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Bernhard Maisch

Publications and source records attributed to Bernhard Maisch.

At least 73 records · Page 4Linked to original sources
PubMed2004

A new but frequent mutation of apoB-100-apoB His3543Tyr.

ApolipoproteinB 100 (apoB-100) is an important component of atherogenic lipoproteins such as LDL and serves as a ligand for the LDL-receptor. Familial defective apolipoproteinB 100 (FDB) is caused by a R3500Q mutation of the apoB gene and results in decreased binding of LDL to the LDL-receptor. So far FDB is the most frequent and best studied alteration of apoB-100. Apart from this, three other apoB mutations, R3500W, R3531C and R3480W, affecting binding to the LDL-receptor are known to date. We screened the apoB gene segment of codons 3448-3561 by denaturing gradient gel electrophoresis (DGGE) analysis in a total of 853 consecutively sampled German patients undergoing diagnostic coronary angiography for suspected CAD. By this, a new single base mutation was detected and confirmed by DNA sequencing. The mutation, CAC(3543)TAC results in a His3543Tyr substitution in apoB-100 (H3543Y). The prevalence of heterozygotes for H3543Y in the study population was 0.47% compared to 0.12% for the known Arg 3500 Gln (R3500Q) mutation. In conclusion, the new mutation is four times more frequent than "classical" FDB and thus appears to be the most common apoB mutation in Germany.

Adult↗
PubMed2004

Detection of anti-hsp70 immunoglobulin G antibodies indicates better outcome in coronary artery bypass grafting patients suffering from severe preoperative angina.

BACKGROUND: Recent findings indicate that molecular chaperones actively participate in myocardial cytoprotection. Moreover, ischemic tolerance can be induced in humans by brief ischemic events. Therefore, we investigated patients with severe angina attacks before coronary artery bypass grafting. We focused on appearance of anti-hsp70 antibodies as an immunologic response to heat shock protein induction by ischemia followed up by hemodynamic measurements perioperatively. We correlated these clinical findings with the presence of antibodies against hsp70 and the antioxidative capacity of patients' sera. METHODS: Thirty-five consecutive patients with coronary artery disease scheduled for coronary artery bypass grafting were included. Seventeen patients had severe angina, and 18 patients suffered from chronic stable angina preoperatively. In the patients' sera, antibodies against hsp70 were detected by enzyme-linked immunosorbent assay, and antioxidative capacity was detected using the chromogen assay. Cardiac output and pulmonary capillary wedge pressure were measured using a thermodilution catheter. We also evaluated C-reactive protein and creatine kinase MB isoenzyme, and performed a conventional leukocyte count. RESULTS: The sera of the 17 patients with severe angina attacks before surgery contained antibodies against hsp70 and a low antioxidative capacity. The interval between a severe angina attack and anti-hsp70 antibody titer are inversely correlated. These patients had better cardiac output and lower pulmonary capillary wedge pressure values after surgery. CONCLUSIONS: Severe angina before cardiac surgery coincided with an improved outcome as measured by hemodynamic variables as compared with chronic stable angina. This finding correlated significantly with a low antioxidative capacity and the presence of antibodies against hsp70. These pathophysiologic mechanisms might therefore play a role in myocardial protection.

Aged↗
PubMed2004

Long-term survival with acquired ventricular septal defect after myocardial infarction.

Acquired ventricular septal defects (VSD) are rare and devastating complications after myocardial infarction. The long-term prognosis with medical therapy is extremely poor. We report on a patient who developed progressive heart failure within 3 months after myocardial infarction due to an unknown VSD. The left ventricular function was severely impaired. After diagnosing VSD by echocardiography, surgical occlusion was performed. In addition, a biventricular pacemaker was applied using epicardial leads. The patient recovered almost completely 6 weeks postoperative. Beside hemodynamic changes, biventricular pacing is potentially sufficient to improve the postoperative outcome of patients with severe heart failure in these conditions.

Aged↗
PubMed2004

Localization of osteoprotegerin, tumor necrosis factor-related apoptosis-inducing ligand, and receptor activator of nuclear factor-kappaB ligand in Mönckeberg's sclerosis and atherosclerosis.

