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Introduction: The biopsy based analyse, with histological, immunohistological and molecular biological analysis of myocardial tissues, represents the only possible tool to investigate the basement of inflammatory cardiomyopathy. Since... more
Introduction: The biopsy based analyse, with histological, immunohistological and molecular biological analysis of myocardial tissues, represents the only possible tool to investigate the basement of inflammatory cardiomyopathy. Since development of this disease assume involvement of extracellular matrix remodelling, the analyze of this process were aimed in this article. Methods and results: Endomyocardial biopsies from patient with inflammatory cardiomyopathy (n=170) were analysed by RT-PCR, Furthermore, histological, immunohistological and biochemical methods (ELISA) were used to estimate the matrix proteins amount in myocardial tissues (n=36). All results were obtained by comparison of patient groups regarding to left ventricular ejection fraction (LVEF), EF>60 versus EF<30. EF<30 group featured significaly increased inflammation cells per surface area: CD3 (p<0.001), CD11a (p<0.02), CD45 (p<0.02), Mac1 (p<0.02) and HLA (p<0.01). The gene expression revealed an increased transcripts number of IL-2 (p<0.01), IL-5 (p<0.01), IL-6 (p<0.02), INF beta (p<0.039), Collagen type I (p<0.001), III (p<0.0014) and IV (p<0.0004) as well Laminin (p<0.001). On the protein level ICTP (p<0.04), MMP9 (p<0.04) and TIMP I (p<0.01) were significaly increased in this group in comparison with EF>60 group. The escalating number of active CD3 cells correlated positively with BNP (ρ=0.624, p<0.0091), adhesion cell number ICAM (ρ=0.682, p<0.01) and VCAM (ρ=0.475, p<0.01) and with uPA (ρ =0.265, p<0.013), as well as with increased quantity of collagen type III per section area (ρ=0.632, p<0.01). The expanded abundance of type I collagen products was clearly dependent of the expression of collagen I gene (ρ=0.575, p<0.002) and uPA (ρ=0.544, p<0.004). Precise correlation between the amount of MMP 9 protein and downward EV values (ρ=− 0.4133, p<0.0073) was also observed in the patient group with EF<30. Conclusion: Myocardial inflammation lead to an imbalance in the MMP/TIMP system with development of myocardial fibrosis with significant correlation to LV-dysfunction. Extracellular matrix remodeling with an imbalance in the MMP/TIMP system plays an important role in the development of left ventricular dysfunction in inflammatory heart disease
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Research Interests: Medicine and Myocarditis
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Research Interests: Chemistry and Dehydration
For the thermal (4 + 2) dimerization of the dienes (I) and (IV) a parallel increase in facial selectivity and reaction rate is observed on going from the (E)‐alkyl‐aryl dienes (IVa) and (IVb) and the (Z)‐dienes (IVc) and (IVd) to the... more
For the thermal (4 + 2) dimerization of the dienes (I) and (IV) a parallel increase in facial selectivity and reaction rate is observed on going from the (E)‐alkyl‐aryl dienes (IVa) and (IVb) and the (Z)‐dienes (IVc) and (IVd) to the (E)‐aryl‐aryl dienes (I).
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Human herpesvirus 6 (HHV-6) and HHV-7 are ubiquitous human pathogens with lymphotropic and neurotropic potential. Both viruses infect cells that express the CD46 complement receptor. Based on their biological properties and their... more
Human herpesvirus 6 (HHV-6) and HHV-7 are ubiquitous human pathogens with lymphotropic and neurotropic potential. Both viruses infect cells that express the CD46 complement receptor. Based on their biological properties and their receptor-dependent cellular tropism, HHV-6 and HHV-7 are detected in cells of different organs and consequently associated with various diseases. In addition to modulation of immune responses, HHV-6 and HHV-7 can directly infect endothelial cells and subsequently enter adjacent tissues. If the cardiovascular system is affected, HHV-6 and HHV-7 infections can be causative for myocarditis, vasospastic endothelial dysfunction, and development of post-infectious or post-inflammatory cardiomyopathies. Reactivation of HHV-6 is often associated with a higher percentage of chest pain, while inhibition of viral RNA is associated with clinical improvement of treated patients. This may be a therapeutic option for HHV-6-positive patients with unexplained cardiac symptoms.
