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Effects of clopidogrel therapy on oxidative stress, inflammation, vascular function, and progenitor cells in stable
Ronnie Ramadan1, Saurabh S Dhawan, Hamid Syed
1*Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA; †Department of Biostatistics and Bioinformatics, Rollins School of Public Health, Atlanta, GA; and ‡Division of Cardiology, Department of Medicine, American University of Beirut, Beirut, Lebanon.
Insights
Clopidogrel therapy in stable coronary artery disease patients primarily offers an antiplatelet effect. It did not improve endothelial function, arterial stiffness, or other cardiovascular disease risk markers.
Area of Science:
- Cardiology
- Pharmacology
- Vascular Biology
Background:
- Atherosclerosis develops from endothelial injury and activation of leukocytes and platelets.
- Clopidogrel, an antiplatelet medication, was investigated for potential broader atheroprotective effects beyond its primary function.
Purpose of the Study:
- To evaluate the pleiotropic effects of clopidogrel therapy in patients with stable coronary artery disease.
- To assess clopidogrel's impact on endothelial function, arterial stiffness, inflammation, oxidative stress, and progenitor cells.
Main Methods:
- A double-blind, placebo-controlled, crossover study involving 41 subjects.
- Participants received clopidogrel (75 mg daily) or placebo for 6 weeks, followed by a crossover to the other treatment.
- Vascular and inflammatory markers were assessed, including flow-mediated dilation, arterial stiffness, CD40 ligand, hs-CRP, aminothiols, and progenitor cells.
Main Results:
- Clopidogrel therapy significantly reduced soluble CD40 ligand, a prothrombotic and proinflammatory marker.
- No significant improvements were observed in endothelial function, arterial stiffness, other inflammatory markers, oxidative stress, or progenitor cells.
Conclusions:
- Clopidogrel therapy in stable coronary artery disease demonstrates a specific antiplatelet effect.
- The study found no evidence of clopidogrel impacting other subclinical cardiovascular disease risk markers.
Background:
Traditional cardiovascular risk factors lead to endothelial injury and activation of leukocytes and platelets that initiate and propagate atherosclerosis. We proposed that clopidogrel therapy in patients with stable coronary artery disease imparts a pleiotropic effect that extends beyond antiplatelet aggregation to other atheroprotective processes.
Methods:
Forty-one subjects were randomized in a double-blind, placebo-controlled, crossover study to receive either clopidogrel 75 mg daily or placebo for 6 weeks and then transitioned immediately to the other treatment for an additional 6 weeks. We assessed (1) endothelial function as flow-mediated dilation of the brachial artery, (2) arterial stiffness and central augmentation index using applanation tonometry, (3) vascular function as fingertip reactive hyperemia index, (4) inflammation by measuring plasma CD40 ligand and serum high-sensitivity c-reactive protein levels, (5) oxidative stress by measuring plasma aminothiols, and (6) circulating progenitor cells, at baseline and at the end of each 6-week treatment period.
Results:
Clopidogrel therapy resulted in a significant reduction in soluble CD40 ligand (P = 0.03), a prothrombotic and proinflammatory molecule derived mainly from activated platelets. However, clopidogrel therapy had no effect on endothelial function, arterial stiffness, inflammatory and oxidative stress markers, or progenitor cells.
Conclusions:
Our findings suggest a solitary antiplatelet effect of clopidogrel therapy in patients with stable coronary artery disease, with no effect on other subclinical markers of cardiovascular disease risk.
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