@article{discovery1561596,
          volume = {38},
          number = {35},
           month = {September},
          author = {ALP Caforio and Y Adler and C Agostini and Y Allanore and A Anastasakis and M Arad and M B{\"o}hm and P Charron and PM Elliott and U Eriksson and SB Felix and P Garcia-Pavia and E Hachulla and S Heymans and M Imazio and K Klingel and R Marcolongo and M Matucci Cerinic and A Pantazis and S Plein and V Poli and A Rigopoulos and P Seferovic and Y Shoenfeld and JL Zamorano and A Linhart},
            note = {This version is the author accepted manuscript. For information on re-use, please refer to the publisher?s terms and conditions.},
           title = {Diagnosis and management of myocardial involvement in systemic immune-mediated diseases: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Disease.},
            year = {2017},
         journal = {European Heart Journal},
           pages = {2649--2662},
             url = {http://discovery.ucl.ac.uk/1561596/},
        abstract = {Systemic immune-mediated diseases (SIDs) include autoimmune and autoinflammatory diseases (AD) affecting at least two-organ systems.1 Autoinflammatory diseases refer to a growing family of conditions characterised by episodes of unprovoked inflammation in the absence of high autoantibody titres or auto reactive T lymphocytes, reflecting a primary innate immune system dysfunction.1 Conversely, autoimmune diseases are characterised by aberrant B, T and dendritic cell responses, leading to a break in tolerance against self-antigens, with predominantly cell-mediated or autoantibody-mediated responses in genetically susceptible individuals.2?11 Autoantibodies (AAbs), when detectable, can promote inflammatory responses via immune complex formation and may directly affect target organ function,10 e.g. resulting, in cardiac autoimmunity, in electrical disturbance, cardiomyocyte dysfunction or loss and heart failure.12?15 However, a dichotomous classification does not reflect clinical evidence and a continuum from purely autoinflammatory to purely autoimmune diseases should be considered (Figure 1).1}
}