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Biomedical subjects

B Maisch

Publications and source records attributed to B Maisch.

At least 199 records · Page 11Linked to original sources
PubMed1995

[The extracellular matrix and cytoskeleton of the myocardium in cardiac inflammatory reaction].

The cardiac cytoskeleton and the extracellular matrix play an essential role for maintaining cellular integrity and function of the myocardium. The network of microtubules and intermediate filaments are disrupted by the inflammatory reaction which depends on resident cells (myocytes, fibroblasts, endothel cells) and on systemic cells (granulocytes, macrophages, monocytes, lymphocytes). Changes in the cardiac cytoskeleton and the extracellular matrix may affect contractile function, since the cytoskeleton organizes the intra- and intercellular architecture. The inflammation in heart disease and the induction of fibrosis are mediated by cytokines and growth factors derived from fibroblast activation and from the B- and T-cell activity. A possible connecting link for the induction of fibrosis is the presentation of the myocardial antigens to the immune system and its subsequent cellular and humoral autoreactive response (Figure 1). Different autoantibodies to sarcolemmal and myolemmal antigens, to laminin, to extracellular matrix proteins, to the collagens and to myofibrils were demonstrated both in endomyocardial biopsy and as circulating autoantibodies in the peripheral blood. The pathophysiological role of the cytoskeleton and the extracellular matrix are well defined for beta-tubulin, fibronectin, laminin, desmin, vimentin, vinculin and collagen: beta-tubulin is increased or altered in dilated cardiomyopathy (DCM). Fibronectin appears in irregular forms in DCM as well. Ultrastructural analysis showed an increased content of laminin in basement membranes. In addition anti-laminin antibodies were found in 73% of patients with myocarditis and in 78% of patients with DCM. Desmin (z-bands) are partly destroyed in DCM. Anti-desmin antibody titers as indicators of a possible secondary immune response are found high in patients with acute myocarditis declining during reconvalescence and are also elevated in DCM. The vimentin of the endothelial cells and the vinculin of the sarcolemmal membrane and the intercalated discs have been demonstrated to be irregularly shaped and increased in content in DCM whereas in myocarditis their appearance and content is still unknown. The intracellular content of collagen type 5 is increased in DCM and in myocarditis. The presence of autoantibodies to components of the cytoskeleton and the extracellular matrix in myocarditis and perimyocarditis is well-described. Antibodies to the myolemma and the sarcolemma are found in almost all patients with perimyocarditis in the serum or bound in the biopsy. Some of them have been known cytolytic in vitro to isolated heart cells. In pericarditis a shift to antibodies to the extracellular matrix, collagen and intermediate filaments is observed among the circulating antibodies.(ABSTRACT TRUNCATED AT 400 WORDS)

Autoantibodies↗
PubMed1995

[Retrospective studies and prospects of therapy for hypertension].