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Background The alarmin S100A8/A9 has been shown to be of importance in several inflammatory cardiovascular disorders. We recently demonstrated the pivotal role of cardiac S100A8/A9 in human and experimental Coxsackievirus B3... more
Background The alarmin S100A8/A9 has been shown to be of importance in several inflammatory cardiovascular disorders. We recently demonstrated the pivotal role of cardiac S100A8/A9 in human and experimental Coxsackievirus B3 (CVB3)-induced myocarditis (MC). Purpose We aimed to evaluate whether serum S100A8/A9 levels are a marker in patients with a recent onset of MC Methods Serum S100A8/A9, hsCRP, and NT pro-BNP levels were analyzed in patients with a recent onset of MC (≤30 days (d), n=29; ejection fraction (EF): 44.3%±13%), dilated cardiomyopathy patients with inflammation (DCMi: n=112; EF: 28.8%±12%) or without inflammation (DCM: n=58; EF: 26.7%±9%), and controls (co: n=25; EF: 68.5%±5%). Blood samples and endomyocardial biopsies (EMB) were collected at time point (T1). In a subgroup, S100A8/A9 serum levels and EMB were available at T1 (n=10) and follow-up (T2, n=10, mean follow-up 8 months). Results MC ≤30 d patients showed a 4.5-fold (p<0.0001), 19.3-fold (p<0.0001), and 4.0-fold (p<0.0001) increase in S100A8/A9, hsCRP, NT pro-BNP levels vs co, respectively. S100A8/A9 levels correlated with the disease activity, displayed by EMB counts of inflammatory cells (CD3: r=0.464, p=0.0128, XY pairs=28, LFA-1: r=0.551, p=0.002, XY pairs=28, Mac-1: r=0.418, p=0.026, XY pairs=28), and the EF (r=0.545, p=0.0027, XY pairs=28). MC ≤30 d patients showed an association between serum S100A8/A9 levels and EMB S100A8 (r=0.482, p=0.060, XY pairs=16), S100A9 (r=0.441, p=0.088, XY pairs=16), nucleotide-binding oligomerization domain containing-protein 2 (NOD2, r=0.55, p=0.035, XY=15), and Nod-like receptor family, pyrin domain-containing 3 protein (NLRP3, r=0.52, p=0.048, XY=15) mRNA levels. Also EMB S100A8 and S100A9 mRNA levels showed a significant correlation with EMB NOD2 and NLRP3 mRNA expression. Serum S100A8/A9 levels were increased by 3.0-fold (p<0.0001) and 1.8-fold (p=0.0005) in DCMi (n=112), and DCM (n=58) patients vs co, respectively. However, the S100A8/A9 levels of DCMi and DCM patients were 1.5-fold (p=0.07) and 2.5-fold (p<0.0001) lower vs MC ≤30 d patients. ROC analyses of S100A8/A9 in MC ≤30 d provided a cut-off of 583 ng/ml with a specificity=92%, sensitivity=86.2%, a PPV=92.6%, a NPV=85.2%, and an AUC=0.934 vs co, which was superior to hsCRP (cut-off=5 mg/l): specificity=95.8%, sensitivity=58.6%, a PPV=94.4%, a NPV=65.7%, AUC=0.885. In the subgroup, S100A8/A9 levels decreased after heart failure medication (T1: 2454±1931 ng/ml vs T2: 934.4±552 ng/ml; p=0.002), reflected by a decrease of EMB inflammatory cells. Baseline serum S100A8/A9 levels predicted the change in EMB CD3 and Mac-1. Conclusions These results support an additional value for S100A8/A9 serum levels as a potential diagnostic biomarker and as a tool to monitor the course of the disease. We provide first evidence that S100A8/A9 is connected to the NOD2-NLRP3 pathway in these patients. Acknowledgement/Funding Novartis
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Research Interests: Pathology, Cancer, Breast Cancer, Immunohistochemistry, Medicine, and 15 moreHumans, Breast Cancer Early Detecion and Treatment, Female, Monoclonal Antibodies, Epidermal Growth Factor Receptor, Myocardium, Metastatic Breast Cancer, Monoclonal Antibody, Cardiotoxicity, Anthracyclines, Trastuzumab, Antineoplastic Agents, Heart Diseases, Breast Neoplasms, and gene amplification
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Introduction: The biopsy based analyse, with histological, immunohistological and molecular biological analysis of myocardial tissues, represents the only possible tool to investigate the basement of inflammatory cardiomyopathy. Since... more
Introduction: The biopsy based analyse, with histological, immunohistological and molecular biological analysis of myocardial tissues, represents the only possible tool to investigate the basement of inflammatory cardiomyopathy. Since development of this disease assume involvement of extracellular matrix remodelling, the analyze of this process were aimed in this article. Methods and results: Endomyocardial biopsies from patient with inflammatory cardiomyopathy (n=170) were analysed by RT-PCR, Furthermore, histological, immunohistological and biochemical methods (ELISA) were used to estimate the matrix proteins amount in myocardial tissues (n=36). All results were obtained by comparison of patient groups regarding to left ventricular ejection fraction (LVEF), EF>60 versus EF<30. EF<30 group featured significaly increased inflammation cells per surface area: CD3 (p<0.001), CD11a (p<0.02), CD45 (p<0.02), Mac1 (p<0.02) and HLA (p<0.01). The gene expression revea...
