BMC cardiovascular disorders · 2026
Heart-reactive antibody levels differentially associate with ventricular function in hereditary cardiomyopathies.
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Schiffer Dennis, Afshar Boshra, Grosser Daria, Pet Juliana, Schmidbauer Lena, Bauser Maximilian, Ramos Gustavo, Boivin-Jahns Valerie, Jahns Roland, Frantz Stefan, Heuschmann Peter, Störk Stefan, Gerull Brenda, Beyersdorf Niklas, Morbach Caroline
Аннотация
BACKGROUND: gCMP are a major cause of cardiovascular morbidity and mortality. While agonistic anti-β1-adrenergic receptor antibodies (anti-β1AR-ECII) have a recognized pathogenic role in idiopathic dilated cardiomyopathy (DCM), the relevance of HRA in gCMP remains unclear.
METHODS: One hundred gCMP patients with confirmed genetic variants in cardiomyopathy genes were compared with 100 age- and sex-matched healthy individuals. Antibody reactivities were quantified using bead-based flow cytometric assays against cardiac antigens: The second extracellular loop of the β1 adrenergic receptor (β1AR-ECII), Troponin I3 (TPI3), Tropomyosin 1 (TPM1), Myosin heavy chain 6 and 7 (MYH6, MYH7) and Myosin light chain 7 (MYL7).
RESULTS: gCMP patients showed higher anti-TPI3 and lower anti-TPM1 antibody levels compared to controls indicating increased induction of the former and loss of the latter in gCMP patients. Age and sex influenced HRA patterns in both groups. Anti-MYH6 and anti-TPM1 antibody levels were negatively associated with left ventricular ejection fraction (LVEF), both overall and within specific gCMP subtypes, including hypertrophic and arrhythmogenic cardiomyopathy. Additionally, anti-MYH6 antibody levels were negatively associated with right ventricular function, measured by tricuspid annular plane systolic excursion (TAPSE).
CONCLUSION: Our findings stress the diagnostic potential of HRA profiling and indicate that gCMP patients might profit from therapeutic targeting of HRA.
METHODS: One hundred gCMP patients with confirmed genetic variants in cardiomyopathy genes were compared with 100 age- and sex-matched healthy individuals. Antibody reactivities were quantified using bead-based flow cytometric assays against cardiac antigens: The second extracellular loop of the β1 adrenergic receptor (β1AR-ECII), Troponin I3 (TPI3), Tropomyosin 1 (TPM1), Myosin heavy chain 6 and 7 (MYH6, MYH7) and Myosin light chain 7 (MYL7).
RESULTS: gCMP patients showed higher anti-TPI3 and lower anti-TPM1 antibody levels compared to controls indicating increased induction of the former and loss of the latter in gCMP patients. Age and sex influenced HRA patterns in both groups. Anti-MYH6 and anti-TPM1 antibody levels were negatively associated with left ventricular ejection fraction (LVEF), both overall and within specific gCMP subtypes, including hypertrophic and arrhythmogenic cardiomyopathy. Additionally, anti-MYH6 antibody levels were negatively associated with right ventricular function, measured by tricuspid annular plane systolic excursion (TAPSE).
CONCLUSION: Our findings stress the diagnostic potential of HRA profiling and indicate that gCMP patients might profit from therapeutic targeting of HRA.