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Our mission is to reduce the burden of cardiovascular disease through percutaneous cardiovascular interventions.
Improving the quality of life and reducing sudden cardiac death by limiting the impact of heart rhythm disturbances.
Our mission is to improve quality of life and longevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
The ESC Working Groups' goal is to stimulate and disseminate scientific knowledge in different fields of cardiology.
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Dr. Wolfgang Linke,
View the Slides from this session in ESC Congress 365
This well-attended session discussed novel potential treatment options in heart failure (HF). The topics included mitochondrial targeting to improve the energetic balance of the failing heart (Prof. H.H. Szeto, USA), detection and targeting of myofilament protein dysfunction (Prof. J. van der Velden, The Netherlands), gene and cell therapy in HF (Prof. S.E. Harding, UK), and tissue engineering applications (Dr. P.L. Soong, Germany).
Hazel Szeto reminded us that many of the available drugs against HF (beta-blockers, ACE inhibitors) target the increase in energy consumption typically associated with this condition. She pointed our attention to cardiolipin, a protein at the inner mitochondrial membrane, which promotes the electron transport along the cristae and is lost in heart failure. She introduced her work on a cell-permeable antioxidant, SS-31 (BendaviaTM), which inhibits HF-associated mitochondrial swelling and oxidative cell death and increases the ATP synthase rate. She provided compelling evidence from 4 different animal models of HF that SS-31 ameliorates hypertensive cardiomyopathy and post-ischemic HF without changing blood pressure.
Jolanda van der Velden talked about changes in myofilament contractile properties in familiar hypertrophic cardiomyopathy, which is mainly a disease of the sarcomere. She summarized her work on changes in myofilament Ca2+ sensitivity and maximum force production in end-stage failing versus donor human heart samples, focusing on HCM hearts with mutations in troponin, tropomyosin, or myosin. She demonstrated that, while changes in Ca2+ sensitivity could go in different directions in different mutations, maximum force was reduced in all HCM hearts. She also highlighted recent advances in novel clinical approaches to target myofilament protein dysfunction using small molecule activators of myosin and troponin.
Sian Harding reviewed recent advances in cardiac gene therapy, focusing on the results of the Calcium Up-regulation by Percutaneous Administration of Gene Therapy in Cardiac Disease (CUPID) and CUPID2 gene therapy trials. These trials evaluate the effectiveness of a gene transfer vector based on adeno-associated virus for delivery of SERCA2a complementary DNA in 39 (CUPID) and 240 (CUPID2) patients with advanced HF. In CUPID2, at one-year follow-up, HF patients had less cardiovascular events after AAV. Prof. Harding went on to discuss advantages and caveats of their gene transfer approach in comparison to other HF therapies involving, e.g., different types of stem cells.
Poh Loong Soong reported on interesting experiments aimed at engineering humanized biological ventricular assist device (BioVAD) tissue structures for the potential use as heart-embracing cardiac grafts in vivo. He demonstrated that electrical stimulation improved the maturation of the BioVADs and that activation of specific signaling pathways increased the contractile activity of the engineered grafts. He showed examples for successful patching of rat hearts using BioVAD-like structures.
Overall, this session provided useful insight by leading experts into a variety of exciting new approaches to HF therapy at various different stages of experimental and clinical development.
Frontiers in the treatment of heart failure
Our mission: To reduce the burden of cardiovascular disease
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