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Copyright © 201 egrated human herpesvirus swers Philip E. Pellett*, Dharam V. Ablashi, Peter F. Ambros, Henri Agut, Mary T. Caserta, Vincent Descamps, Louis Flamand, Agnès Gautheret-Dejean, Caroline B. Hall, Rammurti T. Kamble, Uwe Kuehl,... more
Copyright © 201 egrated human herpesvirus swers Philip E. Pellett*, Dharam V. Ablashi, Peter F. Ambros, Henri Agut, Mary T. Caserta, Vincent Descamps, Louis Flamand, Agnès Gautheret-Dejean, Caroline B. Hall, Rammurti T. Kamble, Uwe Kuehl, Dirk Lassner, Irmeli Lautenschlager, Kristin S. Loomis, Mario Luppi, Paolo Lusso, Peter G. Medveczky, Jose G. Montoya, Yasuko Mori, Masao Ogata, Joshua C. Pritchett, Sylvie Rogez, Edward Seto, Katherine N. Ward, Tetsushi Yoshikawa and Raymund R. Razonable** Department of Immunology andMicrobiology, Wayne State University School of Medicine, Detroit, MI, USA HHV-6 Foundation, Santa Barbara, CA, USA Children’s Cancer Research Institute, Vienna, Austria Service of Virology, Groupe Hospitalier Pitié-Salpêtrière, Paris, France Department of Pediatrics, University of Rochester School of Medicine, Rochester, NY, USA Department of Dermatology, Bichat Claude Bernard Hospital, Paris, France Rheumatology and Immunology Research Center, Université Laval, Quebe...
Steuerung der 1,2‐/ l ,4‐Regioselektivität durch sterische Substituenteneffekte.
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Background: Regarding disease pathogenesis, it has become evident that confinement to analysis of protein-coding regions of the genome is insufficient since many noncoding regions are associated with human diseases. We searched for... more
Background: Regarding disease pathogenesis, it has become evident that confinement to analysis of protein-coding regions of the genome is insufficient since many noncoding regions are associated with human diseases. We searched for elements of the noncoding genome influencing the highly variable course of a cardiomyopathy caused by a common single-stranded RNA virus (CVB3). Methods and Results: Transcriptome mapping of human CVB3 cardiomyopathy hearts showed high long noncoding RNAs (lncRNA) MALAT1 associated with spontaneous virus clearance and recovery, and low MALAT1 with virus persistence and clinical deterioration. Primary [[Unable to Display Character: ]]7kb MALAT1 transcript is only part of a complex RNA processing system generating e.g. mascRNA, a tRNA-like molecule, by a novel biosynthetic pathway. First, we found cell type-specific MALAT1 processing to result in grossly different mascRNA levels, which were highest in leukocytes. Second, CVB3 infection of genetically MALAT1-deficient (MAL...
