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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Cardiovascular drug reviews 20 (2002), S. 0 
    ISSN: 1527-3466
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Endothelin receptor antagonist have been proposed for the treatment of a variety of disorders in which the endothelins may act as pathogenic mediators, such as hypertension, congestive heart failure, and cerebral vasospasm. Bosentan is a nonpeptide competitive antagonist, which can be a good tool for studying the endothelin system. It is specific for the endothelin system and blocks the actions of endothelin at both mammalian receptors (A and B). Bosentan has recently moved into Phase III clinical trial. This review will attempt to overview the experimental and clinical effects of bosentan.〈section xml:id="abs1-2"〉〈title type="main"〉SUMMARYET receptor antagonists, such as bosentan, produce beneficial effects in various pathological conditions. Bosentan, as a mixed ETA/ETB receptor antagonist, may be of particular benefit in heart failure and cerebral vasospasm where ETB receptors are upregulated. For some clinical indications bosentan should be evaluated more vigorously in further controlled clinical trials.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    350 Main Street , Malden , MA 02148 , USA . : Blackwell Science Inc
    Journal of interventional cardiology 17 (2004), S. 0 
    ISSN: 1540-8183
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Stenting of small coronary arteries has been limited by high rates of restenosis, and restenosis after stenting has chiefly been attributed to inflammatory reactions resulting in cell proliferation and intimal hyperplasia. In order to suppress this inflammatory process, we examined the effects of hydrocortisone, an antiinflammatory agent, on restenosis after stenting in a nonrandomized retrospective registry. The study population consisted of 193 patients treated at two hospitals, who underwent stent implantations in coronary arteries of reference diameter 〈3 mm between February 1999 and September 2001. Target lesions included complex, restenotic, diabetic, or chronic total lesions and types of implanted stents were Multi-Link, S-series, and gfx stents. Effect of intravenous administration of hydrocortisone (200 mg) before stenting was compared to control patients who did not receive this treatment. There was no significant difference of early outcomes between the hydrocortisone group and the control group. On angiographic follow-up at 6 months after stenting, the rate of restenosis was significantly lower in patients treated with hydrocortisone as compared with control group (22.8% vs 37%, respectively; P 〈 0.05). The revascularization rate of target lesion at 6 months was also significantly lower in the treated group (16.5% vs 29%, respectively; P 〈 0.05). These results suggest that preprocedural intravenous administration of hydrocortisone reduces restenosis after stenting of small coronary arteries. Prospectively controlled trials will be necessary to confirm this preventive effect of hydrocortisone on coronary in-stent restenosis.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Serum hepatocyte growth factor (HGF) is considered to be a potent marker of vascular endothelial injury. The present study was designed to examine serum HGF levels in atrial fibrillation and after successful direct current (DC) cardioversion.2. We measured serum HGF levels before and 7 days and 1 month after DC cardioversion in 39 patients with atrial fibrillation in whom sinus rhythm was maintained for at least 7 days after DC cardioversion and in 30 age- and sex-matched normal control subjects with sinus rhythm. We also measured acetylcholine-induced changes in forearm blood flow (FBF) using venous occlusive plethysmography in 10 patients.3. Serum HGF levels were significantly higher in the atrial fibrillation patients (both lone atrial fibrillation and with underlying heart disease) than in the controls (0.16 ± 0.07 vs 0.10 ± 0.04 ng/mL; P 〈 0.001). Seven days after successful DC cardioversion, the patients' serum HGF levels had decreased significantly (0.16 ± 0.07 vs 0.12 ± 0.06 ng/mL; P 〈 0.05) and in the 24 patients maintaining sinus rhythm 1 month after DC cardioversion, serum HGF levels decreased to control values (0.10 ± 0.08 ng/mL at 1 month). Serum HGF levels of the 15 patients who had relapsed into atrial fibrillation 1 month after DC cardioversion tended to decrease 7 days after DC cardioversion, but increased again 1 month after DC cardioversion. Percentage changes in FBF between baseline and the highest dose of acetylcholine before and after DC cardioversion were 180 ± 98 and 323 ± 196%, respectively (P = 0.0051). The rate of increase in FBF at the highest dose of acetylcholine between before and after DC cardioversion correlated negatively with the rate of decrease in serum HGF levels between before and after DC cardioversion (r = −0.837; P = 0.0025).4. This study is the first to demonstrate that serum HGF levels increase in atrial fibrillation and decrease after successful DC cardioversion. This may reflect the fact that atrial fibrillation induces vascular endothelial injury.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] We recently reported that mice deficient in the programmed cell death-1 (PD-1) immunoinhibitory coreceptor develop autoimmune dilated cardiomyopathy (DCM), with production of high-titer autoantibodies against a heart-specific, 30-kDa protein. In this study, we purified the 30-kDa protein from heart ...