Vascular calcification may occur at different areas of the vessel wall, including the intima in atherosclerosis and the media in Mönckeberg's sclerosis. Medial calcification of arteries is common in patients with diabetes mellitus or chronic renal failure. Osteoprotegerin (OPG) and receptor activator of nuclear factor-kappaB ligand are essential modulators of bone homeostasis and may be involved in the process of vascular calcification. In this study we investigated arteries from patients with Mönckeberg's sclerosis and atherosclerosis. Apoptosis, which precedes vascular calcification in vitro, was assessed by an in situ ligation assay and was localized to the medial layer of arteries (Mönckeberg's sclerosis) and the neointima (atherosclerosis). Immunohistochemistry and in situ hybridization revealed OPG immunoreactivity and mRNA expression surrounding calcified areas in the medial layer (Mönckeberg's sclerosis), whereas OPG was mainly expressed adjacent to calcified neointimal lesions (atherosclerosis). Receptor activator of nuclear factor-kappaB ligand protein and mRNA were barely or not detectable. Of note, TNF-related apoptosis-inducing ligand, an inducer of apoptosis that is also blocked by OPG, displayed a similar spatial distribution as OPG. In summary, we demonstrate enhanced apoptosis adjacent to vascular calcification, and the concurrent expression of regulators of apoptosis and osteoclastic differentiation, TNF-related apoptosis-inducing ligand and OPG, suggesting their involvement in the pathogenesis of vascular calcification.

Aged↗
PubMed2004

Osteoprotegerin gene polymorphisms in men with coronary artery disease.

Osteoprotegerin (OPG) antagonizes receptor activator of nuclear factor-kappaB ligand (RANKL), the principal regulator of osteoclasts. Of note, OPG-deficient mice display osteoporosis and arterial calcification. Recently, OPG gene polymorphisms have been associated with osteoporosis and early predictors of cardiovascular disease. In this study, we examined OPG gene polymorphisms in 468 men who had absence of coronary artery disease (CAD) or single-, double-, or triple-vessel disease on coronary angiography. Denaturing gradient gel electrophoresis followed by DNA sequencing revealed nucleotide substitutions 149 T-->C, 163 A-->G, 209 G-->A, 245 T-->G, 950 T-->C (all promoter), 1181 G-->C (exon 1), and 6890 A-->C (intron 4), respectively. Although single polymorphisms were not associated with CAD, linkage of polymorphisms 950 and 1181 revealed that haplotypes were overrepresented in men with CAD (chi(2) = 17.05; P = 0.03) with an increased risk of CAD in carriers of genotypes 950 TC/1181 GC and 950 CC/1181 CC (odds ratio, 1.67; 95% confidence interval, 1.02-2.72; P = 0.04). Furthermore, serum OPG levels were correlated with the presence of a C allele at position 950 (P = 0.02). In summary, linkage of genetic variations of the OPG gene at positions 950 and 1181 may confer an increased risk of CAD in Caucasian men.

Alleles↗
PubMed2003

Noninvasive arrhythmia risk stratification in idiopathic dilated cardiomyopathy: results of the Marburg Cardiomyopathy Study.

BACKGROUND: Arrhythmia risk stratification with regard to prophylactic implantable cardioverter-defibrillator therapy is a completely unsolved issue in idiopathic dilated cardiomyopathy (IDC). METHODS AND RESULTS: Arrhythmia risk stratification was performed prospectively in 343 patients with IDC, including analysis of left ventricular (LV) ejection fraction and size by echocardiography, signal-averaged ECG, arrhythmias on Holter ECG, QTc dispersion, heart rate variability, baroreflex sensitivity, and microvolt T-wave alternans. During 52+/-21 months of follow-up, major arrhythmic events, defined as sustained ventricular tachycardia, ventricular fibrillation, or sudden death, occurred in 46 patients (13%). On multivariate analysis, LV ejection fraction was the only significant arrhythmia risk predictor in patients with sinus rhythm, with a relative risk of 2.3 per 10% decrease of ejection fraction (95% CI, 1.5 to 3.3; P=0.0001). Nonsustained ventricular tachycardia on Holter was associated with a trend toward higher arrhythmia risk (RR, 1.7; 95% CI, 0.9 to 3.3; P=0.11), whereas beta-blocker therapy was associated with a trend toward lower arrhythmia risk (RR, 0.6; 95% CI, 0.3 to 1.2; P=0.13). In patients with atrial fibrillation, multivariate Cox analysis also identified LV ejection fraction and absence of beta-blocker therapy as the only significant arrhythmia risk predictors. CONCLUSIONS: Reduced LV ejection fraction and lack of beta-blocker use are important arrhythmia risk predictors in IDC, whereas signal-averaged ECG, baroreflex sensitivity, heart rate variability, and T-wave alternans do not seem to be helpful for arrhythmia risk stratification. These findings have important implications for the design of future studies evaluating prophylactic implantable cardioverter-defibrillator therapy in IDC.

