WEDNESDAY, April 18 (HealthDay News) -- The Fcγ receptors IIa on cardiomyocytes may be the reason why autoantibodies generated in patients with dilated cardiomyopathy can trigger negative inotropic effects, according to a report in the April 24 issue of the Journal of the American College of Cardiology.
Dilated cardiomyopathy (DCM) is associated with autoantibodies that target cardiomyocytes, but how these antibodies impair cardiac function is unknown. Alexander Staudt, M.D., of the Ernst-Moritz-Arndt-Universitat in Greifswald, Germany, and colleagues isolated these antibodies from 11 DCM patients to determine which fragments of the antibodies triggered a response in cardiomyocytes.
The patients' antibodies reduced calcium transients and cell shortening of rat cardiomyocytes, while healthy patients' antibodies did not. However, the same effect was not seen using the isolated Fab portion of the antibody. Reconstituting the Fc portion of the antibody resulted in a regain of the effects on calcium transients and shortening of cardiomyocytes. These cells were found to express the corresponding Fcγ receptor IIa.
These results "should encourage investigators to explore this novel pathway to understand the pathogenesis of DCM and other autoimmune cardiac diseases," wrote Sudhir Gupta, M.D., Ph.D., from the University of California, Irvine, in an accompanying editorial. The antibodies should be used to subclassify patients with DCM and for development of immunoadsorption columns, Gupta added.
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