, patients with cytomegalovirus-DNA persistence in borderline myocarditis had an elevated rate of apoptosis (0.34+/-0.68%, P<.05). Increased rates of apoptosis were found in borderline myocarditis with adenovirus-DNA persistence (0.20+/-0.57%) and in DCM (0.06+/-0.15%). Only a nonsignificant increase of apoptotic cardiocytes was found in DCMi (0.03+/-0.08%). No apoptosis was found in patients with enteroviral genome persistence in borderline myocarditis. CONCLUSIONS: Apoptosis of cardiac cells is increased in myocarditis and dilated cardiomyopathy, being highest in severe active myocarditis. Apoptosis thus contributes to cell death in active myocarditis and may play a role not to be neglected in dilated cardiomyopathy. Enteroviruses seem to have anti-apoptotic effects, because no apoptosis at all was found in the myocardium.

Apoptosis↗
PubMedDate not supplied

Pathophysiology and aetiological diagnosis of inflammatory myocardial diseases with a special focus on parvovirus B19.

Inflammatory processes induced by viral or bacterial infections are believed to be one of the major pathogenetic mechanisms in myocardial diseases. Although the reason for progression to myocardial failure is not fully understood, postulated mechanisms include persistent viral infection alone or in combination with autoimmune processes. A variety of cardiotropic viruses have been identified to elicit myocarditis, with enteroviruses and adenoviruses as the most frequent causative agents in children and adolescents. However, parvovirus B19 (PVB19) has recently emerged as another potential pathogen in adult patients associated with inflammatory heart disease. Many dimensions of inflammatory heart disease coexist while different phases of the disease progress simultaneously: phase 1 is dominated by viral infection, phase 2 by the onset of (probably) multiple autoimmune reactions, and phase 3 by the progression to cardiac dilatation without the role of an infectious agent and cardiac inflammation. Taking these mechanisms into account, screening for viral and bacterial genome by polymerase chain reaction (PCR) and detection of inflammatory infiltrates by immunohistochemistry are considered crucial for establishing an aetiological diagnosis, thereby allowing initiation of specific therapeutic strategies. In a large cohort of 3345 consecutive patients with left ventricular dysfunction evaluated over a period of 10 years, prevalence of PVB19, coxsackievirus (CVB), human cytomegalovirus (HCMV), influenza A virus and adenovirus (ADV) genome was assessed by PCR. Inflammatory infiltrates within the myocardium were detected by immunohistochemistry according to the WHF criteria and by histopathology according to the Dallas criteria of myocarditis. For control, endomyocardial samples of patients with arterial hypertension were studied. Parvovirus B19 was the most often detected virus in all patient subgroups, with positivity ranging from 17% to 33%. Except for PVB19, CVB RNA (3%), ADV (2%) and CMV (3.9%) were the most frequently detected viral genomes. Interestingly, detection of PVB19 genome was significantly correlated with inflammatory heart disease and reduced ejection fraction. Importantly, an aetiological diagnosis requires the immunohistochemical and molecular biological investigation of endomyocardial biopsies. Such an approach may change the management of these diseases in the future. One of the aims of the study was to reveal the underlying dominant pathophysiological mechanisms in a for deciding on the most approriate therapy.

Cardiomyopathy, Dilated↗
PubMedDate not supplied

Humoral immune reactions in uremic pericarditis.

Clinical data from 41 patients with pericarditis or pericardial effusion in acute and chronic renal failure were analyzed in respect to the diagnostic relevance of humoral immune reactions. In patients with pericardial effusion in acute renal failure due to surgery or trauma (n = 10), antimyocardial antibodies were rarely detected. In contrast, in the sera of all patients with pericarditis or pericardial effusion following renal failure in chronic or acute glomerulonephritis (n = 6), complement-fixing antisarcolemmal antibodies of the IgM and IgG classes were observed. In patients in whom pericarditis or pericardial effusion evolved during chronic hemodialysis (n = 25), the incidence of complement-fixing antimyolemmal antibodies was 64%. Only sera with complement-fixing antimyolemmal antibodies induced cytolysis of vital adult cardiocytes in vitro suggesting that the antimyolemmal antibodies may not only play a diagnostic but also a pathogenetic role in 'uremic' pericarditis in vivo.

Acute Kidney Injury↗
PubMedDate not supplied

[Fetal arrhythmias--new immunologic studies and results].

The etiology of fetal arrhythmias is still unknown. We therefore did a research for immunologic causes: antimyolemmal antibodies (AMLA) in mothers and umbilical cord serum resulting from secondary immunopathogenesis caused by myocarditis of the mother. Is there a correlation between immunological and clinical findings giving a possible explanation for fetal arrhythmias? In 21 cases mothers and umbilical cord serum was investigated for AMLA; 16 with fetal atrial premature beats, 4 with fetal tachycardia and 1 with fetal bradyarrhythmia. From 16 mothers with fetal atrial premature beats had 12 AMLA, from these were in 4 cases in the umbilical cord serum AMLA. In 4 cases of fetal tachycardia we found in 1 case AMLA in mothers and umbilical cord serum. In the other 3 cases accessory pathways have been the cause for tachycardia. From 19 healthy persons were found in 3 cases AMLA in mothers serum, umbilical cord serum was negative.

Antibodies, Viral↗
PubMedDate not supplied

[Paradoxic occurrence of symptoms of rheumatic fever after thrombolytic therapy with streptokinase--a case of delayed hypersensitivity?].

We report the case of a 51-year-old patient with a Paget von Schrötter-Syndrome of the right arm who underwent a successful lysis therapy with 9 x 10(6) IU streptokinase (Streptase) i.v. over 3 days. 36 h after ending the lysis therapy he developed a generalized eczema, which was interpreted as a drug-induced allergic reaction of the arthus type (Coombs III). He received methylprednisolone p.o. with an initial dose of 40 mg, tapered to 0 over 5 days. One day after the efflorent rash the patient developed fever for 12 h (with 38.8 degrees C maximum) and a gonarthritis of the left knee, and 24 h later of both knees. An echocardiogram showed a small pericardial effusion without hemodynamic influence. On the following 2 days a minimal proteinuria of 0.28 and 0.22 g/l was found. Subsequently and after a follow-up of 2 years, the patient was totally free of pathologic clinical and laboratory findings. We interpret this unusual case as a delayed hypersensitivity reaction to streptokinase with a paradoxical occurrence of clinical symptoms formally fulfilling the diagnostic criteria of "rheumatic fever".

Arthritis, Reactive↗