PM052 The effect of high-intensity exercise and testosterone supplementation in men with heart...
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Conclusion: Our novel coating technology is robust, haemocompatible and can covalently bind a bioactive molecule to its surface. This has profound potential to improve stent ef- ficacy in vivo. Disclosure of Interest: None Declared PM050 Apoptotic markers in diagnosing inflammatory dilated cardiomyopathy Daiva Bironaite* 1 , Dainius Daunoravicius 2 , Julius Bogomolovas 3 , Arturas Jakubauskas 4 , Dalius Vitkus 5 , Edvardas Zurauskas 2 , Ieva Zasytyte 6 , Kestutis Rucinskas 6 , Algirdas Venalis 7 , Virginija Grabauskiene 2,6 1 Department of Stem Cell Biology, State Research Institute, Center for Innovative Medicine, 2 Department of Pathology, Forensic Medicine and Pharmacology, Vilnius University, Faculty of Medicine, Vilnius, Lithuania, 3 Department of Integrative Pathophysiology, Universitätsmedizin Mannheim, Mannheim, Germany, 4 Center of Immunogenetics, Hematology, Oncology and Transfusion Medicine, Vilnius University, 5 Department of Physiology, Biochemistry and Laboratory medicine, 6 Clinic of Cardiovascular Diseases, Vilnius University, Faculty of Medicine, 7 State Research Institute, Center for Innovative Medicine, Vilnius, Lithuania Introduction: Inflammatory dilated cardiomyopathy (iDCM) is a common debilitating disease with poor prognosis that often requires heart transplantation. It often starts as a myocarditis and is caused by a variety of toxic agents initiating inflammation. The chronic exposure of myocardium to inflammatory insults might subsequently initiate apoptosis or necrosis processes leading to a final destruction of heart tissue. Objectives: This study aimed to test serum and biopsy samples from iDCM patients with the purpose to investigate underlying molecular mechanisms and find reliable prognostic biomarkers for the timely diagnosis of iDCM facilitating purposeful cardio therapy. Methods: A total of 32 (25 males, 7 females; mean age 43.1411.86 years) serum and biopsy samples from patients with iDCM were investigated. Patients were separated in to inflammatory- positive and -negative groups according to expression of inflammatory in- filtrates (CD3, CD45Ro, and CD68). Inflammatory (TNF-a, IL-6, IL-1b) and apoptosis (Caspases 3, 9, 8, Bax, Bcl2, Hsp60) were assayed by the ELISA method, whereas inflam- matory infiltrates (CD3, CD45Ro, CD68) were assayed immunohistochemicaly. Statistical significance of data was analyzed by the Student t test (significance was set at p < 0.05). Results: Data show that inflammatory cytokine IL-6 in serum from patients diagnosed with iDCM was significantly increased (from 3.3 to 10.98 mg/ml; p < 0.05). Another inflam- matory cytokine, TNF-a, was also upregulated (from 7.9 – 14.03 mg/mg protein). In- flammatory infiltrates, such as CD3, CD45Ro and CD68, were upregulated (2.38, 2.1 and 1.63 times; p < 0.05), respectively, in biopsy from iDCM-diagnosed patients. Apoptotic serum markers, such as caspase 9, 8, and 3 were also significantly higher (6.1, 25.6, and 3.55 times; p < 0.05), respectively. Additionally, the increase of Hsp60 in serum was statistically significant (0.419 – 0.36 ng/mg; p < 0.05) supporting the role of an apoptotic myocardial death mechanism in iDCM. Conclusion: Our data show that inflammatory processes induce apoptotic cardiomyocyte death in iDCM. Circulating apoptotic and inflammatory markers, such as caspases 8, 9, 3, Hsp60 and IL-6, respectively, might be a good prognostic tool and signal preventing further heart tissue destruction. Clinically applied anti-inflammatory drugs, together with inhibitors of apoptosis might improve the efficiency of iDCM therapy. Disclosure of Interest: None Declared PM051 The role of collagen in virus-positive dilated cardiomyopathy Daiva Bironaite 1 , Dainius Daunoravicius 2 , Julius Bogomolovas 3 , Arturas Jakubauskas 4 , Dalius Vitkus 5 , Edvardas Zurauskas 2 , Ieva Zasytyte 6 , Kestutis Rucinskas 6 , Algirdas Venalis 7 , Virginija Grabauskiene* 2,6 1 Department of Stem Cell Biology, State Research Institute, Center for Innovative Medicine, 2 Department of Pathology, Forensic Medicine and Pharmacology, Vilnius University, Faculty of Medicine, Vilnius, Lithuania, 3 