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Springer seminars in immunopathology 11 (1989), S. 77-88 
    ISSN: 1432-2196
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion The use of immunosuppressive therapy with prednisolone, cyclophosphamide, cyclosporine or anti-thymocyte serum in experimental virus myocarditis induced by coxsackievirus or EMC virus was associated with greater mortality when administered early in illness. Beneficial effects were not seen by later administration of these agents. Thus, although it would be rather difficult to interpolate the results of animal experiments to man, clinical trials of immunosuppressive therapy against inflammatory myocarditis should be carried out with great caution and only in the setting of a carefully controlled clinical trial. Nonsteroid anti-inflammatory drugs, libuprofen, salicylates and indomethacin, and an immunopotentiating drug, levamisole, worsened experimental coxsackievirus B3 myocarditis and should not be used in acute myocarditis due to Coxsackie B viruses. Interferon has a beneficial effect against viral myocarditis due to coxsackievirus and EMC virus and may be clinically applicable. Moreover, with the development of clinically applicable antiviral agents, immunosuppressive or anti-inflammatory therapy against viral myocarditis, and dilated cardiomyopathy as its sequelae, may well have a different clinical scope in the future.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Idiopathic dilated cardiomyopathy (IDC) is characterized by a thin-walled heart with systolic dysfunction of unknown etiology. Because abnormalities in genes for cytoskeletal proteins related to Z-disc function have recently been reported to cause IDC, genomic organization of the gene for nebulette, a novel actin-binding Z-disc protein, was determined and its sequence variations were searched for in Japanese patients with IDC and healthy controls. The nebulette gene consists of 28 exons, and four sequence variations leading to amino acid replacement (Gln187His, Met351Val, Asn654Lys, and Thr728Ala) were identified in the patients. These variations were also found in the healthy controls and hence they were polymorphisms and not disease-specific mutations. Frequencies of Gln187His, Met351Val, and Thr728Ala variants were similar in the patients and controls. However, the frequency of homozygotes for Lys at codon 654, a variant at a relatively conserved residue in an actin-binding motif, was significantly increased in nonfamilial IDC patients (n=106) as compared with healthy control subjects (n=331) (7.54% vs 1.21%, OR=6.25, P=0.002, 95% CI=1.92–20.29), while this association was not found in familial IDC patients (n=24). These observations suggest that the nebulette polymorphism in the actin-binding motif was a novel genetic marker of susceptibility to nonfamilial IDC.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Herz 25 (2000), S. 249-254 
    ISSN: 1615-6692