Adolescent↗
PubMed2003

Human viral cardiomyopathy.

Viral infection of the heart is relatively common, usually asymptomatic and has a spontaneous and complete resolution. It can, however, in rare cases, lead to substantial cardiac damage, development of viral cardiomyopathy and congestive heart failure. Viral cardiomyopathy is defined as viral persistence in a dilated heart. It may be accompanied by myocardial inflammation and then termed inflammatory viral cardiomyopathy (or viral myocarditis with cardiomegaly). If no inflammation is observed in the biopsy of a dilated heart (<14 lymphocytes and macrophages/mm ) the term viral cardiomyopathy or viral persistence in dilated cardiomyopathy should be applied. The diagnosis of myocarditis and viral cardiomyopathy can be made only by endomyocardial biopsy, implementing the WHO/WHF criteria, and PCR techniques for identification of viral genome. The most frequent cardiotropic viruses detected by endomyocardial biopsy are Parvo B19, enteroviruses, adenoviruses, cytomegalovirus, and less frequently Epstein-Barr virus, and influenza virus.

Animals↗
PubMed2003

[Pregnancy and cardiomyopathies].

This overview on the topic of cardiomyopathy and gestation comprises the diagnostic and therapeutic options of patients with preexistent cardiomyopathies (dilated, hypertrophic, inflammatory, and others) and with cardiomyopathies which have been discovered during or in the 6 months following delivery. CARDIOMYOPATHIES PREEXISTENT BEFORE GESTATION: If cardiomyopathy is present before an intended gestation, the couple should be advised against pregnancy because of the high risk of deterioration both during gestation and peripartum. If pregnancy occurs, according to ESC (European Society of Cardiology) recommendations termination should be advised if the ejection fraction is < 50% and/or the LV dimensions are definitely above normal. If termination is refused, the patient must be checked regularly by both gynecologist and cardiologist, by the latter to perform regular echocardiograms. Termination is not recommended for the hypertrophic (nonobstructive) cardiomyopathies. If atrial fibrillation occurs, anticoagulation with low molecular weight heparin and digoxin and/or Betablockers are recommended for rhythm and rate control. PERIPARTUM CARDIOMYOPATHIES: In peripartum cardiomyopathies, which are discovered clinically postpartum, inflammation of the myocardium sometimes associated with pericarditis is frequently found. For those patients, we recommend heart catheterization with endomyocardial biopsy to allow for the exact diagnosis of the underlying cardiac process (inflammatory and/or viral vs autoreactive myocarditis or noninflammatory or nonviral [= idiopathic] forms). This diagnostic algorithm, which we recommend for any form of dilated cardiomyopathy, bears impact on treatment options beyond the mere heart failure therapy that should be instigated anyhow.

Abortion, Induced↗
PubMed2003

[Excessive hyperchylomicronemia--a rare cause of acute retrosternal and epigastric pain in pregnancy].

CASE REPORT: A 24-year-old woman in her 13th gestational was admitted to our department with acute retrosternal and epigastric pain. She had been transferred from the gynecologic department where she was treated for vaginal bleeding because of abortus imminens. A cardiac cause was excluded by ECG and echo. Clinical chemistry and abdominal ultrasound confirmed the diagnosis of acute pancreatitis. The woman was known in our outpatient department for hyperchylomicronemia and had already had an earlier episode of acute pancreatitis under oral contraception years ago. At current admission, triglycerides were 11,500 mg/dl. To reduce plasma triglycerides, selective lipid apheresis was performed. Apheresis was well tolerated, and the patient became free of pain within the first 30 min of treatment. Triglycerides decreased to 6,600 mg/dl at this session. Keeping to a low-fat diet (< 30 g fat per day), the patient remained healthy and completed pregnancy with the delivery of a healthy girl in her 39th week of pregnancy. CONCLUSION: Selective lipid apheresis is a safe and effective option in the treatment of hyperlipidemic pancreatitis, even in pregnant patients.

Abdominal Pain↗
PubMed2003

Pericardial disease in pregnancy.