Department of Integrative Pathophysiology, Universitätsmedizin Mannheim, Mannheim, Germany, 4 Hematology, Oncology and Transfusion Medicine Center, Vilnius University Hospital Santariskiu Klinikos, 5 Department of Physiology, Biochemistry, Microbiology and Laboratory medicine, 6 Clinic of Cardiovascular Diseases, Vilnius University, Faculty of Medicine, 7 State Research Institute, Center for Innovative Medicine, Vilnius, Lithuania Introduction: Myocarditis may be induced by various bacteria or virus, autoimmune diseases, vasculitis, and chemicals. The progress of acute viral myocarditis is mainly related to the inflammatory response with subsequent deleterious effects, including dilated cardiomyopathy (DCM) which often can be treated only by heart trans- plantation. Therefore, it is clinically important to identify biomarkers that are pre- dictive for viral heart pathology. Objectives: The aim of this study was to investigate prognostic biomarkers of virus- induced cardiomyopathy that might assist in prevention of heart lesion. Methods: We investigated a total of 32 patients (25 males, 7 females; mean age 43.1411.86 years), admitted consecutively, and without undergoing further selection, to a tertiary referral centre for clinically suspected inflammatory DCM. Myocardial biopsies and sera samples from virus-positive and -negative patients were analyzed by the ELISA method for collagen synthesis/degradation (PICP, ICTP, TGF-b1, MMP9, and TIMP1), adiponectin-expression, inflammation (IL6, IL1B, and TNFa) and apoptosis/necrosis (caspases 3, 8, 9, APO1/Fas/CD95, Fas L, Bcl2, Bax, Hsp60 and hsTnT). Results: Our data indicate that myocardial viral infection is related to dysfunction of collagen synthesis and decrease of adiponectin-expression in serum samples, but not to induction of inflammation, apoptosis, necrosis or fibrosis. Actually, markers of the intrinsic and extrinsic apoptotic pathways: Bax, caspase 8, 9, and APO1/Fas/CD95, FasL as well as the myocardial necrotic marker hsTnT, and the inflammatory cytokine IL-6 showed a significant (p < 0.05) decrease in virus-positive heart, suggesting induction of myocarditis subsequent to collagen destruction. In parallel, significant decreases of the N-terminal propeptide of collagen I (PICP) (control - 0.159, virus positive - 0.079 ng/mg protein; p < 0.05) and adiponectin (control - 28.34, virus positive - 15.01 mg/mg protein; p < 0.05) in serum correlated with viral infection. Conclusion: Our data suggest that significant decrease in the serum levels of PICP and adiponectin from virus-infected patients is an informative and prognostic marker of myocarditis and ensuing dilated cardiomyopathy. Drugs stimulating collagen synthesis might be indicated for these patients together with antiviral therapy. Disclosure of Interest: None Declared PM052 The effect of high-intensity exercise and testosterone supplementation in men with heart failure Lourenço S. de Mara 1 , Alexandra A. Lineburge 1 , Anderson Z. Ulbrich 1 , Juliano A. Pacheco 2 , Jamil M. Valente Filho 1 , Eduardo P. Ribeiro 2 , Sabrina W. Sties 1 , Ana I. Gonzáles 1 , Tales de Carvalho* 1 1 Cardiology and Exercise Medicine Center, Santa Catarina State University, 2 Federal University of Santa Catarina, Florianópolis, Brazil Introduction: Heart failure involves endothelial and sexual disorders being considered predictors of poor prognosis. Recently, high-intensity training (HIT) has been considered more effective to improve cardiovascular and respiratory functions. Objectives: To evaluate the effects of HIT and testosterone supplementation therapy in erectile and cardiorespiratory function. Methods: Nineteen heart failure patients (age¼5810 years; ejection fraction¼348%) were randomised to either a high-intensity exercise group (control; n¼9) or a high- intensity exercise group with hormonal supplementation (intervention; n¼10). All of the patients exercised (40 minutes at 90% maximal oxygen consumption) for 12 weeks, three times weekly, and the intervention group received testosterone in the first and sixth weeks. Before and after the study period, cardiopulmonary test measurements, erectile and endothelial function were obtained. Results: Within each group, there was an increase in the maximum oxygen uptake (12% control and 