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Autoantibodies against Cardiac Troponin I in Patients with Dilated Cardio‐myopathy Predict Improvement of Cardiac Function by Immunoadsorption
Author(s) -
Kaya Ziya,
Leuschner Florian,
Trimpert Christiane,
Göser Stefan,
Öttl Renate,
Li Jin,
Felix Stephan,
Dengler Thomas J.,
Hugo Katus A.,
Staudt Alexander
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.668.29
Subject(s) - medicine , immunoadsorption , troponin i , cardiology , dilated cardiomyopathy , autoantibody , antibody , heart failure , myocardial infarction , immunology
Aims: Cardiac troponins in blood are the most preferred markers of myocardial damage. It has been shown that the application of antibodies against cardiac troponin I (cTnI) can induce dilation and dysfunction of the heart in mice. In the present study we investigated the presence of cTnI‐antibody in patients with dilated cardiomyopathy (DCM) and the effect of immunoadsorption (IA) on left ventricular function (LVF). Methods: 51 patients with DCM were included. Every patient underwent heart catheterisation including myocardial biopsy and received IA. LVF was determined by echocardiography before and 6 months after IA. Serum samples from each patient (before, 5 days and 6 month after IA) were screened for the presence of cTnI‐Ab. 22 of the 51 patients had positive cTnI‐Ab‐titers. Whereas LVF of patients with positive cTnI‐Ab‐titers improved after IA by +8.1% during follow up of 6 month (p<0.001 vs. baseline), patients with negative cTnI‐Ab‐titers showed an improvement of +4,1% only (p<0.04 vs. baseline). Furthermore, Patients with positive cTnI‐antibody‐titers showed a significantly better clinical improvement after IA (+1 NYHA‐class) than patients without cTnI‐antibodies (+0.5 NYHA‐class; p<0.05). Conclusion: Immunoadsortion therapy is associated with a pronounced improvement of LVF and NYHA‐Class in patients with detectable antibodies against cardiac troponin I.