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Research Interests: Medicine and Myocarditis
... Kuehl 1 , M. Pauschinger 1 , D. Lassner 2, H.-R Schultheiss 1 , S. Modrow 3 1 Charite, CampusBenjamin Franklin, Department ... co-morbidities L. Mendes, J. Ferreira Santos, L. Pinto, F. Caetano, E Seixo, E Martins, R Cardoso, M.... more
... Kuehl 1 , M. Pauschinger 1 , D. Lassner 2, H.-R Schultheiss 1 , S. Modrow 3 1 Charite, CampusBenjamin Franklin, Department ... co-morbidities L. Mendes, J. Ferreira Santos, L. Pinto, F. Caetano, E Seixo, E Martins, R Cardoso, M. Mendes Sao Bernardo Hospital&#x27; Cardiology ...
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... on the immunohistological and histological proof of intramyocardial inflammation in myocarditis and dilated cardiomyopathy M. Noutsias, E. Noutsias, HP Schultheiss, U. Kuehl Charite - CampusBenjamin Franklin, Department of Cardiology... more
... on the immunohistological and histological proof of intramyocardial inflammation in myocarditis and dilated cardiomyopathy M. Noutsias, E. Noutsias, HP Schultheiss, U. Kuehl Charite - CampusBenjamin Franklin, Department of Cardiology & Pneumonology, Berlin, Germany ...
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Human herpesvirus 6 (HHV-6) and HHV-7 are ubiquitous human pathogens with lymphotropic and neurotropic potential. Both viruses infect cells that express the CD46 complement receptor. Based on their biological properties and their... more
Human herpesvirus 6 (HHV-6) and HHV-7 are ubiquitous human pathogens with lymphotropic and neurotropic potential. Both viruses infect cells that express the CD46 complement receptor. Based on their biological properties and their receptor-dependent cellular tropism, HHV-6 and HHV-7 are detected in cells of different organs and consequently associated with various diseases. In addition to modulation of immune responses, HHV-6 and HHV-7 can directly infect endothelial cells and subsequently enter adjacent tissues. If the cardiovascular system is affected, HHV-6 and HHV-7 infections can be causative for myocarditis, vasospastic endothelial dysfunction, and development of post-infectious or post-inflammatory cardiomyopathies. Reactivation of HHV-6 is often associated with a higher percentage of chest pain, while inhibition of viral RNA is associated with clinical improvement of treated patients. This may be a therapeutic option for HHV-6-positive patients with unexplained cardiac symptoms.
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Research Interests: Pathology, Cancer, Breast Cancer, Immunohistochemistry, Medicine, and 15 moreHumans, Breast Cancer Early Detecion and Treatment, Female, Monoclonal Antibodies, Epidermal Growth Factor Receptor, Myocardium, Metastatic Breast Cancer, Monoclonal Antibody, Cardiotoxicity, Anthracyclines, Trastuzumab, Antineoplastic Agents, Heart Diseases, Breast Neoplasms, and gene amplification
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... Kuehl 1 , M. Pauschinger 1 , D. Lassner 2, H.-R Schultheiss 1 , S. Modrow 3 1 Charite, CampusBenjamin Franklin, Department ... co-morbidities L. Mendes, J. Ferreira Santos, L. Pinto, F. Caetano, E Seixo, E Martins, R Cardoso, M.... more
... Kuehl 1 , M. Pauschinger 1 , D. Lassner 2, H.-R Schultheiss 1 , S. Modrow 3 1 Charite, CampusBenjamin Franklin, Department ... co-morbidities L. Mendes, J. Ferreira Santos, L. Pinto, F. Caetano, E Seixo, E Martins, R Cardoso, M. Mendes Sao Bernardo Hospital&#x27; Cardiology ...