15% intervention; p<0.05, both groups), and in the OUES (22% control and 14% intervention; p<0.05, both groups), a decrease in the VE/VCO 2 slope (5%; p<0.05, intervention group). There was an increase in erectile function scores (110.7%; control and 98.8% intervention; p <0.05, both groups) and in the per- centage of flow-mediated dilation (56.3% control and 92,3% intervention; not signif- icant in both groups). Conclusion: Testosterone treatment, in addition to HIT, does not have an added beneficial effect compared with exercise alone on the improvement of cardiorespiratory and erectile function. Disclosure of Interest: None Declared GHEART Vol 9/1S/2014 j March, 2014 j POSTER/2014 WCC Posters e71 POSTER ABSTRACTS
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Conclusion: Our novel coating technology is robust, haemocompatible and can covalentlybind a bioactive molecule to its surface. This has profound potential to improve stent ef-ficacy in vivo.Disclosure of Interest: None Declared
PM050
Apoptotic markers in diagnosing inflammatory dilated cardiomyopathy
Daiva Bironaite*1, Dainius Daunoravicius2, Julius Bogomolovas3, Arturas Jakubauskas4,Dalius Vitkus5, Edvardas Zurauskas2, Ieva Zasytyte6, Kestutis Rucinskas6, Algirdas Venalis7,Virginija Grabauskiene2,61Department of Stem Cell Biology, State Research Institute, Center for Innovative Medicine,2Department of Pathology, Forensic Medicine and Pharmacology, Vilnius University, Faculty ofMedicine, Vilnius, Lithuania, 3Department of Integrative Pathophysiology, UniversitätsmedizinMannheim, Mannheim, Germany, 4Center of Immunogenetics, Hematology, Oncology andTransfusion Medicine, Vilnius University, 5Department of Physiology, Biochemistry andLaboratory medicine, 6Clinic of Cardiovascular Diseases, Vilnius University, Faculty of Medicine,7State Research Institute, Center for Innovative Medicine, Vilnius, Lithuania
Introduction: Inflammatory dilated cardiomyopathy (iDCM) is a common debilitatingdisease with poor prognosis that often requires heart transplantation. It often starts as amyocarditis and is caused by a variety of toxic agents initiating inflammation. The chronicexposure of myocardium to inflammatory insults might subsequently initiate apoptosis ornecrosis processes leading to a final destruction of heart tissue.Objectives: This study aimed to test serum and biopsy samples from iDCM patients withthe purpose to investigate underlying molecular mechanisms and find reliable prognosticbiomarkers for the timely diagnosis of iDCM facilitating purposeful cardio therapy.Methods: A total of 32 (25 males, 7 females; mean age 43.14�11.86 years) serum andbiopsy samples from patients with iDCM were investigated. Patients were separated in toinflammatory- positive and -negative groups according to expression of inflammatory in-filtrates (CD3, CD45Ro, and CD68). Inflammatory (TNF-a, IL-6, IL-1b) and apoptosis(Caspases 3, 9, 8, Bax, Bcl2, Hsp60) were assayed by the ELISA method, whereas inflam-matory infiltrates (CD3, CD45Ro, CD68) were assayed immunohistochemicaly. Statisticalsignificance of data was analyzed by the Student t test (significance was set at p < 0.05).Results: Data show that inflammatory cytokine IL-6 in serum from patients diagnosed withiDCM was significantly increased (from 3.3 to 10.98 mg/ml; p < 0.05). Another inflam-matory cytokine, TNF-a, was also upregulated (from 7.9 – 14.03 mg/mg protein). In-flammatory infiltrates, such as CD3, CD45Ro and CD68, were upregulated (2.38, 2.1 and1.63 times; p < 0.05), respectively, in biopsy from iDCM-diagnosed patients. Apoptoticserum markers, such as caspase 9, 8, and 3 were also significantly higher (6.1, 25.6, and3.55 times; p < 0.05), respectively. Additionally, the increase of Hsp60 in serum wasstatistically significant (0.419 – 0.36 ng/mg; p < 0.05) supporting the role of an apoptoticmyocardial death mechanism in iDCM.Conclusion: Our data show that inflammatory processes induce apoptotic cardiomyocytedeath in iDCM. Circulating apoptotic and inflammatory markers, such as caspases 8, 9, 3,Hsp60 and IL-6, respectively, might be a good prognostic tool and signal preventingfurther heart tissue destruction. Clinically applied anti-inflammatory drugs, together withinhibitors of apoptosis might improve the efficiency of iDCM therapy.
