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Biomedical subjects

B Maisch

Publications and source records attributed to B Maisch.

At least 37 records · Page 2Linked to original sources
PubMed2004

[Complicated course of Churg-Strauss syndrome with eosinophilic perimyocarditis and pericardial tamponade].

HISTORY: A 30-year-old patient suffered from a dry cough and increasing dyspnea since two years; he further complained about non radiating chest pain and weight loss of 15 kg in the past 8 weeks. EXAMINATIONS: Physical examination revealed pulsus paradoxus and distended neck veins. On chest x-ray, signs of cardiomegaly without infiltrations were found. Echocardiographic studies demonstrated a large pericardial effusion with signs of pericardial tamponade. Pericardiocentesis and pericardioscopy was performed and pericardial as well as epimyocardial biopsy samples were taken. Serum studies revealed increased markers of myocardial infarction and hypereosinophilia without clinical evidence of parasitic, myeloproliferative, or neoplastic diseases. Diagnosis of acute eosinophilic myocarditis was established in the epimyocardial biopsy samples. DIAGNOSIS, TREATMENT AND COURSE: Based on the clinicopathologic findings, we diagnosed Churg Strauss syndrome with cardiac involvement. We instilled 500 mg triamcinolone intrapericardially and initiated systemic treatment with corticosteroids which resulted in normalization of the blood eosinophil count. During a follow up of 18 months, no recurrence of pericardial effusion was detected. However, while trying to reduce the steroids below 15 mg prednisolone equivalent per day, eosinophil numbers raised and wheezing increased. We suggested an immunosuppressive therapy including cyclophosphamide according to the Fauci protocol, which was denied by the patient due to potential adverse side effects. CONCLUSION: We suggest a detailed invasive strategy including endomyocardial biopsy to rule out viral myocarditis before immunosuppressive therapy with steroids is initiated in patients with suspected cardiac involvement in Churg Strauss syndrome.

Adult↗
PubMed2004

[Premedication visits. Economizing at the cost of the patient?].

The older the patient, the higher the risk of perioperative cardiac complications. Therefore, patients at risk have to be identified and the appropriate diagnostic or therapeutic measures initiated. The most important factor in this context is whether a planned surgery can be postponed. Several strategies have been developed (e.g. Goldman index, Eagle criteria) and the American Heart Association (AHA/ACC) has produced guidelines concerning perioperative diagnosis and therapy of cardiac risk patients. The common goal of these strategies is always the risk classification of the patient by combining the operative risk and the risk factors of the patient. The further procedure (diagnostic or therapeutic measures) is based on the risk classification. If further invasive therapy proves to be necessary, the determining factor is the period of time for which the operation can be delayed. This appears to be about 3 months but if this is not possible the outcome could be improved with a beta-blocker therapy in advance. A working group from the university hospital in Marburg has developed a strategy for risk classification and further diagnostic and therapeutic measures as outlined in this article.

Adrenergic beta-Antagonists↗
PubMed2004

[Significance of aldosterone antagonist therapy].

Since the introduction of ACE-inhibitors into clinical practice, the diuretic treatment with the classical aldosterone antagonist spironolactone has disappeared. It was generally believed that chronic treatment with ACE-inhibitors significantly reduces aldosterone secretion via reduction of angiotensin II-dependent aldosterone formation. However, aldosterone "escape" occurs: Even during chronic treatment with ACE-inhibitors, plasma levels of aldosterone rise again, which is associated with increased cardiovascular risk. Furthermore, extrarenal actions of aldosterone have been demonstrated, which detrimentally affect coagulation, autonomic activity, inflammatory signalling, hemodynamics, and fibrosis, subsequently leading to cardiovascular damage. Recently published studies (RALES, EPHESUS) convincingly support the concept of detrimental cardiovascular aldosterone actions even during chronic ACE-inhibition. In addition to those cardiovascular effects, aldosterone antagonism has beneficial impacts on ascites, chronic renal disease, renal volume regulation, and hypokalemia induced by diuretics. Of note, aldosterone dependent mechanisms are believed to be even involved in essential hypertension, and the value of aldosterone antagonism is currently tested in those patients. In conclusion, an old-fashioned, previously abandoned treatment strategy is currently celebrating its revival.

Aldosterone↗
PubMed2004

[Extracardiac causes of right ventricular insufficiency].

