Effect of testosterone on post-myocardial infarction remodeling and function

doi:10.1016/S0008-6363(02)00701-0

Cardiovascular Research 2003 57(2):370-378; doi:10.1016/S0008-6363(02)00701-0
© 2003 by European Society of Cardiology

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Effect of testosterone on post-myocardial infarction remodeling and function

Matthias Nahrendorf^a^,1, Stefan Frantz^a^,1, Kai Hu^a, Constantin von zur Mühlen^a, Maria Tomaszewski^a, Heidi Scheuermann^a, Ralf Kaiser^a, Virginija Jazbutyte^a, Stephanie Beer^a, Wolfgang Bauer^a, Stefan Neubauer^b, Georg Ertl^a, Bruno Allolio^a^,* and Frank Callies^a

^aMedical University Hospital Wuerzburg, Josef-Schneider-Strasse 2, 97080 Wuerzburg, Germany
^bDepartment of Cardiovascular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, UK

b.allolio{at}medizin.uni-wuerzburg.de

^* Corresponding author. Tel.: +49-931-2013-6109; fax: +49-931-2013-6283.

Background: Men and women are differently affected by coronaryartery disease, suggesting an important role of sex steroids.Moreover, testosterone (T) treatment is increasingly used inelderly males. Therefore, we examined effects of chronic anabolicT administration on left ventricular (LV) remodeling after myocardialinfarction (MI). Methods: Adult male rats were treated withintramuscular placebo, testosterone undecanoate (T), or wereorchiectomized. After 2 weeks, animals underwent sham-operation(sham) or left coronary artery ligation. Left ventricular remodelingand function was assessed by serial magnetic resonance imaging(MRI) at weeks 2 and 8 and hemodynamic investigation at week8. Results: In sham operated animals T administration increasedserum T levels and led to cardiac hypertrophy, but not to anupregulation of ANP mRNA. The ${alpha}$ /β-MHC ratio was significantlyhigher after T treatment due to an increase in ${alpha}$ -MHC. As a potentialmechanism for this "physiologic" form of hypertrophy, IGF-1mRNA expression was significantly increased in T treated animals.After coronary artery ligation, infarct size and mortality weresimilar among the groups. Left ventricular hypertrophy was enhancedby T treatment. However, in vivo LV end-diastolic pressure andwall stress were decreased by T, whereas other hemodynamic parameters(mean arterial pressure, cardiac output, etc.) remained unchanged.Conclusion: Chronic anabolic T treatment led to a specific "physiologic"pattern of myocardial hypertrophy with a significant increasein LV weight, but without differences in ANP and with an upregulationin ${alpha}$ /β-MHC, possibly mediated by IGF-1. Testosterone treatmenthad no detrimental effects following MI. Reduced wall stressand LVEDP may even improve long-term outcome.

KEYWORDS Heart failure; Hormones; Hypertrophy; Infarction; Remodeling

¹ Both authors contributed equally.

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