Future trends in hypertensive treatment have to rely on our past and present experience with antihypertensive drugs as well as on emerging concepts of blood pressure regulation, on which some new drugs in the "pipeline" are based. Early detection of hypertension, before organ manifestations particularly in the heart, the kidney and the vessels occur, remain mandatory since in most of the patients with mild and moderate hypertension the high blood pressure is not diagnosed at all or treated inadequately. Prevention of cardiac, vascular, renal or metabolic complications has always been better for the patient and less costly than their repair or reparation. Our present treatment goals have often not reached far enough. Normalisation of blood pressure demonstrates only surrogate efficacy of our treatment. Our ultimate goal has to be improvement of total or cerebrovascular or cardiovascular and cardiac mortality. Important steps on that road are the prevention or reparation of cardiac hypertrophy, of the increased extracellular matrix and collagen deposition, the conservation of vascular integrity including both coronary and systemic microangiopathy and macroangiopathy. For the patient this means integrated care of his associated disorders that is of coronary artery disease, diabetes mellitus, lipid disorders, overweight and the metabolic syndrome. True health efficacy (= reduction of total or cerebro- and cardiovascular mortality) has been demonstrated so far only by blood pressure reduction with diuretics (thiazides) and beta-blockers in long term studies, whereas sufficient surrogate efficacy, the lowering of blood pressure, has been demonstrated with almost all the others drugs either in mono- or in combinationtherapy. Together with ACE-inhibitors, which have demonstrated their prognostic value in patients with heart failure of different causes, thiazides (as the most representative diuretic) and betablockade can be considered first line drugs in the treatment of hypertension. Long-term mortality trials for ACE-inhibitors in hypertension are needed, however, to prove that the anticipated benefit from the heart failure megatrials can also be taken for granted for hypertensive patients without coronary artery disease as well. All other drugs should not or not yet be considered first line medication, although treatment behavior in the US and in Europe shows wide-spread use of calcium antagonists in short- and long-acting dihydropyridine type hypertensive patients. No peer reviewed journal has so far published a randomized double-blind trial with the endpoint of total or cardiovascular mortality in hypertension using calcium antagonists. A recent case control study, as well as the preliminary data from MIDAS and GLANT, for which event rates are available in abstract form, suggest that short acting calcium-antagonists of the dihydropyridine type, though controlling blood pressure well, are not reducing mortality but show a trend to increase cardiovascular events particularly when given in higher doses. In contrast the unpublished data from a Chinese megatrial with dihydropyridines (STONE) demonstrate effective blood pressure reduction and benefit in mortality in a population that differs from patients in Europe and in the USA because of the low prevalence of coronary artery disease. No randomized, double blindly acquired data on mortality as the primary end of antihypertensive treatment are yet available for verapamil, diltiazem and the new class of longer acting calciumantagonists. Only when speculating from trials with calcium antagonists in coronary artery disease e.g. the DAVIT II study, one could imagine so far that prognostic benefit may be expected from drugs that do not or very little activate the adrenergic and the renin-angiotensin-aldosterone system and the baroreceptors and reduce or at least maintain heart rate. The need for double blind, randomized trials with the different Ca-antagonists is obvious, before a further w

Antihypertensive Agents↗
PubMed1994

Coxsackievirus B3 infection leads to cell death of cardiac myocytes.

In order to address the question whether the virus or immune reactions to the heart induce cardiac damage in the murine model of coxsackievirus B3 induced myocarditis, calcium-resistant cardiac myocytes of a myocarditis susceptible strain of mice were isolated and exposed to myocarditic coxsackievirus B3. The tetrazolium salt MTT was used to visualize the effect of the virus upon cell viability by inverse light microscopy and by an EA test. Coxsackievirus B3 infected isolated adult cardiac myocytes as well as infected cultured cardiac fibroblasts were examined. In vitro the virus killed the myocytes within 16 h of infection whereas the fibroblasts survived the infection. Since coxsackievirus B3 is able to kill cardiac myocytes by itself, immunosuppressive treatment of acute coxsackievirus B3 induced myocarditis may be harmful by eliminating host immune defence mechanisms and, therefore, may lead to an enhanced viral spread and virus induced myocyte necrosis in the heart.

Animals↗
PubMed1994

Pericardioscopy and epicardial biopsy--new diagnostic tools in pericardial and perimyocardial disease.

Pericardioscopy is a new diagnostic tool for macroscopic visualization of alterations in both the epicardium and pericardium. We report on 35 patients with pericardial effusion due to inflammatory perimyocardial disease. After puncture of the pericardial effusion, an 8F sheath was introduced over a guidewire under X-ray control. The pericardial pressures were measured; the fluid was removed by aspiration and exchanged with 100 ml of body-warm saline until the pericardial fluid was clear. To visualize the peri- and epicardium, for video- and photo documentation, two sorts of 8F endoscope were used, either a flexible fibreglass version or a rigid 110 degree one--both made by Storz. Cytology of the fluid and optically guided and controlled epicardial and pericardial biopsies were performed to classify the form of pericarditis. A specific diagnosis of viral pericarditis could thus be established in seven cases--by in situ hybridization for cytomegalovirus (n = 3) and by microneutralization test for enteroviruses and/or coxsackievirus B4 isolation (n = 4); of lymphocytic perimyocarditis in 16; of bacterial pericarditis in seven and antibody-mediated autoreactive pericarditis in five cases.

Adult↗
PubMed1994

Regulation of the structural remodelling of the myocardium: from hypertrophy to heart failure.