Evidence for manifest right ventricular dysfunction is considered a critical threshold in the development of a fatal event after acute pulmonary embolism. While the acute event impressively reflects the clinical significance of right ventricular function, various disorders such as idiopathic pulmonary arterial hypertension, secondary pulmonary hypertension in lung diseases, carcinoid heart disease, and portopulmonary hypertension can lead to chronic right ventricular failure. Adapted treatment makes it possible to alleviate the patients' distress and presumably also improve the prognosis. The clinical picture of right ventricular insufficiency can also be imitated in constrictive or adhesive pericarditis and pericardial tamponade. Pericardiocentesis of the tamponade provides initial hemodynamic improvement. Causal treatment is based on cytological findings and/or results of epicardial or pericardial biopsy to classify malignant and nonmalignant effusions. Cardiac surgery with pericardiolysis and (partial) pericardial resection remains the method of choice for symptomatic constrictive pericarditis.

Acute Disease↗
PubMed2004

Escape from cardiomyocyte apoptosis by enterovirus persistence due to elevated soluble Fas-receptors.

BACKGROUND: Apoptosis causes loss of contractile cardiomyocytes in inflammatory heart disease. Despite recent examinations, the influence of virus infection on apoptosis remained ill-defined. METHODS: Apoptosis was assessed in left ventricular endomyocardial biopsies by the TUNEL method frompatients with chronic myocarditis and adeno-, cytomegalo- and enterovirus persistence. Soluble Fas-ligands, sFas-receptors, TNF-alpha, IL-6, IL-10 and IFN-gamma were measured using ELISA technique. RESULTS: Elevated (P < 0.05) rates of apoptosis were found in patients with autoimmune myocarditis. Apoptosis was increased (P < 0.05) in the case of cytomegalovirus persistence, but not significantly increased in the presence of adenoviral genome. No evidence for apoptosis, but elevated concentrations of soluble Fas-receptors were found only in the case of enterovirus persistence. In turn, elevated percentages of apoptosis and normal soluble Fas-receptor concentrations were found in patients with chronic myocarditis. Serum levels of soluble Fas-ligands, TNF-alpha, IL-6, IL-10 and IFN-gamma did not predict changes in TUNEL-positivity. CONCLUSIONS: Escape mechanisms to protect cardiomyocytes from apoptosis are yet not known for enterovirus infections. Soluble Fas-receptors have to be considered to counteract binding of soluble Fas-ligands that results in the blockade of apoptosis induction. It is a new finding that soluble Fasreceptors were elevated in the presence of enterovirus genome in the heart. Inhibition of apoptosis can impair virus clearing and prolong its replication with a potential worse outcome. In turn, sufficient protection from apoptosis in autoimmune myocarditis should reduce loss of cardiomyocytes. Therefore, the interaction of the Fas components could provide a new therapeutic target in myocarditis.

Adenoviridae Infections↗
PubMed2004

Giant left atrial mass in an asymptomatic patient.

A large atrial myxoma, attached in an atypical location, was identified in the left atrium of a 70 year old patient. Although the tumour occupied a large part of the left atrium the patient remained in sinus rhythm and displayed no symptoms.

Aged↗
PubMed2003

[LDL-Apheresis for the treatment of hyperchylomicronemia-induced pancreatitis].

Severe hyperchylomicronemia due to defects of lipoprotein lipase or apoC-II is a rare cause for acute pancreatitis. Food with a high content of fat, as well as alcoholic or hormonal influences, can lead to excessive hypertriglyceridemia. Especially hyperchylomicronemia due to hormonal influences during pregnancy are troublesome. Here, we are confronted with both the risk to the mother as well as the vital risk to the unborn. Conventional plasma apheresis has been used to successfully eliminate chylomicrons and, thus, the primary cause of chylomicron-induced pancreatitis. Most recently, we reported the use of selective LDL-apheresis in a 24-year-old pregnant woman (thirteenth week of pregnancy), who was admitted with the signs of acute pancreatitis to our hospital. The patient was known to have a history of severe hyperchylomicronemia and she had also been treated several years before for acute pancreatitis by LDL-apheresis. Her triglycerides were severely elevated (11500 mg/dl) and, in order to achieve a rapid decrease of chylomicrons, we decided to treat her by selective LDL-apheresis utilizing HELP-apheresis. The treatment was well tolerated and within half an hour the patient was free of any abdominal pain. However, due to the enormous triglyceride load, we needed to change the precipitate filters several times and at the end of the treatment triglyceride levels were 6600 mg/dl. Under a low-fat diet (<30 gram fat per day), the follow-up was uneventful and the patient delivered a healthy baby at the end of week 39. We conclude that LDL-apheresis is a safe and rapid procedure to eliminate chylomicrons in chylomicron-induced pancreatitis.

