Patients with heart failure recover differently after acute decompensation. Since the reasons for these different courses are largely unclear, there are also no adequate therapeutic options yet. However, we have recently made a key observation by showing that the development of anti-myocardial autoantibodies is associated with poor clinical outcome. The type and strength of this autoimmune response is hypothesised to contribute to how heart failure progresses.
Rationale and aim
We want to analyse in detail the autoantibody response after acute decompensation of heart failure. A better understanding of this autoantibody response should form the basis for new diagnostic tests and ideally also pave the way for an immunotherapy of heart failure.
Autoantibodies are detected in the blood of patients with acutely decompensated heart failure – directly at the time of decompensation and up to 18 months later. In parallel, the composition of leukocytes in peripheral blood is also analysed. For the detection of the anti-myocardial autoantibodies and for cellular immunophenotyping, we use immunofluorescence, FACS and so-called antigen chips. These biochips have a large number of binding sites in a very small space and thus make it possible to find out which antigenic target structures the autoantibodies recognise.
Significance and outlook
From the characterisation of the anti-myocardial autoantibody response after acute decompensation of heart failure we expect to be able to name diagnostically important parameters and to point out ways for new immunotherapeutic procedures. This applies especially to the variant of heart failure with preserved pump function (HFpEF).
Medizinische Klinik und Poliklinik I, Universitätsklinikum Würzburg, Zentrum für Innere Medizin (ZIM), Oberdürrbacher Straße 6, Haus A3, 97080 Würzburg, Deutschland
Deutsches Zentrum für Herzinsuffizienz Würzburg | Comprehensive Heart Failure Center | Am Schwarzenberg 15 | Haus A15 | 97078 Würzburg