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Preventive Arterial Wall Phenotype and Low-dose Fluvastatin/Valsartan Combination

Not Applicable
Completed
Conditions
Atherosclerosis
Interventions
Registration Number
NCT03393377
Lead Sponsor
University Medical Centre Ljubljana
Brief Summary

The study was designed to test whether short-term treatment with a very low-dose combination of fluvastatin and valsartan could induce improvement of endothelial function, arterial stiffness, vascular inflammation, oxidative stress and expression of protective genes in subjects with moderate cardiovascular risk.

Detailed Description

The largest population that suffers from cardiovascular events are subjects at moderate cardiovascular risk. However, no effective and safe preventive treatment is available for this population. This study aimed to investigate whether their arterial wall phenotype could be turned to a preventive direction by low-dose fluvastatin/valsartan combination (low-flu/val).

Twenty males at moderate cardiovascular risk (as classified by SCORE) were blindly randomised into the intervention group (n=10, low-flu/val: 10 mg/20mg) or control group (n=10, placebo). At inclusion and after 30 days of treatment, brachial flow-mediated dilatation (FMD), beta stiffness coefficient, carotid pulse wave velocity (c-PWV), carotid-femoral PWV, reactive hyperaemia index, high-sensitivity C-reactive protein (hs-CRP), interleukin 6, vascular cell adhesion molecule 1, total antioxidant status and expression of several protective genes (SIRT1, mTOR, NF-κB1, NFE2L2, PRKAA1) were followed.

Recruitment & Eligibility

Status
COMPLETED
Sex
Male
Target Recruitment
20
Inclusion Criteria
  • moderate cardiovascular risk according to Systematic Coronary Risk Estimation (SCORE) risk charts of the European Society of Cardiology
  • males
  • aged between 40 and 55 years
Exclusion Criteria
  • diabetes mellitus
  • manifest peripheral artery disease or carotid artery disease
  • acute infection
  • chronic diseases
  • present therapy with fluvastatin and/or valsartan

Study & Design

Study Type
INTERVENTIONAL
Study Design
PARALLEL
Arm && Interventions
GroupInterventionDescription
intervention groupfluvastatin 10 mg and valsartan 20 mgreceived fluvastatin 10 mg and valsartan 20 mg (low-flu/val) for 30 days
control groupplaceboreceived placebo for 30 days
Primary Outcome Measures
NameTimeMethod
gene Nrf2/NFE2L230 days

Hs00975961_g1

gene AMPK/PRKAA130 days

Hs01562315_m1

brachial flow-mediated dilatation (FMD)30 days

FMD measured by ultrasound on right brachial artery (as result of reactive hyperaemia)

reactive hyperaemia index (RHI)30 days

RHI measured by Endopat device

gene mTOR30 days

Hs00234522_m1

vascular cell adhesion molecule 1 (VCAM1)30 days

inflammatory marker

beta stiffness coefficient30 days

assessed by ultrasound employing e-Tracking on right common carotid artery

gene NF-kB130 days

Hs00765730_m1

carotid pulse wave velocity (c-PWV)30 days

assessed by ultrasound employing e-Tracking on right common carotid artery

carotid-femoral PWV (cf-PWV)30 days

cf-PWV measured by Sphygmocor device

high-sensitivity C-reactive protein (hs-CRP)30 days

inflammatory marker

interleukin 6 (IL-6)30 days

inflammatory marker

total antioxidant status (TAS)30 days

marker of oxidative stress

gene SIRT130 days

Hs01009006_m1

Secondary Outcome Measures
NameTimeMethod
brachial flow-mediated dilatation (FMD)10 weeks after treatment completion

FMD measured by ultrasound on right brachial artery (as result of reactive hyperaemia)

reactive hyperaemia index (RHI)10 weeks after treatment completion

RHI measured by Endopat device

beta stiffness coefficient10 weeks after treatment completion

assessed by ultrasound employing e-Tracking on right common carotid artery

carotid pulse wave velocity (c-PWV)10 weeks after treatment completion

assessed by ultrasound employing e-Tracking on right common carotid artery

carotid-femoral PWV (cf-PWV)10 weeks after treatment completion

cf-PWV measured by Sphygmocor device

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