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<jats:p>Introduction: Inflammation and/or viral infection are both relevant for extracellular matrix remodeling. Therefore the effects of myocardial inflammation on ECM remodeling are analyzed in this study.</jats:p>... more
<jats:p>Introduction: Inflammation and/or viral infection are both relevant for extracellular matrix remodeling. Therefore the effects of myocardial inflammation on ECM remodeling are analyzed in this study.</jats:p> <jats:p> # Methods and results: Endomyocardial biopsies were obtained from 20 patients with established DCM (2.11±0.44 CD3 cells/mm <jats:sup>2</jats:sup> ) and 29 DCMi patients (18.91±6.41 CD3 cells/mm <jats:sup>2</jats:sup> ) comparable in age (51.45±3.15 vs. 48.48±2.39 years), LVEDD (72.7±2.2 vs. 69.76±1.06mm) and EF (26±2.99 vs. 25.86±2.0%). Total collagen content was quantified by picosiriusredstaining while the MMP2, MMP3 and TIMP1 expression was evaluated by immunohistochemistry. The MMP1, MMP3 and TIMP1 and ICTP expression in the serum was quantified by Elisa. and levels of IL6 and IL8 were measured by BioPlexAssays. Furthermore various cytokines and proteases were evaluated by real-time-PCR. In DCMi patients both CD3-lymphocyte infiltration (8.95fold, p&lt;0.001) and IL6 expression (2.93fold, p=0.0067) were significantly increased vs. DCM as well as the mRNA-expression of TNF-alpha (p&lt;0,049). The cellular inflammation correlated with the grade of fibrosis (p&lt;0.01) which is 2.43fold elevated in DCMi (p&lt;0.01). This may be caused by the increased MMP expression in DCMi, demonstrated by elevated MMP1 serum level (1.64fold increased, p&lt;0.01 vs. DCM) and slightly increased MMP-2 (1.41fold) and MMP-3 (1.6fold) expression in biopsies. In contrast, the serum levels of TIMP1 were reduced to 83.14% in DCMi (p=0.06 vs. DCM) and correlated negatively to the serum MMP3 expression (p&lt;0.01) indicating an imbalance in the proteasessystem. The transcripts amount of collagen type I (ρ = −0.80; <jats:italic>P</jats:italic> &lt;0.0091) and III (ρ = −0.80; <jats:italic>P</jats:italic> &lt;0.0091), inflammatory cytokines TGF beta (ρ =−0.67; <jats:italic>P</jats:italic> &lt;0.044) and INF beta (ρ = −0.47; <jats:italic>P</jats:italic> &lt;0.05) as well amount of ICTP (ρ = −0.89; <jats:italic>P</jats:italic> &lt;0.0011) was positively correlated with decreased LVEF from DCMi patients. The increased number of CD3 active cells in DCM biopsies was positively linked to the protein amount of TIMP1 as well to the mRNA amount of MMP9. </jats:p> <jats:p>Conclusion: Myocardial inflammation in patients with DCMi leads to an imbalance in the MMP/TIMP-system, which attributes to the development of myocardial fibrosis.</jats:p>
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<jats:p>The clinical phenotype of human dilated cardiomyopathy (DCM) encompasses a broad spectrum of etiologically distinct disorders. We obtained the cardiac expression profile of a DCM subtype (DCMi-B19) characterized by cardiac... more
<jats:p>The clinical phenotype of human dilated cardiomyopathy (DCM) encompasses a broad spectrum of etiologically distinct disorders. We obtained the cardiac expression profile of a DCM subtype (DCMi-B19) characterized by cardiac inflammation and parvovirus B19 (B19) persistence, to identify possible new therapeutic targets in humans. By microarray analysis and TaqMan PCR endomyocardial biopsies from DCMi-P19 patients (n=8) were compared to controls w/o cardiac disease. In DCMi-B19 an expression profile with dysbalance between several gene regulatory networks was observed. Tab. 1/2 classify deregulated genes in a group closely correlated (p&lt;0.01) with left ventricular ejection fraction (EF) and another one w/o correlation to EF. CCN1 was the most strongly upregulated of the EF-independent genes which encompass further members of the CCN1 regulatory network including CCN2=CTGF. In contrast the genes in tab. 2 are closely EF-correlated. We have previously shown that CCN1 is induced in endothelial cells by pro-inflammatory cytokines in vitro, which may also be the mechanism of its induction in human DCMi-B19 hearts. Two recent studies described the potential of CCN1 to promote migration/adhesion of CD34+ stem cells, and of activated monocytes via alphaMbeta2 integrin. This suggests that the CCN1 induction in DCMi-B19 may influence the influx of CD34+ stem cells and activated monocytes to the inflamed heart, and obviously this may occur independent of hemodynamic impairment. B19 viruses infect cardiac microvascular endothelium, and endothelial CCN1 induction may therefore be involved in disease pathogenesis by altering circulating cell interactions with the inflamed heart.</jats:p> <jats:p> <jats:table-wrap orientation="portrait" position="anchor"> <jats:label>Table 1:</jats:label> <jats:caption> <jats:p> <jats:bold>EF-Independent Gene Deregulation</jats:bold> </jats:p> </jats:caption> <jats:graphic xmlns:xlink="http://www.w3.org/1999/xlink" orientation="portrait" position="float" xlink:href="5901T1.jpeg" /> </jats:table-wrap> <jats:table-wrap orientation="portrait" position="anchor"> <jats:label>Table 2:</jats:label> <jats:caption> <jats:p> <jats:bold>EF-Correlated Gene Deregulation</jats:bold> </jats:p> </jats:caption> <jats:graphic xmlns:xlink="http://www.w3.org/1999/xlink" orientation="portrait" position="float" xlink:href="5901T2.jpeg" /> </jats:table-wrap> </jats:p>
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Aims: We analysed possible influence of perforin-dependent infiltration upon long-term mortality in patients with inflammatory cardiomyopathy (CMi). We previously demonstrated that left ventricular...
