© 2006 European Society of Cardiology
Thalidomide attenuates the development of fibrosis during post-infarction myocardial remodelling in rats
a Research Institute for Internal Medicine, Rikshospitalet University Hospital, University of Oslo N-0027 Oslo, Norway
b Institute for Surgical Research, Rikshospitalet University Hospital, University of Oslo N-0027 Oslo, Norway
c Department of Cardiology, Ullevål University Hospital Norway
d Section of Endocrinology, Rikshospitalet University Hospital, University of Oslo N-0027 Oslo, Norway
e Section of Clinical Immunology and Infectious Diseases, Rikshospitalet University Hospital, University of Oslo N-0027 Oslo, Norway
f Medical Department, Diakonhjemmet Hospital Oslo, Norway
* Corresponding author. Tel.: +47 23 07 36 29; fax: +47 23 07 36 30. E-mail address: arne.yndestad{at}klinmed.uio.no
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Abstract |
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Background: Inflammation plays a pathogenic role in the development of heart failure (HF). The aim of this study was to examine the effect of treatment with the immunomodulating drug thalidomide in a rat model for post-myocardial infarction (MI) HF.
Methods: Rats were subjected to MI by left coronary artery ligation or sham-operated. Seven days after surgical intervention rats were randomised to treatment with thalidomide or vehicle for 8 weeks.
Results: Our main findings were: (i) thalidomide treatment did not affect cardiac function or the hypertrophic response, as determined by haemodynamic measurements and heart chamber weights, respectively. (ii) HF rats treated with thalidomide had a minor reduction in septum and relative wall thickness (p<0.05), indicating an anti-remodelling effect. (iii) Thalidomide appeared to have immunostimulatory effects on the myocardium as evident by increased MIP-1
gene expression (p<0.05). (iv) Treating HF rats with thalidomide reduced myocardial collagen content, as assessed by markedly decreased levels of hydroxyproline (
40% reduction; p<0.05), accompanied by lower TGF-β1 gene expression (p<0.05).
Conclusion: Although thalidomide had no effect on cardiac function, our results suggest that intervention with thalidomide may have beneficial effects in post-MI HF by attenuating collagen accumulation and development of myocardial fibrosis.
Key Words: Heart failure • Myocardial infarction • Inflammation • Fibrosis • Cytokine • Intervention
Received August 23, 2005; Revised January 3, 2006; Accepted February 8, 2006
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