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Biomedical subjects

Bernhard Maisch

Publications and source records attributed to Bernhard Maisch.

At least 19 recordsLinked to original sources
PubMed2007

Osteoprotegerin expression in dendritic cells increases with maturation and is NF-kappaB-dependent.

Dendritic cells (DC) comprise a unique leukocyte population which controls primary immune responses. Recent studies indicate that DC express osteoprotegerin (OPG), a secreted tumor necrosis factor receptor homolog, which regulates DC survival, monocyte chemotaxis, and B cell development and function by ligating TNF family member receptor activator of NF-kappaB ligand (RANKL). The precise regulators of OPG expression in DC have not been investigated. In this study, we assessed OPG mRNA steady state levels by Northern blot analysis and OPG protein secretion by an immunoassay in monocyte-derived DC of different maturation, and the effect of different cytokines and hormones on OPG expression. OPG was upregulated with maturation of DC, whereas pretreatment of DC with 1alpha,25(OH)(2) vitamin D(3), tamoxifen, or dexamethasone, agents that inhibit differentiation of DC, decreased OPG expression. In vivo, OPG was found to be colocalized with mature CD83(+) DC in human tonsils by immunofluorescence confocal microscopy analysis. Furthermore, OPG was upregulated by TNF superfamily members TNF-alpha, anti-CD40, and RANKL, and by ligands of the Toll-like/IL-1 receptor family including IL-1beta, double-stranded RNA (poly I:C), or lipopolysaccharide (LPS), all of which induce maturation of DC. Gene silencing by small interfering RNA (siRNA) directed against transcription factor NF-kappaB abrogated the expression of OPG as demonstrated by real-time PCR. In summary, we describe that the expression of OPG by DC increases with maturation and is NF-kappaB-dependent, possibly regulating immune responses in lymphoid tissues.

Blotting, Northern↗
PubMed2006

Clinical and immunologic characteristics in peripartum cardiomyopathy.

Peripartum cardiomyopathy (PPCM) is a rare disorder of dilated cardiomyopathy and left ventricular dysfunction occurring in the last month of pregnancy or within 5 months postpartum. Outcome of PPCM is highly variable, comprising clinical improvement and rapid deterioration unresponsive to medical treatment requiring heart transplantation or even death. In this study, we report the clinicopathologic findings of 10 patients with PPCM who were retrospectively identified in our cardiomyopathy registry. During a follow-up of 69+/-27 months, no patient died or required orthotopic heart transplantation. Left ventricular ejection fraction was 38+/-7% at the time of diagnosis and 53+/-7% during follow-up. While all patients had sinus rhythm at the time of diagnosis, three patients presented with left bundle branch block. We found no evidence of viral infection in endomyocardial biopsy samples of seven patients by PCR. Histopathologic findings revealed the presence borderline myocarditis in two of seven patients (29%). Circulating autoantibodies to cardiac tissue of any kind were observed in all patients. In conclusion, in our retrospective observational study, no patient diagnosed with PPCM died or received orthotopic heart transplantation. Improvement of left ventricular ejection fraction was present in eight patients (80%), while LV dysfunction persisted in four patients. Our findings support the hypothesis of an underlying autoimmune pathomechanism in this rare disease.

Adult↗
PubMed2006

Non-compaction cardiomyopathy in an adult with hereditary spherocytosis.

A 23-year old male (199 cm, 88 kg) presented muscular weakness due to skeletal myopathy and symptoms of heart failure NYHA functional class II. Total creatine kinase was increased up to 830 U/l, but troponin was negative. Prior episodes of intermittent atrial fibrillation were reported and 6 years ago splenectomy was performed due to hereditary spherocytosis. Cardiac magnetic resonance imaging revealed the spongy appearance of non-compacted left ventricular myocardium. This impaired fetal morphogenesis occurred predominantly in the apical to midventricular anterior, lateral and inferior segments. Non-compaction cardiomyopathy was initially described in paediatric patients. Occasional associations with other congenital disorders are known, e.g., Barth syndrome, which is an X-linked disease characterized by cardio-skeletal myopathy of variable severity and neutropenia. To our knowledge, combined occurrence of non-compaction cardiomyopathy, skeletal myopathy and hereditary spherocytosis has not previously been reported.

