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J Am Coll Cardiol, 2003; 41:2299, doi:10.1016/S0735-1097(03)00488-1
© 2003 by the American College of Cardiology Foundation
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LETTER TO THE EDITOR

Reply

Robert J. Scheubel, MD

Department of Cardiothoracic Surgery, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Str. 40, D-06097 Halle (Saale), Germany

robert.scheubel{at}medizin.uni-halle.de


We thank Dr. Marin-Garcia for the interest in our study (1). He is right in stating that our citation of his study (2) "indicating disturbed mitochondrial gene expression" is inaccurate. We regret such inaccuracies, which must have occurred during several reformulations of our text. The reasons for the reduced activities in complex III and complex V in his tachypacing-induced failure model (2) remain undetermined at present. However, we are happy that Dr. Marin-Garcia agrees to our conclusion that a depressed complex I activity in failing human myocardium may not be due to generalized damage of mitochondrial deoxyribonucleic acid.


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1. Scheubel RJ, Tostlebe M, Simm A, et al. Dysfunction of mitochondrial respiratory chain complex I in human failing myocardium is not due to disturbed mitochondrial gene expression. J Am Coll Cardiol. 2002;40:2174–2181[Abstract/Free Full Text]

2. Marin-Garcia J, Goldenthal MJ, Moe GW. Abnormal cardiac and skeletal muscle mitochondrial function in pacing-induced cardiac failure. Cardiovasc Res. 2001;52:103–110[CrossRef][Medline]





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