Why the study?
Does chronic treatment with ivabradine improve endothelium-dependent vasodilatation in human apoB-100 transgene dyslipidaemic mice?
Does chronic treatment with ivabradine improve endothelium-dependent vasodilatation in human apoB-100 transgene dyslipidaemic mice?
Heart rate reduction with ivabradine improves endothelial function in a dyslipidemic mouse model, suggesting potential benefits beyond its anti-ischemic effects.
Ivabradine has proven therapeutic efficacy for cardiac ischaemia and, until proved otherwise, is a very specific inhibitor of the cardiac sinoatrial node I(f) current. In the current issue of the British Journal of Pharmacology, Drouin et al. demonstrated that chronic treatment of the human apoB-100 transgene dyslipidaemic mouse with ivabradine significantly improved endothelium-dependent vasodilatation to ACh in renal and cerebral arteries and that the beneficial effects of ivabradine result secondarily to the lowering of heart rate. These data suggest that drugs that target the I(f) current have potential benefits not only as anti-ischaemics but also as agents for the treatment of endothelial dysfunction.
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Chris R. Triggle (2008) studied this question.
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