Adult↗
PubMed2006

Endomyocardial fibrosis in Churg-Strauss syndrome assessed by cardiac magnetic resonance imaging.

Cardiac involvement frequently occurs in hypereosinophilic syndrome. The endocardium seems to be most susceptible to disturbances deriving from eosinophilia as seen in Loeffler's endocarditis. Hypereosinophilia and cardiac involvement are also seen in Churg-Strauss syndrome. The present report deals with a patient with Churg-Strauss syndrome who exhibited marked endomyocardial fibrosis that was visualized by cardiac magnetic resonance imaging. Loeffler's endocarditis is the classical endocardial manifestation of hypereosinophilic syndrome. Similarities between Loeffler and Churg-Strauss syndromes had been described previously. Potentially, endocardial involvement is more common even in Churg-Strauss syndrome than expected so far. The significance of these findings remains to be shown.

Adult↗
PubMed2006

Familial inflammatory dilated cardiomyopathy.

BACKGROUND: Systematic family screening has recently identified dilated cardiomyopathy as an inherited disorder in up to 30% of cases. Mutations in genes encoding proteins responsible for myocardial architecture have been identified, but additional pathophysiological mechanisms including inflammatory reactions have been proposed. AIMS: Identification and characterization of familial DCM, where at least one affected family member fulfils the criteria for inflammatory DCM may lead to a better understanding of the aetiology and pathogenesis of (inflammatory) DCM. METHODS AND RESULTS: Ten families were examined. In six families, clinical characteristics and mode of inheritance were compatible with pure fDCM, fDCM with conduction defect and autosomal recessive fDCM. In four families, (auto-)immune features were diagnosed in affected and non-affected family members. CONCLUSIONS: Familial DCM with an inflammatory component was identified as a specific subgroup of familial DCM. In most cases, the inflammatory process seems to modify, i.e. aggravate, the "classic, cytoskeletopathic" familial DCM, but in some, especially when taking clinical and genetic aspects into account, inflammatory (auto-)immune features can be addressed as the leading pathogenetic principle. Further elucidation of these families may provide a better insight into pathophysiologic processes and may aid in the development of specific therapeutic strategies.

Adult↗
PubMed2006

Echocardiographic findings mimicking type A aortic dissection.

BACKGROUND: Type A aortic dissection is a rare, but life-threatening disease. The prognosis is determined by an accurate and immediate diagnosis. CASE STUDY: A patient with suspected type A dissection based on outward transesophageal echocardiography (TEE) findings is reported. Renewed TEE showed dilation of the ascending aorta with pronounced wall thickness. A membrane-like structure was found in the ascending aorta. M-mode technique revealed movement of the suspected membrane that was partially in parallel to the aortic wall. Thus, there were severe doubts on the presence of type A dissection. By contrast, typical intimal rupture was found in the descending aorta. Computed tomography (CT) and angiography showed aortic dilation and an extended wall hematoma deriving from the entry at the descending part. There was no evidence of type A dissection. CONCLUSION: TEE is a noninvasive diagnostic tool to assess aortic dissection of type A with a sensitivity of 90-98% that is equal to CT or magnetic resonance imaging (MRI) solely. Complementary use of CT or MRI could improve the diagnostic accuracy. False-positive findings could result from echocardiographic artifacts concealing an intimal flap in the ascending aorta. Echo reverberations in dilated or calcified aortas had been judged to account for this phenomenon. In the present case, it could be assumed that the extended wall hematoma in accordance with vessel dilation mimicked the membrane-like structure. Oscillation or flutter of the suspicious intimal flap independently of aortal wall movement seem to be mandatory to avoid false-positive diagnoses. Ancillary findings such as flow signals, intimal fenestration or thrombosis are helpful to enhance the diagnostic specificity of TEE.

Aortic Dissection↗
PubMed2006

Molecular basis of obesity and the risk for cardiovascular disease.

