Why the study?
Does fluvastatin improve endothelial function, oxidative stress, and inflammation in patients with arterial hypertension and normal LDL-cholesterol?
Does fluvastatin improve endothelial function, oxidative stress, and inflammation in patients with arterial hypertension and normal LDL-cholesterol?
Fluvastatin does not improve endothelial function, oxidative stress, or inflammation in hypertensive patients with normal LDL-cholesterol, arguing against its use in this population without other risk factors.
Answers are grounded in this paper and cite their sources.
No endothelial benefit with fluvastatin in hypertensive patients with normal LDL; challenges pleiotropic vascular effects beyond lipid lowering.
OBJECTIVE: Patients with arterial hypertension are characterized by impaired endothelial function and increased cardiovascular risk. Statins have been proposed as a potential treatment option in hypertension, even in those with normal low-density lipoprotein (LDL)-cholesterol levels. We tested whether fluvastatin reduces oxidative stress and inflammation, and improves endothelial function in patients with arterial hypertension and normal LDL-cholesterol. METHODS: In a cross-over designed, double-blind randomized trial, 26 patients with arterial hypertension and LDL-cholesterol below 160 mg/dl were treated for 2 weeks with either placebo or fluvastatin 80 mg/day. Endothelium-dependent vasodilation (EDV) was assessed as the forearm blood flow (FBF) response to intra-arterial infusion of acetylcholine (ACH, 12 and 48 μg/min), and endothelium-independent vasodilation (EIV) as the FBF response to nitroprusside (3.2 and 12.8 μg/min). Furthermore, we measured reduced to oxidized glutathione (GSH/GSSG) ratio in red blood cells, total antioxidant capacity in plasma (TAC) and high-sensitivity C-reactive protein (hs-CRP) levels. RESULTS: Fluvastatin lowered LDL-cholesterol from 118 ± 16 to 90 ± 25 mg/dl (P < 0.0001), but had no effect on blood pressure, high-density lipoprotein (HDL)-cholesterol or triglycerides. EDV and EIV were unaffected by fluvastatin treatment (e.g. increase of FBF 48 μg/min: 339 ± 285% during placebo versus 268 ± 194% during fluvastatin, n.s.). Finally, GSH/GSSG ratio, TAC and hs-CRP levels were similar between fluvastatin and placebo treatment. CONCLUSION: Fluvastatin treatment did not improve endothelial function, oxidative stress or inflammation in patients with arterial hypertension and normal LDL-cholesterol levels. These data argue against the usefulness of statins in patients with arterial hypertension in the absence of hypercholesterolemia or other additional risk factors.
No takes yet. Share an insight, caveat, or question.
Schneider et al. (2011) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: