Why the study?
Does add-on aliskiren to valsartan improve endothelial-dependent vasodilation in hypertensive patients with ischemic heart disease?
Does add-on aliskiren to valsartan improve endothelial-dependent vasodilation in hypertensive patients with ischemic heart disease?
Adding aliskiren to valsartan in hypertensive patients with ischemic heart disease does not improve endothelial function but significantly reduces resting heart rate.
Aliskiren add-on does not improve FMD; challenges dual RAAS blockade for endothelial benefit while confirming heart rate reduction in hypertensive IHD.
The aim of this study was to evaluate the add-on effect of aliskiren to valsartan on endothelial-dependent vasodilation in hypertensive patients with ischemic heart disease (IHD). After 4 weeks of treatment with 80 mg of valsartan, 28 patients were allocated to either continued treatment with valsartan or an add-on treatment with valsartan plus 150 mg of aliskiren. Aliskiren significantly decreased plasma renin activity, whereas endothelium-dependent vasodilation measured by flow-mediated dilation (FMD) did not change. In contrast, heart rate significantly decreased (73.1 ± 9.8 to 66.3 ± 7.0 beats per minute at baseline and 24 weeks, respectively [P = .009]) and the standard deviation of the R-R intervals (SDNN) significantly increased in the aliskiren group. The add-on aliskiren to valsartan therapy may not improve endothelial functions, although it significantly reduced resting heart rate via regulation of the autonomic nervous system in hypertensive patients with IHD.
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Ozeki et al. (2014) studied this question.
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