Adult↗
PubMed2003

In vitro simulation of therapeutic plasmatic fibrinolysis.

One type of therapy for thromboembolism is plasmatic thrombolysis. Several plasminogen activators (PA) are clinically available, including urokinase (u-PA), tissue plasminogen activator (t-PA), streptokinase (SK), plasminogen-streptokinase-activator-complex (PSAC), or mutants of t-PA such as reteplase (RP) or tenecteplase (TP). Therapeutic plasmatic fibrinolysis was simulated, using the PA at relevant plasma concentrations, and plasmin (Pli) and PA activities were determined. Normal citrated plasma was supplemented with 31 to 1,000 IU/mL u-PA, 0.31 to 20 microg/mL t-PA, 125 to 4,000 IU/mL SK, 12.5 to 400 U/mL PSAC, 125 to 4,000 U/mL RP, or 0.31 to 10 microg/mL TP. Ten IU/mL urokinase was also incubated with pooled plasma of stroke patients, that was previously oxidized with the singlet oxygen (1O2) donor chloramine T (CT), to destroy plasmatic PAI-1 and alpha2-antiplasmin. After 0 to 80 minutes (37 degrees C), 50-microL samples were withdrawn and added to 100 microL 1.5 M arginine, pH 8.7, and oxidized with 50 microL of 20 mM CT. For determination of plasmin activity, 10 microL thereof was incubated with 150 microL 1.5 M arginine, pH 8.7, and 100 microL 20 mM CT preoxidized (15 minutes 37 degrees C) pooled normal citrate buffered EDTA-plasma for 30 minutes (37 degrees C). For determination of [PA+Pli]-activity, arginine was added after this incubation. 25-microL 6 mM Val-Leu-Lys-pNA were added and deltaA/h at room temperature (RT) was monitored, using a microtiterplate reader. [PA+Pli]-Pli = PA. The PA concentration required to induce 25% [ED25] of the maximally inducible Pli-activity in plasma (= 1 U/mL = 45 mg/L = 0.53 micromol/L active Pli; deltaA = 363 +/- 8 mA/h RT) after 10 minutes (37 degrees C) were 320 IU/mL u-PA, 8 microg/mL t-PA, 140 U/mL PSAC, 6,000 IU/mL SK, 720 U/mL RP, and approximately 150 microg/mL TP. The approximate activity half-lives of the PA in plasma were 30 minutes for u-PA, 30 minutes for t-PA, greater than 80 minutes for SK, greater than 80 minutes for PSAC, 50 minutes for RP, and 80 minutes for TP. The present study shows--for the first time--a combined kinetic in vitro simulation of the plasmatic activity of six different PAs. At clinically used concentrations, RP induces the highest plasmatic Pli activity. Due to unselective generation of plasmin in plasma, all PA are of some danger in inducing severe hemorrhagias. Clinical thrombolysis might be improved by usage of more physiologic activators of thrombolysis, such as activators of polymorphonuclear neutrophils.

Fibrinolysin↗
PubMed2002

Intrapericardial treatment of autoreactive pericardial effusion with triamcinolone; the way to avoid side effects of systemic corticosteroid therapy.

AIMS: To evaluate efficacy and safety of intrapericardial treatment with the crystalloid corticosteroid triamcinolone in autoreactive pericardial effusion. METHODS AND RESULTS: Two hundred and sixty consecutive patients with pericarditis/myopericarditis underwent pericardiocentesis, pericardioscopy (Storz-AF1101B1), and epicardial biopsy with pericardial fluid and tissue analyses. By polymerase chain reaction for cardiotropic viruses/bacteria in pericardial effusion and epicardial biopsies as well as by immunohistochemistry and immunocytochemistry of epicardial and endomyocardial biopsies, 84/260 patients were classified as autoreactive pericarditis and underwent intrapericardial instillation of triamcinolone (group 1: 54 patients, 50% males, mean age 48.9 +/- 14.3 years, triamcinolone 600 mg x m(-2) x 24 h(-1); group 2: 30 patients, 46.7% males, mean age 52.5 +/- 12.7 years, triamcinolone 300 mg x m(-2) x 24 h(-1)). Intrapericardial administration of triamcinolone resulted in symptomatic improvement and prevented effusion recurrence in 92.6% vs 86.7% of the patients after 3 months and in 86.0% vs 82.1% after 1 year in groups 1 and 2, respectively (P>0.05). There were no treatment-related acute complications. During the follow-up, 29.6% of the patients developed transitory iatrogenic Cushing syndrome in group 1 in contrast to 13.3% in group 2 (P<0.05). Conclusion Intrapericardial treatment of autoreactive pericarditis with 300 mg x m(-2) x 24 h(-1) of triamcinolone prevented recurrence of symptoms and relapse of effusion as effectively as the 600 mg x m(-2) x 24 h(-1) regimen, but with significantly fewer side effects.