GHEART Vol 9/1S/2014 j March, 2014 j POSTER/2014 WCC Posters
Disclosure of Interest: None Declared
PM051
The role of collagen in virus-positive dilated cardiomyopathy
Daiva Bironaite1, Dainius Daunoravicius2, Julius Bogomolovas3, Arturas Jakubauskas4,Dalius Vitkus5, Edvardas Zurauskas2, Ieva Zasytyte6, Kestutis Rucinskas6, Algirdas Venalis7,Virginija Grabauskiene*2,61Department of Stem Cell Biology, State Research Institute, Center for Innovative Medicine,2Department of Pathology, Forensic Medicine and Pharmacology, Vilnius University, Faculty ofMedicine, Vilnius, Lithuania, 3Department of Integrative Pathophysiology, UniversitätsmedizinMannheim, Mannheim, Germany, 4Hematology, Oncology and Transfusion Medicine Center,Vilnius University Hospital Santariskiu Klinikos, 5Department of Physiology, Biochemistry,Microbiology and Laboratory medicine, 6Clinic of Cardiovascular Diseases, Vilnius University,Faculty of Medicine, 7State Research Institute, Center for Innovative Medicine, Vilnius,Lithuania
Introduction: Myocarditis may be induced by various bacteria or virus, autoimmunediseases, vasculitis, and chemicals. The progress of acute viral myocarditis is mainlyrelated to the inflammatory response with subsequent deleterious effects, includingdilated cardiomyopathy (DCM) which often can be treated only by heart trans-plantation. Therefore, it is clinically important to identify biomarkers that are pre-dictive for viral heart pathology.Objectives: The aim of this study was to investigate prognostic biomarkers of virus-induced cardiomyopathy that might assist in prevention of heart lesion.Methods: We investigated a total of 32 patients (25 males, 7 females; mean age43.14�11.86 years), admitted consecutively, and without undergoing further selection, toa tertiary referral centre for clinically suspected inflammatory DCM. Myocardial biopsiesand sera samples from virus-positive and -negative patients were analyzed by the ELISAmethod for collagen synthesis/degradation (PICP, ICTP, TGF-b1, MMP9, and TIMP1),adiponectin-expression, inflammation (IL6, IL1B, and TNFa) and apoptosis/necrosis(caspases 3, 8, 9, APO1/Fas/CD95, Fas L, Bcl2, Bax, Hsp60 and hsTnT).Results: Our data indicate that myocardial viral infection is related to dysfunction ofcollagen synthesis and decrease of adiponectin-expression in serum samples, but not toinduction of inflammation, apoptosis, necrosis or fibrosis. Actually, markers of the intrinsicand extrinsic apoptotic pathways: Bax, caspase 8, 9, and APO1/Fas/CD95, FasL as well asthe myocardial necrotic marker hsTnT, and the inflammatory cytokine IL-6 showed asignificant (p < 0.05) decrease in virus-positive heart, suggesting induction of myocarditissubsequent to collagen destruction. In parallel, significant decreases of the N-terminalpropeptide of collagen I (PICP) (control - 0.159, virus positive - 0.079 ng/mg protein; p <0.05) and adiponectin (control - 28.34, virus positive - 15.01 mg/mg protein; p < 0.05) inserum correlated with viral infection.Conclusion: Our data suggest that significant decrease in the serum levels of PICP andadiponectin from virus-infected patients is an informative and prognostic marker ofmyocarditis and ensuing dilated cardiomyopathy. Drugs stimulating collagen synthesismight be indicated for these patients together with antiviral therapy.Disclosure of Interest: None Declared
PM052
The effect of high-intensity exercise and testosterone supplementation in men withheart failure
Lourenço S. de Mara1, Alexandra A. Lineburge1, Anderson Z. Ulbrich1, Juliano A. Pacheco2,Jamil M. Valente Filho1, Eduardo P. Ribeiro2, Sabrina W. Sties1, Ana I. Gonzáles1,Tales de Carvalho*11Cardiology and Exercise Medicine Center, Santa Catarina State University, 2Federal Universityof Santa Catarina, Florianópolis, Brazil
Introduction: Heart failure involves endothelial and sexual disorders being consideredpredictors of poor prognosis. Recently, high-intensity training (HIT) has been consideredmore effective to improve cardiovascular and respiratory functions.Objectives: To evaluate the effects of HIT and testosterone supplementation therapy inerectile and cardiorespiratory function.Methods: Nineteen heart failure patients (age¼58�10 years; ejection fraction¼34�8%)were randomised to either a high-intensity exercise group (control; n¼9) or a high-intensity exercise group with hormonal supplementation (intervention; n¼10). All of thepatients exercised (40 minutes at 90% maximal oxygen consumption) for 12 weeks, threetimes weekly, and the intervention group received testosterone in the first and sixth weeks.Before and after the study period, cardiopulmonary test measurements, erectile andendothelial function were obtained.Results: Within each group, there was an increase in the maximum oxygen uptake(12% control and 15% intervention; p<0.05, both groups), and in the OUES (22%control and 14% intervention; p<0.05, both groups), a decrease in the VE/VCO2 slope(5%; p<0.05, intervention group). There was an increase in erectile function scores(110.7%; control and 98.8% intervention; p <0.05, both groups) and in the per-centage of flow-mediated dilation (56.3% control and 92,3% intervention; not signif-icant in both groups).Conclusion: Testosterone treatment, in addition to HIT, does not have an added beneficialeffect compared with exercise alone on the improvement of cardiorespiratory and erectilefunction.Disclosure of Interest: None Declared
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