Aggressive statin therapy (atorvastatin 80 mg qd) for 6 months significantly reduced the expression of CX3CL1 and CX3CR1 in patients with coronary artery disease, unlike conventional therapy.
Observational (n=145)
Does aggressive statin therapy reduce CX3CL1 and CX3CR1 expression compared to conventional therapy in patients with coronary artery disease?
Aggressive statin therapy significantly reduces the expression of the pro-atherogenic fractalkine (CX3CL1) and its receptor in patients with coronary artery disease, suggesting a potential mechanism for plaque stabilization.
OBJECTIVE: Recent data derived primarily from studies in animal models suggest that fractalkine (CX3CL1) and its cognate receptor, CX3CR1, play a role in atherogenesis. We, therefore, hypothesized that enhanced CX3CL1/CX3CR1 expression may promote atherogenesis in patients with coronary artery disease (CAD). METHODS AND RESULTS: We examined the plasma levels of CX3CL1 and CX3CR1 expression in peripheral blood mononuclear cells (PBMC) in various CAD populations (30 patients with previous myocardial infarction, 40 patients with stable angina, 40 patients with unstable angina, and a total of 35 controls) and used various experimental approaches to characterize CX3CL1-mediated leukocyte responses. We found that the plasma levels of CX3CL1 are greatly increased in CAD, particularly in unstable disease. The parallel increase of CX3CR1 expression in PBMC was predominantly attributable to an expansion of the (CX3CR1+)(CD3+)(CD8+) T cell subset and was associated with enhanced chemotactic, adhesive, and inflammatory responses to CX3CL1. Statin therapy for 6 months reduced the expression of CX3CL1 and CX3CR1, reaching statistical significance for both parameters only during aggressive (atorvastatin, 80 mg qd) but not conventional (simvastatin, 20 mg qd) therapy. Consequently, the functional responses of the PBMC to CX3CL1 including migration, adhesion, and secretion of interleukin-8 were attenuated by the treatments. CONCLUSIONS: Our results suggest that the CX3CL1/CX3CR1 dyad may contribute to atherogenesis and plaque destabilization in human CAD.
Damås et al. (Fri,) conducted a observational in Coronary artery disease (n=145). Statin therapy (atorvastatin) vs. Conventional therapy (simvastatin 20 mg qd) was evaluated on Plasma levels of CX3CL1 and CX3CR1 expression. Aggressive statin therapy (atorvastatin 80 mg qd) for 6 months significantly reduced the expression of CX3CL1 and CX3CR1 in patients with coronary artery disease, unlike conventional therapy.
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