Atherosclerosis and cardiovascular disease (CVD) are the main causes of death in the Western world, for both men and women. The onset and development of diseases of the cardiovascular and cerebrovascular system are strongly dependent on multiple risk factors that promote pathologic conditions like atherosclerosis, hypertension and thrombosis. Besides genetic factors also environmental influences such as diet composition are known to be closely related to CVD. In this context obesity has been postulated as an independent cardiovascular risk factor. Data from the Framingham Heart Study have consistently shown that increasing degrees of obesity are accompanied by greater rates of CVD. At present, obesity affects 10-35% of the European and US population and increases steadily. As obesity is a serious health problem which promotes metabolic abnormalities (insulin resistance, hyperinsulinemia and dyslipidemia) and dramatically increases the risk for CVD, this review will focus on the epidemiologic and genetic background of obesity. Furthermore, the molecular mechanisms involved in obesity development and their contribution to CVD will be discussed.

Adipose Tissue↗
PubMed2006

Acute heart failure--basic pathomechanism and new drug targets.

In view of the high incidence of heart failure and sudden cardiac death, efforts in the development of compounds which target-specific mechanisms such as a reduced expression of SERCA2, the Ca2+ pump of sarcoplasmic reticulum, of hypertrophied cardiomyocytes of pressure-overloaded or infarcted hearts should be strengthened. Lead compounds for correcting a dysregulated gene expression are the carnitine palmitoyltransferase-1 (CPT-1) inhibitors etomoxir and oxfenicine. Since bypassing the CPT-1 inhibition by a medium-chain fatty acid diet had a lesser effect on myosin V1 proportion than on lipid droplet number, one has to infer also other mechanisms such as PPARalpha activation (FOXIB/PPARalpha). In view of the intricate interrelationship between depressed pump function and malignant arrhythmias, stimulation of endogenous antiarrhythmogenic mechanisms linked to an enhanced production of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) could potentially provide alternatives to the administration of 1 g EPA and DHA ethyl esters (minimum 84% EPA + DHA) for secondary prevention of myocardial infarction. The apparently greater efficacy of omega-3 fatty acids in post-myocardial infarction patients (GISSI-Prevention study) compared with ICD patients (SOFA study) can be attributed to the greater ischemia-induced release of membrane-bound EPA and DHA and a better compliance (one vs. four capsules daily).

Acute Disease↗
PubMed2006

Management strategies in pericardial emergencies.

BACKGROUND: The most frequent pericardial emergency is cardiac tamponade, but complications of an acute coronary syndrome and aortic dissection may also involve the pericardium. Acute pericarditis can also represent a medical emergency due to chest pain of upsetting intensity. Decompensations in chronic advanced constriction and in the clinical course of purulent pericarditis necessitate critical care as well. DIAGNOSIS AND MANAGEMENT: The diagnosis of cardiac tamponade is based on clinical presentation and physical findings, confirmed by echocardiography and cardiac catheterization. Tamponade is an absolute indication for urgent drainage, either by pericardiocentesis or surgical pericardiotomy. The approach for pericardiocentesis can be subxiphoid or intercostal using echocardiographic or fluoroscopic guidance. Urgent drainage, combined with intravenous antibiotics, is also mandatory in suspected purulent pericarditis. If confirmed, it should be combined with intrapericardial rinsing (best by a surgical drainage). Pericardiocentesis is contraindicated in cardiac tamponade complicating aortic dissection. This condition should immediately lead to cardiac surgery. Although pericardiectomy is the only treatment for permanent constriction, this procedure is contraindicated when extensive myocardial fibrosis and/or atrophy are demonstrated. CASE STUDY: Iatrogenic tamponade may occur during percutaneous mitral valvuloplasty, implantation of pacemakers, electrophysiology and radiofrequency ablation procedures, right ventricular endomyocardial biopsy, percutaneous coronary interventions, and rarely during Swan-Ganz catheterization. The authors report on a 79-year-old who suffered coronary perforation and cardiac tamponade during elective stent implantation. Tamponade was successfully treated with pericardiocentesis and implantation of a membrane-covered graft stent. Subsequent recurrent pericarditis/postpericardial injury syndrome with moderate pericardial effusion was initially treated with aspirin and then with aspirin and colchicine. At 6 months, the patient is in stable remission even after withdrawal of colchicine. CONCLUSION: Natural history of pericardial diseases can be complicated with pericardial emergencies requiring prompt diagnosis, intensive care with hemodynamic monitoring, and early aggressive management. Medical supportive measures, drainage of pericardial effusion, surgical pericardiotomy, and pericardiectomy should be applied when needed with no delay. This procedural approach also applies to iatrogenic interventions leading to tamponade.

