Effect of acute changes in oxygen tension on flow-mediated dilation. Relation to cardiovascular risk

Ole Fröbert; Pernille Holmager; Ken michael Jensen; Erik Berg Schmidt; Ulf Simonsen

doi:10.1080/14017430701466402

January 1, 2008Scandinavian Cardiovascular JournalOpen Access

Effect of acute changes in oxygen tension on flow-mediated dilation. Relation to cardiovascular risk

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Why the study?

Do acute changes in oxygen tension or atorvastatin treatment affect flow-mediated dilation in patients with cardiovascular risk?

Structured PICO

Do acute changes in oxygen tension or atorvastatin treatment affect flow-mediated dilation in patients with cardiovascular risk?

P

Population

40 participants across two studies: 10 males with increased cardiovascular risk (mean age 44) and 10 matched controls without risk factors (mean age 44) in study 1; 20 persons with cardiovascular risk (mean age 50) in study 2.

I

Intervention

Inhalation of hypoxic gas (12.5% O2) and 100% O2 supplementation; Study 2 also included atorvastatin 80 mg/day for 3 months.

C

Comparator

Normoxia (21% O2, 79% N2) and baseline measurements before atorvastatin treatment.

O

Outcome

Endothelial responsiveness evaluated by brachial ultrasound and flow-mediated/nitroglycerin-mediated dilation (FMD/NMD).surrogate

Hypoxia reduces endothelial vasodilation and oxygen supplementation causes vasoconstriction, physiological effects that are not modified by high-dose atorvastatin therapy.

Implication

Acute oxygen tension changes may impair endothelial function in at-risk patients; leaves open atorvastatin effects beyond lipid lowering.

Abstract

OBJECTIVE: Oxygen-dependent changes in vascular diameters may be detrimental when the endothelium is dysfunctional. DESIGN: Endothelial responsiveness was evaluated by brachial ultrasound and flow-mediated/nitroglycerin-mediated dilation (FMD/NMD). FMD/NMD was investigated in males with increased risk of cardiovascular disease (mean age 44+/-2 years, n=10) and matched controls without risk factors (44+/-2 years, n=10). FMD/NMD was assessed during normoxia (21% O2, 79% N2), while inhaling hypoxic gas (12.5% O2, FMDHyp/NMD), and 100% O2 supplementation (FMDO2/NMD). In a second study we addressed the effect of lipid lowering. Twenty persons with cardiovascular risk (mean age 50+/-2 years) were treated with atorvastatin (80 mg/day) and FMD/NMD was measured during normoxia, hypoxia and oxygen supplementation before, after 1 day and 3 months. RESULTS: Oxygen supplementation evoked vasoconstriction, while FMDHyp/NMD was reduced compared to FMD/NMD. Atorvastatin significantly lowered total cholesterol, LDL cholesterol, and ADMA after 1 day of treatment, while triglycerides, ApoB and hsCRP were lowered after 3 months. Atorvastatin did not change FMD/NMD irrespective of oxygen tension. CONCLUSION: Irrespective of risk factors or atorvastatin, hypoxia reduced endothelial vasodilation while oxygen supplementation evoked vasoconstriction.