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Prof. Rudolf De Boer
Session number: 117Session title: Cardiomyopathies: what are the mechanisms?Authors: Rudolf De Boer (Groningen, Netherlands)
The session: “Cardiomyopathies: what are the mechanisms?” was part of the Basic Science Translational track and dealt with various aspects of cardiomyopathies. The session was chaired by Dr. H.P. Schultheiss (Berlin, Germany) and Dr. R. de Boer (Groningen, the Netherlands).
The first talk was given by Dr. A. Keren (Jerusalem, Israel) who discussed various aspects of dilated cardiomyopathy (DCM). DCM is a severe cardiomyopathy, and currently, the main etiological factors include myocarditis, genetic mutations, autoimmunity and autoantibodies, and toxic agents. The use of immunosuppressive therapy was discussed but remains controversial.
The second talk was given by Dr. P. van der Meer (Groningen, the Netherlands), who discussed translational approaches to the study of hypertrophic cardiomyopathy (HCM). HCM is characterized by focal hypertrophy and age dependent penetrance. Interesting and compelling cell and animal studies were discussed, which help to explain these features of HCM.
The third talk was delivered by Dr. F. Smih (Toulouse, France) and was about diabetic cardiomyopathy. Diabetic cardiomyopathy is characterized by multiple pathological changes in the myocardium, such as hypertrophy, lipotoxicity and apoptosis. A model of diabetic cardiomyopathy overexpressing apolipoprotein O (APOO) was discussed as it strikingly encompasses these features. It was discussed that targeting of APOO may offset the deleterious effects of diabetes on the heart.
The final talk was on Tako-Tsubo cardiomyopathy, and given by Dr. A.R. Lyon (London, United Kingdom). Tako-Tsubo is a rare cardiomyopathy, although likely underdiagnosed. Dr. Lyon shared convincing data from several experimental models showing that the presence of estrogen protects against Tako-Tsubo, while depletion of estrogen is harmful. This helps to explain why women more often suffer from this disease. Furthermore, he showed interesting data on adrenaline and noradrenaline, and beta1- and beta2-adrenergic receptors, further clarifying the pathophysiology of this intriguing disease.
Sessions like this one help to provide clinicians with deeper insight into pathophysiology, and provide clinical background for those who have a more basic orientation.
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