Adult↗
PubMed2002

Neoplastic pericardial effusion. Efficacy and safety of intrapericardial treatment with cisplatin.

AIMS: To evaluate the clinical efficacy, safety, and long-term effect of intrapericardial treatment with cisplatin in large neoplastic pericardial effusions. METHODS AND RESULTS: Out of the registry of 260 patients undergoing pericardiocentesis, 42 patients with neoplastic pericardial effusion (69% males, mean age 58.8+/-13.2 years) were selected for treatment with cisplatin (single instillation of 30 mg.m(-2) x 24h(-1)) in addition to the tumour-specific systemic chemotherapy. All patients underwent clinical examination, echocardiography, pericardiocentesis, pericardioscopy, and epicardial biopsy. Pericardial effusion and biopsy analyses included biochemistry, cytology, serology, microbiology, histology, immunohistology, and PCR. The following malignancies were established: lung cancer, 52.4%; breast cancer, 19.0%; Hodgkin's disease, 4.8%; oesophageal cancer, 2.4%; mesothelioma, 2.4%; colon cancer, 4.8%; and undifferentiated cancer of unknown origin, 14.2%. Cisplatin appeared to prevent recurrence of pericardial effusion during the first 3 months of the follow-up in 92.8%, and after 6 months in 83.3% of the patients. Lung cancer patients had fewer effusion relapses at the 6 months follow-up (4.5%) than breast cancer patients (37.5%)(P<0.05). Myocardial ischemia occurred after 1/42 cisplatin instillations, but there were no other complications. CONCLUSION: Intrapericardial treatment with cisplatin appeared to successfully prevent recurrences of neoplastic pericardial effusion. The treatment was more successful in lung than in breast cancer patients.

Aged↗
PubMed2002

[Amiodarone induced pulmonary toxicity].

BACKGROUND: Antiarrhythmic therapy with class III drug amiodarone (Cordarex(R)) for supraventricular and ventricular tachycardia is commonly used because of its high efficacy and absent negative inotropy. Pulmonary toxicity of amiodarone possibly leading to lung fibrosis is a rare, but severe side effect of chronic therapy. In contrast to patients with coronary artery disease, there are only a few data about pulmonary toxicity in patients with dilated cardiomyopathy. CASE REPORT: We report on two patients with dilated cardiomyopathy who received amiodarone because of symptomatic non-sustained or sustained ventricular tachycardia. After 6 weeks resp. 8 months of treatment with amiodarone both patients developed pulmonary toxicity. Other causes of pulmonary toxicity were ruled out by bronchoscopy, bronchoalveolar lavage and biopsy. Pulmonary function improved in both patients within some weeks after discontinuation of amiodarone. CONCLUSIONS: This report deals with two cases of amiodarone induced pulmonary toxicity in dilated cardiomyopathy leading to respiratory insufficiency. Pulmonary toxicity is a rare, but potentially lethal side effect of amiodarone. Reversibility of pulmonary changes in case of an early drug discontinuation is shown. Because of severe reduced left ventricular function in dilated cardiomyopathy, heart failure symptoms could conceal clinical signs of pulmonary amiodarone toxicity. Therefore, pulmonary function should be controlled periodically during amiodarone therapy including bronchoscopy, bronchoalveolar lavage, biopsy and measurement of diffusion capacity.

Adult↗
PubMed2001

The genotoxic risk of hospital, pharmacy and medical personnel occupationally exposed to cytostatic drugs--evaluation by the micronucleus assay.

The aim of this study was to evaluate the genotoxicity of cytostatic drugs in hospital and pharmacy employees (n=100), occupationally exposed. The micronucleus assay was used to study lymphocytes in 247 peripheral blood samples. Samples were collected at "baseline level" without any cytostatic drugs exposure before recruiting or after at least 3 weeks without cytostatic drugs contact and at three times (cycle 1-3) post-exposure. Samples from 60 office employees served as controls. Furthermore, our results were compared to urinary analyses of cytostatic drugs (oxazaphosporines, anthracyclines, platinum) which were collected in parallel to the cytogenetic investigation. Statistical analyses were performed under consideration of age, gender and X-ray exposure. The frequency of micronuclei was significantly related to the age of the subjects (r(Spearman)=0.16; P<0.05). However, there were no significant differences in micronucleus rates between controls and exposed hospital workers. Similarly, micronucleus rates were not significantly different at the various sampling time points and there was no correlation between duration of employment and micronucleus rates. Furthermore, no correlation between current biomonitoring data of exposure (urine tests) and micronuclei frequency was found. Therefore, significantly increased genotoxic damage of the lymphocytes investigated in this study could not be demonstrated.