The Framingham heart study has shown that arterial hypertension is the major aetiological factor for the development of heart failure. In the presence of heart failure, various regulatory systems may be operative. These include the Frank-Starling mechanism, the neurohormonal system, regulation of cardiac growth and peripheral oxygen delivery. Recently, the interrelationship of the neuroendocrine system and cardiac growth has been examined. In the pressure or volume overloaded heart, growth of the myocardium involves the enlargement of cardiac myocytes, an adaptation governed by ventricular loading. Non-myocyte cell growth, including cardiac fibroblasts, may also occur. However, the haemodynamic load does not appear to be its major physiological stimulus. Cardiac fibroblast activation is responsible for the accumulation of type I and III collagens, the major fibrillar proteins of the myocardial collagen matrix, while vascular smooth muscle cell growth accounts for medial thickening of coronary resistance vessels. This structural remodelling of the cardiac interstitium represents a major determinant of pathological hypertrophy: it accounts for abnormal myocardial stiffness and impaired coronary reserve, thereby leading to ventricular diastolic and systolic dysfunction and ultimately the appearance of symptomatic heart failure. Several lines of evidence suggest that circulating and tissue renin-angiotensin-aldosterone systems are involved in the structural remodelling of the non-myocyte compartment, including the 'cardioprotective' effects of angiotensin converting enzyme (ACE) inhibition or the beneficial effects of anti-aldosterone treatment that were found to prevent myocardial fibrosis in renovascular hypertension due to unilateral renal ischaemia under experimental conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Pericardial diseases, with a focus on etiology, pathogenesis, pathophysiology, new diagnostic imaging methods, and treatment.

Recent advances in the study of pericardial disorders have opened new diagnostic windows to the heart through the pericardial sac, with the development of pericardioscopy and thoracoscopy. Specific diagnosis of inflammatory, postinflammatory, autoreactive, or neoplastic pericardial disease can now be made by epicardial and pericardial biopsy and by cytologic analysis of the pericardial fluid. In perimyocarditis, optically guided epicardial biopsy gives more disease-specific results than does endomyocardial biopsy in the same patients. For viral and tuberculous pericarditis, molecular techniques such as polymerase chain reaction and in situ hybridization are available. Immunologic characterization of lymphocytic cells and antibodies demonstrates increased reactivity in viral, autoimmune, and neoplastic disorders of the heart. Doppler echocardiographic features in tamponade are reviewed thoroughly. Advantages and problems of pericardectomy in constrictive disease are noted, and finally, a pragmatic clinical and scientific approach for improved diagnosis of pericardial diseases is outlined.

Cardiac Tamponade↗
PubMed1994

[Accelerated idioventricular rhythm].

The term accelerated idioventricular rhythm describes an ectopic ventricular rhythm with 3 or more consecutive ventricular premature beats with a rate faster than the normal ventricular intrinsic escape rate of 30 to 40 beats per minute, but slower than ventricular tachycardia. Accelerated idioventricular rhythm differs from ventricular tachycardia by additional features such as the onset with a long coupling interval, the end by a gradual decrease of the ventricular rate or increase of the sinus rate and, last but not least, by a good prognosis. Clinically, accelerated idioventricular rhythm can occur in any form of structural heart disease and occasionally in adults or children without structural heart disease. Accelerated idioventricular rhythm most often can be seen in patients with coronary artery disease. Its occurrence after thrombolysis during acute myocardial infarction is a marker of successful reperfusion. Since accelerated idioventricular rhythm is usually hemodynamically well tolerated and not associated with malignant ventricular tachycardias; as a rule, no specific treatment other than care of the underlying heart disease is necessary. The present overview discusses electrocardiographic criteria, possible mechanisms, and the clinical significance of accelerated idioventricular rhythms.

Accelerated Idioventricular Rhythm↗
PubMed1994

Detection of cytomegalovirus genome by in situ hybridization in paraffin embedded endomyocardial biopsy specimens of viral myocarditis.

