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Atorvastatin Reduces Plasma Inflammatory and Oxidant Biomarkers in Patients With Risk of Atherosclerotic
Fadia Mayyas1, Duha Baydoun1, Rasheed Ibdah2,3
11 Department of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan.
Insights
Atorvastatin therapy significantly reduces key markers of oxidative stress and inflammation, including C-reactive protein (CRP) and myeloperoxidase (MPO), in patients at risk for atherosclerotic cardiovascular disease (ASCVD). This effect is independent of its cholesterol-lowering benefits.
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- Oxidative stress and inflammation are implicated in endothelial injury and coronary artery disease (CAD).
- Key inflammatory factors promoting oxidative damage include endothelin-1 (ET-1), myeloperoxidase (MPO), and C-reactive protein (CRP).
- Statins, like atorvastatin, are recommended for patients with atherosclerotic cardiovascular disease (ASCVD) risk.
Purpose of the Study:
- To evaluate the impact of atorvastatin on plasma biomarkers of inflammation and oxidation.
- To assess these effects in patients with moderate to very high risk of ASCVD.
Main Methods:
- 210 cardiology patients were stratified by ASCVD risk.
- Moderate- (20 mg/d) to high-intensity (40 mg/d) atorvastatin was administered.
- Plasma levels of lipids, ET-1, CRP, MPO, nitrite, lipid peroxides (TBARS), and SOD activity were measured at baseline and 12 weeks.
Main Results:
- Baseline inflammatory markers (CRP, MPO, ET-1, nitrite) were higher in very high-risk patients; SOD activity was lower.
- Atorvastatin significantly reduced LDL cholesterol, total cholesterol, CRP, MPO, nitrite, and TBARS.
- Atorvastatin increased SOD activity in moderate to very high-risk ASCVD patients, independent of lipid reduction.
Conclusions:
- Elevated CRP, ET-1, nitrite, and MPO are linked to increased ASCVD risk.
- Moderate and high-intensity atorvastatin effectively reduces plasma oxidative stress and inflammation.
- These anti-inflammatory and antioxidant effects occur irrespective of ASCVD risk level and lipid-lowering action.
Background:
Oxidative stress and inflammation are associated with endothelial injury and coronary artery disease. Inflammatory factors that promote oxidative damage include endothelin-1 (ET-1), myeloperoxidase (MPO), and C-reactive protein (CRP). Current guidelines recommend the use of statins in patients with risk of atherosclerotic cardiovascular disease (ASCVD).
Aim:
To assess the impact of atorvastatin on plasma inflammatory and oxidant biomarkers in patients with moderate to very high risk of ASCVD.
Method:
Two hundred ten patients presented to the cardiology clinic were included and stratified into low, moderate, high, and very high risk of ASCVD. Moderate- (20 mg/d) to high-intensity (40 mg/d) atorvastatin was prescribed. Plasma levels of lipids, ET-1, CRP, MPO, total nitrite, lipid peroxides (thiobarbituric acid reactive substances [TBARS]), and superoxide dismutase (SOD) activities were measured at baseline and 12 weeks after treatment.
Result:
Relative to low-risk patients, baseline plasma inflammatory markers of CRP, MPO, ET-1, and nitrite were higher in patients with very high risk of ASCVD, whereas plasma SOD was lower (all P < .05). Use of high and moderate atorvastatin therapy significantly reduced low-density lipoprotein and total cholesterol levels, as well as plasma levels of CRP, MPO, nitrite, and TBARS, and increased plasma SOD activity in patients with moderate to very high risk of ASCVD, independent of lipid-lowering effects.
Conclusions:
Key markers of oxidative stress/inflammation such as CRP, ET-1, total nitrite, and MPO are associated with an increased risk of ASCVD. Moderate- and high-intensity atorvastatin use reduces plasma oxidative stress and inflammation regardless of ASCVD risk and independent of its lipid-lowering effect.
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