doi: 10.1161/CIRCULATIONAHA.106.684480
(Circulation. 2007;115:e384.)
© 2007 American Heart Association, Inc.
Correspondence |
Response to Letter Regarding Article, "Cardiac Troponin I but Not Cardiac Troponin T Induces Severe Autoimmune Inflammation in the Myocardium"
Department of Internal Medicine III, University of Heidelberg, Heidelberg, Germany
Institute of Vegetative Physiology, University of Cologne, Koeln, Germany
Departments of Pathology and Molecular Microbiology and Immunology, The Johns Hopkins Medical Institutions, Baltimore, Md
We thank Drs Conti and Volpe for their valuable comments regarding our article.1 We agree with their opinion that autoimmunity to troponins might have additional influence on the pathogenesis of cardiovascular diseases. In our recent publication, we describe how the induction of an immune response to troponin I (TnI) can induce a severe inflammation and fibrosis and then dilation and dysfunction of the myocardium. Furthermore, we show that preimmunization before the ligation of the left anterior descending artery leads to increased inflammation and ischemia-induced infarct size.1
In our discussion, we mainly focus on the effects of inducing autoimmunity toward the myocardium, and we do not discuss the possible implications of our findings on the development of atherothrombosis. Our results demonstrate an important effect for inducing an autoimmune response against TnI (the preferred marker of myocardial damage and risk stratification in acute coronary syndrome) in heart failure. These findings may aid in developing new approaches to the early treatment of heart failure in some patients and initiating further (clinical) studies to investigate the role of TnI release during acute cardiac damage and induction of autoimmunity against TnI in postinfarct remodeling and its role in heart failure. Additionally, as Drs Conti and Volpe mention, it has recently been reported that increased levels of troponins can be found in patients without acute coronary syndrome and that these levels correlate to 10-year mortality.2 These results are supported by our recent findings that levels of increased antibody titers against TnI can be found not only in patients with acute coronary syndromes but also in some subjects without a known history for cardiovascular diseases (Z. Kaya, MD, unpublished data, 2006), where they also may be useful as predictors for future heart disease and mortality.
In conclusion, we agree with Drs Conti and Volpe that more basic and clinical studies need to be performed to elucidate the role of autoimmunity to troponins as predictors of heart failure and atherothrombosis.
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Acknowledgments |
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Sources of Funding
This work was supported by the Ernst und Berta Grimmke Stiftung (Dr Kaya); the Deutschen Forschungsgemeinschaft, research grants KA 1797/3-1 (Dr Kaya) and SFB 612 (Dr Pfitzer); and in part by the National Institutes of Health, research grants HL077611 and HL067290 (Dr Rose).
Disclosures
Dr Katus developed the troponin T assay and holds a patent on this assay jointly with Roche Diagnostics. The other authors report no conflicts.
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References |
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 Top References |
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1. Göser S, Andrassy M, Buss SJ, Leuschner F, Volz CH, Ottl R, Zittrich S, Blaudeck N, Hardt SE, Pfitzer G, Rose NR, Katus HA, Kaya Z. Cardiac troponin I but not cardiac troponin T induces severe autoimmune inflammation in the myocardium. Circulation. 2006; 114: 1693–1702.
2. Zethelius B, Johnston N, Venge P. Troponin I as a predictor of coronary heart disease and mortality in 70-year-old men: a community-based cohort study. Circulation. 2006; 113: 1071–1078.
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