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Updated: Jul 6, 2026

On-Chip Endothelial Inflammatory Phenotyping
Published on: July 21, 2012
Integrin expression on monocytes and lymphocytes in unstable angina short term effects of atorvastatin
Minodora Dobreanu1, D Dobreanu, Andrea Fodor
1Department of Clinical Biochemistry-Immunology, University of Medicine and Pharmacy, Târgu Mureş, Romania. dobreanu@orizont.net
Insights
Atorvastatin significantly reduced monocyte and lymphocyte activation markers in patients with unstable angina. These anti-inflammatory effects of statins may improve cardiovascular outcomes beyond cholesterol reduction.
Area of Science:
- Cardiology
- Immunology
- Pharmacology
Background:
- Inflammatory processes in coronary plaques are key to acute atherothrombotic events.
- Statins, potent lipid-lowering drugs, possess anti-inflammatory and immunomodulatory properties independent of cholesterol reduction.
Purpose of the Study:
- To investigate the impact of atorvastatin on monocyte and lymphocyte activation in patients with unstable angina (UA) and mild primary hypercholesterolemia.
- To assess if atorvastatin's effects are linked to its cholesterol-lowering capabilities.
Main Methods:
- A study involving 22 patients (12 UA, 10 stable coronary heart disease) after a 4-week drug-free baseline.
- Treatment with atorvastatin 20 mg/day for 8 weeks.
- Flow cytometry was used to measure monocyte and lymphocyte activation markers (CD14, HLA-DR, CD11b, 11c, 49d) pre- and post-treatment.
Main Results:
- Patients with UA exhibited higher baseline expression of monocyte CD11b, 11c, CD14, and T lymphocyte CD11b compared to stable patients (p < 0.001).
- Atorvastatin treatment led to a significant decrease in these activation markers in UA patients.
- Reductions in adhesion molecules, C-reactive protein (CRP), and soluble intercellular adhesion molecule-1 (sICAM-1) were observed.
Conclusions:
- Atorvastatin effectively reduces monocyte and lymphocyte activation in patients with unstable angina.
- These immunomodulatory effects may contribute to the clinical benefits of atorvastatin in coronary artery disease, irrespective of lipid-lowering.
- Further research into these non-lipid-lowering mechanisms is warranted.
Abstract:
Inflammatory reactions in coronary plaques play an important role in the pathogenesis of acute atherothrombotic events. The most powerful class of lipid-lowering drugs available-statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors)--have additional actions, unrelated to cholesterol reduction, including anti-inflammatory and immunomodulatory properties. This study sought to determine if atorvastatin affects monocyte and lymphocyte activation in patients with unstable angina and mild primary hypercholesterolemia. Following a 4-weeks hypolipemiant-free baseline period, 22 patients-12 with unstable angina (UA) and 10 patients with stable coronary heart disease (SCHD) - were treated with Atorvastatin 20 mg/day. Lipopolysaccharide (LPS)-receptor (CD14) and HLA-DR expression on monocytes and beta-integrins (CD11b, 11c, 49d) on monocytes and lymphocytes were measured by flow cytometry before and after treatment with atorvastatin for 8 weeks. Monocyte CD11b, 11c and CD14 expression and T lymphocytes CD11b expression were significantly (p < 0.001) higher in UA patients before treatment when compared with that in SCHD patients. In patients with UA, they decreased markedly with atorvastatin treatment. The reduction in expression of adhesion molecule on monocytes and lymphocytes and the concentrations of CRP and sICAM-1 may crucially contribute to the clinical benefit of atorvastatin in coronary artery disease, independent of cholesterol lowering effects.
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