M. Hausberg et al., Effect of fluvastatin on endothelium-dependent brachial artery vasodilation in patients after renal transplantation, KIDNEY INT, 59(4), 2001, pp. 1473-1479
Background Hypercholesterolemia may affect both endothelial function and ar
terial distensibility (DC). Renal transplant recipients (NTX) exhibit advan
ced structural and functional alterations of arterial vessel walls. The aim
of this double-blind, randomized trial was to evaluate the effects of fluv
astatin (FLU) on brachial artery flow-mediated vasodilation (FMD) and DC in
hypercholesterolemic NTX.
Methods. Eighteen NTX received FLU 40 mg/day and 18 NTX placebo (PLA). Befo
re and after six months of treatment, the brachial artery diameter and DC a
t rest were measured by a Doppler frequency analysis in the M mode, and the
n changes in diameter during reactive hyperemia (to assess endothelial-depe
ndent FMD) and after 400 mug sublingual nitroglycerin (to assess endotheliu
m-independent vasodilation-NMD).
Results. FLU, but not PLA, treatment resulted in significant decreases in t
otal (from 288 +/- 10 to 239 +/- 8 mg/dL, P < 0.05) and low-density lipopro
tein cholesterol (from 182 <plus/minus> 779 to 138 +/- 8 mg/dL, P < 0.05).
Blood pressure did not differ between FLU- and PLA-treated patients and was
not affected by either treatment. Also, the brachial artery baseline diame
ter was not different between groups and was not affected by FLU or PLA. Br
achial artery how at rest and during reactive hyperemia as measured by puls
ed Doppler did not differ between groups. Brachial artery FMD increased wit
h FLU from 0.23 <plus/minus> 0.08 to 0.54 +/- 0.08 mm (P < 0.05), whereas P
LA did not alter FMD (0.22 <plus/minus> 0.07 vs. 0.14 +/-: 0.05 mm at basel
ine and after six months of PLA treatment, respectively, P = NS). In contra
st, NMD did not change significantly with either treatment (0.76 +/- 0.13 v
s. 0.83 +/- 0.15 mm at baseline and after 6 months of FLU treatment, respec
tively, P = NS, and 0.64 +/- 0.09 vs. 0.66 +/- 0.10 mm at baseline and afte
r 6 months of PLA treatment, respectively, P = NS). Also, brachial artery D
C was not altered by FLU (6.4 +/- 1.0 vs. 5.8 +/- +/- 0.6 x 10(-3)/kPa, P =
NS) or PLA treatment (5.8 +/- 0.6 vs. 6.8 +/- 0.8 x 10(-3)/kPa, P = NS).
Conclusions. In hypercholesterolemic NTX, the HMG-CoA reductase inhibitor F
LU significantly improves brachial artery FMD as a measure of endothelial f
unction after six months of treatment. In contrast, FLU does not have a ben
eficial effect on brachial artery DC.