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L-arginine improves endothelial function and reduces LDL oxidation in patients with stable coronary artery disease
Wei-Hsian Yin1, Jaw-Wen Chen, Chingmin Tsai
1Division of Cardiology, Cheng-Hsin General Hospital, and Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Insights
Oral L-arginine supplementation improved endothelial function and reduced low-density lipoprotein (LDL) oxidation in patients with stable coronary artery disease (CAD). This study highlights L-arginine
Area of Science:
- Cardiovascular Medicine
- Nutritional Science
- Biochemistry
Background:
- Stable coronary artery disease (CAD) patients often experience endothelial dysfunction and increased oxidative stress.
- Investigating the impact of oral L-arginine on these markers is crucial for therapeutic strategies.
Purpose of the Study:
- To evaluate the effects of oral L-arginine on endothelial function, oxidative stress, and inflammatory markers in stable CAD patients.
- To compare L-arginine with vitamin C as an active control for these effects.
Main Methods:
- A randomized, crossover study involving 31 stable CAD patients.
- Patients received oral L-arginine (10g) or vitamin C (500mg) daily for 4 weeks, with a 2-week washout period.
- Endothelial function, lipid profiles, inflammatory markers, and LDL oxidation susceptibility were assessed.
Main Results:
- Both L-arginine and vitamin C significantly improved brachial artery flow-mediated dilatation.
- Neither L-arginine nor vitamin C altered lipid profiles or circulating inflammatory markers.
- L-arginine significantly increased the lag time of LDL oxidation, indicating reduced susceptibility.
Conclusions:
- Oral L-arginine supplementation enhances endothelial function in stable CAD patients.
- L-arginine effectively reduces low-density lipoprotein (LDL) oxidation in this patient group.
- L-arginine shows potential as a therapeutic agent for managing oxidative stress in CAD.
Background:
We investigated the effects of oral L-arginine on endothelial function, intravascular oxidative stress, and circulating inflammatory markers in patients with stable coronary artery disease (CAD).
Methods:
Thirty-one stable CAD patients were randomly assigned to oral L-arginine (10 g) or vitamin C (500 mg, an antioxidant, as active control) daily for 4 weeks, with crossover to the alternate therapy after 2 weeks off therapy, in this study. Brachial artery endothelial function studies were performed and serum concentrations of lipids and inflammatory markers were measured at baseline, at the end of each 4-week treatment period and at the 2-week wash-out period. Susceptibility of low-density lipoprotein (LDL) particles to oxidation, a marker of oxidative stress, was determined in 11 patients at random before and after 4-week treatment of oral L-arginine.
Results:
We demonstrates that consumption of either L-arginine or vitamin C significantly increased brachial artery flow-mediated dilatation (mean diameter change from baseline of 4.87%, P<0.0001 and of 3.17%, P=0.0003, respectively). Neither oral L-arginine nor vitamin C affected lipid profiles and circulating levels of inflammatory markers. However, in the 11 patients whose LDL susceptibility to oxidation was determined, lag time significantly increased by 27.1% (P=0.045) after consumption of L-arginine for 4 weeks.
Conclusions:
Oral L-arginine supplement improved endothelial function and reduced LDL oxidation in stable CAD patients.
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