Antineoplastic Agents↗
PubMed2001

[ Update 2001. Myocarditis--cardiomyopathy].

Myocarditis is a common cardiological disease. New molecular biological and immunohistological methods have confirmed the persistence of viral infection and chronic myocardial inflammation in a considerable number of patients. A causal link between viral myocarditis and the development of dilated cardiomyopathy has been recognized. This has prognostic implications and helps for the decision of a specific immunosuppressive, immunomodulatory and antiviral therapy.

Antihypertensive Agents↗
PubMed2001

[Fulminant course of falciparum malaria].

HISTORY AND ADMISSION FINDINGS: A 57-year-old white man had been travelling in Kenya for vacation until 14 days before admission. Due to apprehension about side effects, the patient had refused any malaria prophylaxis. Ten days before admission he developed low grade temperatures and suffered from pain in the limbs, from nausea and vomiting. A new episode of tachyarrhythmia was diagnosed two days before admission and was treated by his general practitioner. Finally he was admitted to our hospital because of high temperatures, chills and progressive clinical deterioration. Autopsy revealed prominent congestion of liver, spleen and cerebral vessels as well as subdural and subarachnoidal hemorrhage. INVESTIGATIONS: In both thin and thick peripheral blood smears Plasmodium parasites were demonstrated in approximately 30% of the eryhthrocytes and the diagnosis of Plasmodium falciparum was immediately confirmed by an immunological test. TREATMENT AND COURSE: Due to the fulminant clinical and neurological deterioration with progressive hypoxaemia, the patient required ventilator therapy already one hour after admission. Therapy with chinine and doxycycline was initiated and exchange transfusion was considered. However, due to hyperkalaemia and cardiac arrest, the patient died 4 hours after admission due to parasitic hemolysis. CONCLUSIONS: Severe Plasmodium falciparum infection in non-immunized patients is a medical emergency and requires immediate diagnosis and treatment. Malaria should always be considered in the differential diagnosis in persons who have travelled to endemic areas and presenting not only with temperatures, but also with non-specific clinical signs, like cardiac arrhythmias. Although never entirely effective, chemoprophylaxis is highly recommended.

Anti-Bacterial Agents↗
PubMed2001

[Prevention of atrial arrhythmias by pacing].

BACKGROUND: Atrial fibrillation is the most frequent arrhythmia. It can impair quality of life considerably. Due to thromboembolic complications it contributes to the patients' morbidity and mortality and to the costs for their medical treatment. PREVENTION: In chronic atrial fibrillation there is a need for adequate anticoagulation and heart rate control. In paroxysmal and intermittent atrial fibrillation it should be sought to prevent its progression to chronic atrial fibrillation. Since atrial fibrillation initiates negative processes of remodeling within the atrial myocardium, it has the tendency to perpetuate itself. From a theoretical point of view, it can be expected that all means which prevent episodes of atrial fibrillation or which terminate it immediately after its onset, are able to prevent or at least to delay the progression to chronic atrial fibrillation. Pharmacologic treatment is usually used to prevent recurrences of atrial fibrillation. Based on the actual data it can also be expected that pacemakers with special preventive pacing algorithms are able to reduce the atrial arrhythmic burden. Besides consequent overdrive pacing, more sophisticated algorithms like "suppression of premature atrial contractions", "post exercise response", "automatic rest rate" or "post mode-switch pacing" have been developed. They can be applied either alone or in combination with special lead positions (interatrial septal pacing or pacing of the triangle of Koch) or special stimulation configurations like dual site right atrial pacing or biatrial pacing. These pacing strategies cover the most relevant onset mechanisms of atrial fibrillation. Furthermore, there are algorithms to treat atrial tachyarrhythmias actively by antitachycardia pacing (ATP). First clinical results have shown that about 2/3 of the diagnosed atrial tachyarrhythmias could be terminated by these means immediately after their onset. ONGOING TRIALS: This article gives an overview over the principles of pacing in the management of atrial arrhythmias and ongoing clinical trials in this field. Before a definite judgement on the clinical relevance of these new preventive and therapeutic pacing strategies can be given, the results of these ongoing controlled clinical studies have to be analyzed.

Algorithms↗