    Keywords: Key Words Cardiomyopathy ; Myocarditis ; Virus ; Hepatitis C ; Interferon ; Hypertrophy ; Heart failure ; Schlüsselwörter Kardiomyopathie ; Myokarditis ; Virus ; Hepatitis C ; Interferon ; Hypertrophie ; Herzinsuffizienz
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Der Zusammenhang zwischen einer Hepatitis-C-Virus-Infektion und dem Auftreten einer hypertrophischen und einer dilatativen Kardiomyopathie wurde erst vor kurzem erkannt. In einem gemeinsamen Forschungsprojekt der “Committees for the Study of Idiopathic Cardiomyopathy” wurden Hepatitis-C-Virus-Antikörper bei 74 (10,6%) von 697 Patienten mit hypertrophischer Kardiomyopathie und bei 42 (6,3%) von 663 Patienten mit dilatativer Kardiomyopathie gefunden, wobei diese Prävalenz signifikant höher ist als bei freiwilligen Blutspendern in Japan. Hepatitis-C-Virus-Antikörper wurden bei 650 (5,4%) von 11 967 Patienten, die zur Behandlung in fünf Universitätskliniken waren, gefunden. Verschiedene kardiale Veränderungen wurden beobachtet, wobei Arrhythmien am häufigsten auftraten. Diese Beobachtungen legen nahe, daß eine Hepatitis-C-Virus-Infektion eine wichtige Ursache für eine Reihe bisher ungeklärter Herzerkrankungen ist. In einem gemeinsamen Forschungsprojekt mit dem “National Cardiovascular Center” und der Juntendo-Universität versuchten wir Hepatitis-C-Virus-Genome in Paraffinscnitten von autoptischen Herzen nachzuweisen. Von 106 untersuchten Herzen wurde das β-Aktin Gen bei 61 Herzen (52,6%) nachgewiesen. Bei diesen Proben wurden die Hepatitis-C-Virus-RNA in 13 Herzen (21,3%) und Negativstränge bei vier Herzen (6,6%) gefunden. Eine Hepatitis-C-Virus-RNA wurde bei sechs Herzen (26,0%) mit hypertrophischer Kardiomyopathie, drei Herzen (11,5%) mit dilatativer Kardiomyopathie und bei vier Herzen (33,3%) mit Myokarditis identifiziert. Diese Hepatitis-C-Virus-RNA-positiven Proben wurden zwischen 1979 und 1990 eingebettet, und daher kann gefolgert werden, dass Hepatitis-C-Virus-RNA noch aus paraffineingebettetem Gewebe, das mehrere Jahre gelagert wurde, amplifiziert werden kann. Vor kurzem untersuchten wir den Einfluss von Interferon auf eine Myokardschädigung, die mit einer akuten Hepatitis C einhergeht. Da TL-201-SPECT sensitiver war als die Elektrokardiographie oder Echokardiographie, um eine Hepatitis-C-Virus-induzierte Myokardschädigung nachzuweisen, verwandten wir T1-SPECT-Scores, um den Einfluss von Interferon auf eine Myokardschädigung zu untersuchen. SPECT-Scores verbesserten sich bei acht (53%) von 15 Patienten nach einer Interferonbehandlung. Zirkulierende Hepatitis-C-Viren verschwanden nach einer Interferontherapie bei allen elf Patienten, die entweder eine Besserung oder keine Zustandsveränderung aufwiesen; bei zwei Patienten mit schwerer Erkrankung waren Hepatitis-C-Virus-Genome im Blut noch nachweisbar. Obwohl diese Studie noch vorläufig ist, erscheint eine Interferontherapie erfolgversprechend bei Myokarderkrankungne, die durch eine Hepatitis-C-Virus-Infektion verursacht werden.
