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Cardiovascular Research 1999 43(1):117-124; doi:10.1016/S0008-6363(99)00075-9
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Chronic high-dose creatine feeding does not attenuate left ventricular remodeling in rat hearts post-myocardial infarction

Michael Horna, Helga Remkesa, Charlotte Dienescha, Kai Hub, Georg Ertlb and Stefan Neubauera,*

aMedizinische Universitätsklinik Würzburg, Josef-Schneider-Straße 2, 97080 Würzburg, Germany
bKlinikum Mannheim, Abteilung Kardiologie, Heidelberg University, Heidelberg, Germany

* Corresponding author. Tel.: +49-931-2013158; fax: +49-931-2012291 s.neubauer{at}mail.uni-wuerzburg.de

Objective: In heart failure, cardiac energy metabolism is compromised. The failing myocardium is characterized by reduced contents of both phosphorylated (phosphocreatine) and non-phosphorylated (free) creatine content as well as decreased energy reserve via creatine kinase (creatine kinase reaction velocity). These changes may contribute to cardiac dysfunction. The purpose of the present study was to determine whether chronic feeding with high-dose dietary creatine prevents the derangement of energy metabolism and the development of left ventricular remodeling in a rat model of heart failure, i.e. post-myocardial infarction (MI). Methods and results: Rats were subjected to sham operation or left coronary artery ligation. Surviving rats were fed with 0% (untreated) or 3% creatine (related to weight of diet) for 8 weeks. Creatine feeding increased serum creatine levels significantly ~2-fold. Thereafter, hearts were isolated, perfused and left ventricular pressure–volume curves obtained. Steady state and dynamic (CK reaction velocity) high-energy phosphate metabolism was determined with 31P NMR spectroscopy. In both MI groups (treated n=8, untreated n=7), pressure–volume curves were shifted right- and downward compared to both sham groups (treated n=5, untreated n=7), i.e. creatine had no effect on left ventricular remodeling. Likewise, similar reductions of phosphocreatine, free creatine and creatine kinase reaction velocity (untreated sham 12.0±0.7 mmol/lxs; untreated MI 7.8±0.7*; treated sham 13.6±1.0; treated MI 7.2±1.1*; * p<0.025 sham vs. MI) were found in both MI groups. Conclusions: Chronic creatine feeding of post-MI rats is ineffective in preventing the functional and energetic derangements occurring post-MI. Inspite of increased serum creatine levels, neither the normal nor the failing heart accumulates additional creatine.

KEYWORDS Creatine; 31P NMR spectroscopy; Heart failure; ATP; Phosphocreatine; Isolated rat heart


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