Key result
Thalidomide treatment in rats with post-myocardial infarction heart failure reduced myocardial collagen content by approximately 40% (p<0.05), though it did not affect cardiac function.
Why the study?
Does thalidomide attenuate fibrosis and improve cardiac function in a rat model of post-MI heart failure?
RCT
randomised
Does thalidomide attenuate fibrosis and improve cardiac function in a rat model of post-MI heart failure?
Effect estimate: approximately 40% reduction
p-value: p=<0.05
In a rat model of post-MI heart failure, thalidomide attenuated myocardial fibrosis and collagen accumulation without affecting overall cardiac function.
No clinical role for thalidomide in post-MI HF; leaves open whether fibrosis reduction improves outcomes in translational models.
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-1alpha gene expression (p<0.05). (iv) Treating HF rats with thalidomide reduced myocardial collagen content, as assessed by markedly decreased levels of hydroxyproline ( approximately 40% reduction; p<0.05), accompanied by lower TGF-beta(1) 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.
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Yndestad et al. (2006) conducted an RCT in post-myocardial infarction heart failure. Thalidomide vs. vehicle was evaluated on myocardial collagen content (hydroxyproline levels) (approximately 40% reduction, p=<0.05). Thalidomide treatment in rats with post-myocardial infarction heart failure reduced myocardial collagen content by approximately 40% (p<0.05), though it did not affect cardiac function.
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