Cytomegalovirus (CMV) genes were detected by in situ hybridization in 25 Chinese patients with viral myocarditis (VMC). The positive hybridization signals were found in cardiomyocytes (6 cases, 24%), capillary endothelial cells (4 cases, 16%) and interstitial cells (7 cases, 28%). The difference between VMC and control group (16 cases died of brain trauma and 10 cases of congenital heart diseases was statistically significant. There was no definite pathomorphological relationship between the detection of CMV genes and myocardial lesions. The results suggest that CMV infection may be one of the causes of myocarditis and chronic stimulation of the immune system induced by CMV may be a possible pathogenesis of this disease.

Adolescent↗
PubMed1994

[Löffler endocarditis fibroplastica with simultaneous infectious endocarditis].

The clinical and immunological 8-year follow-up of a 45-year old female with hypereosinophilic syndrome and cardiac involvement of Löffler's fibroplastic endocarditis which was complicated by infective endocarditis during immunosuppressive treatment is presented. All 3 stages of the disease were documented by clinical and histologic data: stage 1 by biopsy proven eosinophilic myocarditis and arteritis, stage 2 with Berlin blue positive parietal thrombosis, and the fibrotic features of stage 3 both by fibrosis in the latest biopsies and by echocardiography. It was remarkable, however, that this classic clinical case of Löffler's endocarditis lacked a few serological markers postulated to be found regularly, e.g., a positive staining for the cationic protein and major ribonucleases. Instead, the patient demonstrated all the immunological features of autoreactive myocarditis with cytolytic, complement fixing antimyolemmal antibodies. After an initial loading dose of 120 mg prednisolone per day for 6 weeks (11/1986), the steroid dosage was reduced to 40 mg (12/1986) and diminished to 15 mg/day in 1988 to 1989. Finally, the patient was on 4 mg prednisolone per day for almost 4 years. In 1987, azathioprine was added in the dose of 150 mg/day for 6 weeks. In 3/1994 the patient developed infective endocarditis with streptococcus sanguis and presented with dyspnoea. By echocardiography a large floating structure was diagnosed on the anterior mitral leaflet and the left atrium was enlarged by severe mitral regurgitation. Infective endocarditis was successfully treated with antibiotics, but mitral regurgitation made valve replacement obligatory.

Autoantibodies↗
PubMed1994

[Fever and lung abscesses in anorexia nervosa after infusion therapy].

A 26 year old female patient was admitted to our hospital because of septic temperatures and chills. In the patient's history renal insufficiency has been known for several years due to agenesia of the right and pyelonephritic renal congestion of the left kidney. Long lasting anorexia nervosa had been treated by psychotherapeutical interventions for years and when failing it necessitated repeated intravenous nutrition by central venous lines. The prominent symptom of the intravenously treated young woman was fever up to 39.7 degrees C and pneumonia, which was considered by the first treating clinic to be caused directly by diminished immunoreactivity in malnutrition and preuremia. The chest X-ray confirmed pneumonia and revealed multiple abscesses in both lungs (Figure 1). After being transferred to our intensive care unit the pathophysiological context became obvious. From inspection (positive jugular pulsation), from auscultation (holosystolic murmur at the left parasternal border) tricuspid incompetence due to infective endocarditis was suspected. This was confirmed immediately by TM and two-dimensional transthoracic echocardiography, which showed a large vegetation on the anterior tricuspid valve leaflet (Figures 2a and 2b). Tricuspid regurgitation was also ascertained by color flow echocardiography (Figure 2c). Several blood cultures were positive for staphylococcus aureus. Clinical and laboratory recovery was achieved by antibiotic therapy with vancomycin and cephtazidim for 3 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[Aortic and mitral valve endocarditis after infection of the pacemaker pocket].

The case of a 76-year-old diabetic patient with known aortic valve sclerosis is reported. One week after implantation of a permanent pacemaker system (indication: 2nd degree AV-block type Mobitz) he developed fever. Large endocarditic vegetations were found on the aortic and mitral valve (blood cultures: were positive for Staphylococcus aureus). Also from the pacemaker bed Staphylococcus aureus was isolated and an antibiotic treatment including vancomycin was started. Nevertheless the patient developed insufficiencies of both the aortic and mitral valves and became hemodynamically unstable. Due to cerebral embolisms and further deterioration of the patient's overall clinical state the already planned operative replacement of the aortic and mitral valve could not be performed. The patient died because of left ventricular failure after pacemaker infection which was complicated by endocarditis.