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Foxo3 is a transcription factor involved in cell metabolism, survival, and inflammatory disease. However, mechanistic insight in Foxo3 effects is still limited. Here, we investigated the role of Foxo3 on natural killer (NK) cell responses... more
Foxo3 is a transcription factor involved in cell metabolism, survival, and inflammatory disease. However, mechanistic insight in Foxo3 effects is still limited. Here, we investigated the role of Foxo3 on natural killer (NK) cell responses and its effects in viral myocarditis. Effects of Foxo3 on viral load and immune responses were investigated in a model of coxsackie virus B3 myocarditis in wild-type (WT) and Foxo3 deficient mice. Reduced immune cell infiltration, viral titres, and pro-inflammatory cytokines in cardiac tissue were observed in Foxo3-/- mice 7 days post-infection (p.i.). Viral titres were also attenuated in hearts of Foxo3-/- mice at Day 3 while interferon-γ (IFNγ) and NKp46 expression were up-regulated suggesting early viral control by enhanced NK cell activity. CD69 expression of NK cells, frequencies of CD11b+CD27+ effector NK cells and cytotoxicity of Foxo3-/- mice was enhanced compared to WT littermates. Moreover, microRNA-155 expression, essential in NK cell ac...
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Parvovirus B19 (B19V) is a causative agent of inflammatory cardiomyopathy and impaired cellular endothelial regeneration with consecutive endothelial dysfunction and microvascular disease. B19V was recently identified as strong inductor... more
Parvovirus B19 (B19V) is a causative agent of inflammatory cardiomyopathy and impaired cellular endothelial regeneration with consecutive endothelial dysfunction and microvascular disease. B19V was recently identified as strong inductor of apoptosis with impaired function of circulating angiogenic cells. Since as yet no therapeutic option for chronic B19V infection exists, we tested whether antiviral treatment with the thymidine analog telbivudine was effective on clinical outcome in B19V-cardiomyopathy and in suppressing B19V replication in vitro . Patients (6 male, 2 female) with B19V associated chronic myocarditis were enrolled in a pilot trail to receive 600 mg o.d. of telbivudine for 6 months. Transcriptional activity of B19V was silenced in all but one patient after end of telbivudine therapy resulting in a significant suppression of B19V load in endomyocardial biopsies (EMB; 2245 to 629 genome equivalents (GE/µg isolated nucleic acids; p 2 on immunohistochemical analysis. Left ventricular ejection fraction improved significantly from 45% to 55% (p in vitro data showed suppressed B19V replication after 48 hours. Pretreatment of early outgrowth endothelial progenitor cells and endothelial colony forming cells with telbivudine resulted in a significant reduction of apoptosis in vitro (39% and 60%, both p
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... 717 Cardiomyopathy associated with Emery-Dreifuss muscular dystrophy, echocardiographic and biomarker study M. Marchel1, V. Stepien1, A. Madej2, R. Steckiewicz1, J. Kochanowski1, KJ Filipiak1, I. Hausmanowa-Petrusewicz2 , G. Opolski1... more
... 717 Cardiomyopathy associated with Emery-Dreifuss muscular dystrophy, echocardiographic and biomarker study M. Marchel1, V. Stepien1, A. Madej2, R. Steckiewicz1, J. Kochanowski1, KJ Filipiak1, I. Hausmanowa-Petrusewicz2 , G. Opolski1 1Medical University of Warsaw ...