Aged↗
PubMed2006

Management of patients with suspected (peri-)myocarditis and inflammatory dilated cardiomyopathy.

Inflammatory cardiomyopathy and myocarditis are considered acquired forms of dilated cardiomyopathy. Whereas consensus documents on the diagnosis of myocarditis and perimyocarditis do exist, guidelines on the specific treatment have been established only for the management of pericardial diseases, which at least partly can be applied in analogy to myocarditis. Presently, feasible clinical pathways are available, which can lead to a correct diagnosis and specific treatment. This is illustrated with two cases of fulminant myocarditis, in one with successful diagnosis and treatment of a cardiac sarcoid and another one in which diagnostic nihilism led to a lethal outcome in giant cell myocarditis at necropsy. A case of active parvo B19-positive myocarditis demonstrates the role of immunoglobulin treatment under these conditions.

Adult↗
PubMed2006

Heart rate variability in patients with cardiac hypertrophy--relation to left ventricular mass and etiology.

BACKGROUND: Decreased heart rate variability (HRV) has been shown to reflect disturbances of the autonomic nervous system that is related to increased cardiovascular mortality. Most studies investigated HRV in patients with systolic left ventricular dysfunction due to remote myocardial infarction or dilated cardiomyopathy. To date, only few data are available on HRV in patients with predominant diastolic dysfunction in the presence of cardiac hypertrophy of different etiologies. METHODS: Time domain analysis of HRV was performed from digital 24-hour Holter electrocardiogram recordings in 86 patients with sinus rhythm and cardiac hypertrophy, which was due to aortic valve stenosis in 33 patients, hypertrophic cardiomyopathy in 29 patients, and hypertensive heart disease in 24 patients. Heart rate variability analysis was compared with 91 healthy controls. RESULTS: The SD of all normal-to-normal R-R intervals (SDNN) was reduced in patients with aortic valve stenosis, hypertrophic cardiomyopathy, and hypertensive heart disease when compared with controls (SDNN 119 +/- 42 vs 154 +/- 36 milliseconds, P < .001). The extent of cardiac hypertrophy indexed by echocardiography based left ventricular mass calculation and increased patient age were independent predictors for depression of SDNN. CONCLUSIONS: Cardiac hypertrophy of various etiologies is related to decreased HRV on 24-hour Holter electrocardiogram. Both the patient age and the extent of left ventricular hypertrophy are independently associated with depression of HRV. These findings are independent of the cause of cardiac hypertrophy. The significance of these findings remains to be determined by future studies.

Aged↗
PubMed2006

Asymmetric dimethylarginine is an independent risk factor for coronary heart disease: results from the multicenter Coronary Artery Risk Determination investigating the Influence of ADMA Concentration (CARDIAC) study.

BACKGROUND: Asymmetric dimethylarginine (ADMA) plasma levels have been shown to be elevated in diseases related to endothelial dysfunction such as hypertension, hyperlipidemia, diabetes mellitus, and others. It has been shown that ADMA predicts cardiovascular mortality in patients who have coronary heart disease (CHD). However, the question whether ADMA is an independent risk factor for CHD still remains unresolved. METHODS: The CARDIAC study is a multicenter case-control study, designed to detect differences in ADMA plasma levels between patients with CHD and controls from the general population. We included in our analysis 131 cases and 131 controls, matched for age, sex, and body mass index. RESULTS: We found that cases had higher ADMA plasma levels than controls (0.70 micromol/L [0.59-0.87 micromol/L] vs 0.60 micromol/L [0.54-0.69 micromol/L], P < .001). To evaluate the predictive power of ADMA regarding CHD, we calculated 2 multivariate logistic regression models including laboratory parameters and traditional risk factors. The odds ratio for ADMA in the multivariate model including the laboratory characteristics was 2.59 (1.61-4.17; P < .001); the odds ratio for the multivariate model including other risk factors was 6.04 (2.56-14.25; P < .001) for the third tertile (>0.72 micromol/L) versus the first (<0.58 micromol/L). CONCLUSIONS: We conclude from the results of our study that ADMA is an independent risk factor for CHD.

Aged↗