BACKGROUND: There is no evidence that pregnancy affects susceptibility to pericardial disease. However, when such a condition occurs, its proper diagnosis and management may be crucial for the outcome of the pregnancy. INCIDENCE AND DIAGNOSIS: Hydropericardium is the most frequent form of pericardial involvement in pregnancy. It is typically a small, clinically silent pericardial effusion present in the third trimester in approximately 40% of healthy pregnant women. Small amounts of fetal pericardial fluid (< 2 mm in echocardiography, in diastole) can be detected after 20 weeks of gestation. Larger effusions should raise clinical concern for hydrops fetalis, Rh disease, hypoalbuminemia, and infectious or autoimmune disorder. Wide varieties of etiologic forms of pericardial diseases occur sporadically in pregnant women. Significant symptoms, electrocardiographic changes, or physiologic impairment warrant hospitalization. TREATMENT: Most pericardial disorders are managed during pregnancy as in nonpregnant patients (i.e., nonsteroidal antiinflammatory drugs for acute, antibiotics and drainage for purulent pericarditis, and corticosteroids for systemic autoimmune disorders). However, colchicine is contraindicated in pregnancy, and pericardiocentesis should be performed only for very large effusions causing clinical signs of cardiac tamponade or if presence of suppurative, tuberculous or neoplastic pericardial effusion is suspected. Echocardiographic guidance of pericardiocentesis is preferred to fluoroscopic guidance in order to avoid fetal X-ray exposure. Pericardiectomy should be reserved for significant pericardial constriction and resistant bacterial infections. Delivery of normal infants in term after pericardiocentesis or pericardiectomy is expected, whenever natural history of causative disease allows. Pericardiectomy itself is not a contraindication for subsequent successful pregnancies.

Colchicine↗
PubMed2003

Genetics of human hypertension.

BACKGROUND: Hypertension is a multifactorial disease involving interactions among genetic, environmental, demographic, vascular and neuroendocrine factors. Essential hypertension is the most frequent diagnosis in this syndrome, indicating that a monocausal etiology has not been identified. However, a number of risk factors underlying essential hypertension have also been identified including age, sex, genetics, demographic factors, and others. Remarkable progress in molecular biological research has been achieved in clarifying the molecular basis of Mendelian hypertensive disorders. Causative genes and chromosomal fragments harboring disease susceptibility genes have been identified, e. g., for glucocorticoid-remediable aldosteronism, Liddle's syndrome, mineralocorticoid excess. MOLECULAR GENETIC STUDIES: Molecular genetic studies have now identified mutations in eight genes that cause Mendelian forms of hypertension and nine genes that cause Mendelian forms of hypotension in humans. No single genetic variant has emerged from linkage or association analyses as consistently related to blood pressure level in every sample and in all populations. However, a number of polymorphisms in candidate genes have been associated with differences in blood pressure. Most prominent have been the polymorphisms in the renin-angiotensin-aldosterone system. CONCLUSION: Essential hypertension is likely to be a polygenic disorder that results from the inheritance of a number of susceptibility genes and involves multiple environmental determinants. These determinants complicate the study of blood pressure variations in the general population. The complex nature of the hypertension phenotype makes large-scale studies indispensable, when screening of familial and genetic factors is intended.

Chromosome Mapping↗
PubMed2003

Abdominal fat and sympathetic overactivity. From calorie intake to postmenopausal hypertension.

BACKGROUND: Epidemiologic studies have found an association between overweight and increased mortality arising primarily from cardiovascular disorders. A major determinant is a chronically raised sympathetic nervous system activity which can arise from calorie intake-dependent and -independent mechanisms. Calorie-dependent parameters reflecting sympathetic overactivity are an increased body fat mass and body mass index. VISCERAL FAT: Although influenced by calorie intake to a certain extent, visceral fat accumulation is a mechanism which is determined also by estrogen deficiency (postmenopausal hypertension) or enhanced corticoid influences. It is hypothesized that excess catecholamines trigger various adverse processes which, if they persist, can lead or aggravate hypertension and insulin resistance. Visceral but not peripheral fat mass was correlated with atherogenic metabolites. EXCESS CATECHOLAMINE SYNDROME: The present focus on visceral fat accumulation strengthens the concept of an "excess catecholamine syndrome" of which the "metabolic syndrome" appears as one consequence. It is proposed to further assess the potential of transthoracic echocardiography as routine imaging method for the prediction of visceral fat accumulation and its adverse health consequences.

Abdomen↗