    Notes: Abstract The importance of hepatitis C virus infection has been recently noted in patients with hypertrophic cardiomyopathy or dilated cardiomyopathy. In a collaborative research project of the Committees for the Study of Idiopathic Cardiomyopathy, hepatitis C virus antibody was found in 74 of 697 patients (10.65) with hypertrophic cardiomyopathy and in 42 of 663 patients (6.3%) with dilated cardiomyopathy; these prevalences were significantly higher than that found in volunteer blood donors in Japan. Hepatitis C virus antibody was detected in 650 of 11,967 patients (5.4%) seeking care in 5 academic hospitals. Various cardiac abnormalities were found, and arrhythmias were the most frequent. These observations suggest that hepatitis C virus infection is an important cause of a variety of otherwise unexplained heart diseases. As a collaborative research with National Cardiovascular Center and Juntendo University, we tried to detect hepatitis C virus genomes using paraffin section of autopsied hearts. Among 106 hearts examined, β-actin gene was amplified in 61 hearts (52.6%). Among these, hepatitis C virus RNA was detected in 13 hearts (21.3%), and negative strands in 4 hearts (6.6%). Hepatitis C virus RNA was found in 6 hearts (26.0%) with hypertrophic cardiomyopathy, 3 hearts (11.5%) with dilated cardiomyopathy, 4 hearts (33.3%) with myocarditis. These hepatitis C virus RNA positive samples were obtained between 1979 and 1990, indicating that hepatitis C virus RNA can be amplified from paraffin-embedded hearts preserved for many years. More recently, we examined the effect of interferon on myocardial injury associated with active hepatitis C. As TL-201-SPECT was a more sensitive method to detect myocardial injury induced by hepatitis C virus than electrocardiography or echocardiography, we used to T1-SPECT scores to evaluate the effect of interferon on myocardial injury. SPECT scores improved in 8 patients (53%) out of 15 patients in whom interferon therapy was completed. Circulating hepatitis C virus disappeared after interferon therapy in all 11 patients with improvement or no change, but hepatitis C virus genomes persisted in the blood in 2 aggravated patients. Although this study is preliminary, interferon therapy is a promising treatment for myocardial diseases caused by hepatitis C virus infection.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1615-2573
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of prednisolone (PN) on viral myocarditis was studied experimentally with encephalomyocarditis virus myocarditis in BALB/c mice, PN was administered intramuscularly, 10 mg/kg, once a day, on days 4–13. Control mice were injected with distilled water. The mortality of the PN group was significantly higher than that of the control group (P〈0.05). The antibody synthesis was impaired and virus clearance from the hearts was delayed in the PN group. The present experiment suggests that early administration of steroids will aggravate the course of acute viral myocarditis.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1615-2573
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of inactivated virus vaccine was studied in an animal model of viral myocarditis. Encephalomyocarditis (EMC) virus, 5×106 plaque-forming units (pfu)/ml, was inactivated by 1 : 4000 formalin. Four-week-old CD-1 mice were injected subcutaneously and after 7 days intravenously with 0.1 ml vaccine. Seven days after the second vaccine, a significant rise in neutralizing antibody titers was found in the sera (1 : 40-1 : 2560,n=10), but not in mice without vaccine treatment (n=10). Seven days after the second vaccine, 100 pfu of live EMC virus was inoculated intraperitoneally. None of ten mice with vaccine treatment died or showed myocardial lesions after challenge with EMC virus, whereas all ten mice without vaccine died 5–7 days after EMC virus inoculation and showed severe myocardial lesions. Thus, virus-specific vaccine prevented development of myocarditis due to EMC virus.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1615-2573
    Keywords: DNA fragmentation ; Fas antigen ; Heart failure ; Mouse ; Programmed cell death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has recently been speculated that progressive deterioration of left ventricular function in chronic heart failure is due to the ongoing loss of viable cardiac myocytes. However, as there is little direct evidence of significant apoptosis contributing to the pathogenesis in cardiac myocytes in vivo, the significance of apoptosis in heart failure remains to be clarified. We investigated the role of apoptosis in heart failure induced by encephalomyocarditis virus myocarditis. DBA/2 mice were inoculated with the virus (day 0), then killed, and their hearts were extracted 3 to 28 days later. Internucleosomal DNA fragmentation, chromatin binding dye staining, and in situ terminal transferase deoxyuridine triphosphate (dUTP) endlabeling were used to detect apoptosis. Internucleosomal DNA fragmentation (DNA ladder) was clearly demonstrated on days 5 to 14 in the virusinfected hearts when myocardial necrosis and infiltration of mononuclear cells were prominent in the hearts. Apoptotic cells demonstrated morphological changes typical of apoptosis (condensation of chromatin and nuclear fragmentation). Both Fas antigen and Fas ligand immunoreactivity were detected in the infiltrating mononuclear cells. The in situ terminal transferase dUTP end-labeling method demonstrated condensed nuclei of infiltrating mononuclear cells on day 7. However, nuclei of cardiac myocytes surrounded by the cellular infiltration were absent. The main source of apoptotic cells in the heart in mice with viral myocarditis appeared to be the infiltrating mononuclear cells.
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