Aged↗
PubMed1994

Anemia with LDH-elevation in a patient with aortic valve replacement.

In a 63-year old patient with a history of aortic valve replacement in 1986, a reduced hemoglobin of 91 g/l was found by a family physician. Since serum LDH was also increased, the patient was diagnosed to suffer from mechanically induced, hemolytic anemia and presented at our hospital for further diagnosis and evaluation of the aortic valve prosthesis.

Anemia, Hemolytic↗
PubMed1994

[Biventricular inflow tract compression by chronic organized hemopericardium in Caplan syndrome].

We report the case of a 59-year old patient with the rare combination of silicosis and rheumatoid arthritis, which is called Caplan's syndrome. The patient presented with right heart failure caused by a pericardial tumor compressing the right and the left ventricle. By means of several imaging techniques it was possible to elucidate the topographic relations of the tumor. Definite signs of malignant growth were not found. Despite his elevated perioperative risk we decided to operate on the patient. During the operation macroscopic and histologic evidence revealed that the tumor was not a neoplastic process but consisted of an organized hemopericardium. This demonstrates that pericarditis in rheumatoid arthritis can be hemorrhagic and can mimick a malignant pericardial tumor. The decision to operate was first supported by the findings of the applied imaging techniques, the normal endomyocardial biopsy, and the clinical course and were later confirmed in situ.

Caplan Syndrome↗
PubMed1994

[Malignant angiosarcoma of the right atrium in pregnancy. Diagnostic and therapeutic problems].

Primary tumors of the heart, in contrast to secondary metastatic tumors show a very rare occurrence. About 25% of all primary cardiac tumors are malignant with angiosarcomas being the most frequent type of tumor. The clinical presentation include pericardial tamponade by hemorrhagic pericardial effusion, right heart failure, lung embolism and thoracal pain. Diagnostic procedures include echocardiography, magnetic resonance imaging, CT scan, angiography, pericardioscopy and finally surgical exploration. We report on a 27-year old pregnant woman (23rd week) with a malignant primary angiosarcoma of the right atrium. The patient was admitted to the hospital with progressive shortening of breath due to pericardial tamponade from pericardial effusion. A tumor of the right atrium was detected by echocardiography. Diagnostic procedures had to consider the pregnancy of the patient. Transesophageal echocardiography, magnetic resonance imaging and finally angiography of the right heart with tumor biopsy were performed. Histological examination did not show any signs of malignancy. After corticosteroids pericardial effusion disappeared. Surgical exploration of the tumor was not performed because of the pregnancy. Two weeks later the patient underwent emergency surgery because of progressive heart failure due to obstruction of the tricuspidal valve by the tumor. Thereby intrauterine death of the fetus occurred. The tumor was removed and the right atrium was reconstructed using a Dacron patch. Adjuvant chemotherapy was performed. Eight months later the tumor recurred and heart transplantation was performed. two months later pulmonary metastases were found. the patient died 20 months after onset of symptoms. This is a rare case of the very unusual coincidence of pregnancy and a primary malignant heart tumor.

Adult↗
PubMed1994

[Diagnosis of Ebstein's anomaly with transesophageal echocardiography].

We describe a 63-year old female patient presenting with increasing dyspnea on exertion. The chest X-ray was suggestive but not compelling for Ebstein's anomaly. Although Ebstein's anomaly is most often discovered first in childhood, rare cases, such as ours, are described in late adulthood, however. Obesity may be one reason why it was not possible in our patient to detect the characteristic features in transthoracic echocardiography. The diagnosis of Ebstein's anomaly could be established only by transesophageal echocardiography: There the right atrium was grossly enlarged due to the distal insertion of the septal tricuspid valve leaflet. Colour flow echocardiography clearly demonstrated severe tricuspid valve incompetence. No additional congenital or acquired cardiac disorder could be detected. Cardiac catheterization confirmed the echocardiographical findings, whereas magnetic resonance tomography did not show the abnormal insertion of the tricuspid valve leaflet. If Ebstein's anomaly is suspected and cannot be ascertained by transthoracic echocardiography, transesophageal echocardiography can be employed to definitely diagnose this fairly rare form of congenital heart disease in an adult population.

Angina Pectoris↗