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J Am Coll Cardiol, 1998; 32:2057-2064 © 1998 by the American College of Cardiology Foundation |
a Fundación Jiménez Díaz, Universidad Autónoma, Madrid, Spain
* Hospital Clínico, Madrid, Spain
Hospital Gómez Ulla, Universidad Complutense, Madrid, Spain
Parke Davis Spain, Barcelona, Spain
Manuscript received January 6, 1998; revised manuscript received July 21, 1998, accepted August 26, 1998.
Address for correspondence: Dr. Jesús Egido, Research Laboratory, Fundación Jiménez Díaz, Avda. Reyes Católicos 2. 28040 Madrid
evasc{at}uni.fjd.es
Objectives. To study the effect of the 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA)-reductase inhibitor atorvastatin on the potential mechanisms involved in the recruitment of monocytic cells into the vessel wall.
Background. Inhibitors of HMG-CoA-reductase reduce cardiovascular mortality though the mechanisms yet elucidated. Most ischemic events are secondary to disruption of atherosclerotic plaques highly infiltrated by macrophages.
Methods. Atherosclerosis was induced in the femoral arteries of rabbits by endothelial damage and atherogenic diet for 4 weeks. Then, animals were switched to standard chow and randomized to receive either no treatment or atorvastatin (5 mg/kg/d) and killed after 4 weeks.
Results. Atorvastatin induced a significant reduction in serum lipids and in lesion size. Arterial macrophage infiltration was abolished by the treatment, and monocyte chemoattractant protein-1 (MCP-1) was significantly diminished in the neointima and in the media. Nuclear factor kappa-B (NF-
B) was activated in the 60% of the lesions, both in macrophages and vascular smooth muscle cells (VSMC), of the untreated group while only in 30% of the atorvastatin group. NF-B activity was also lower in the uninjured aorta and liver of treated compared with untreated rabbits. In cultured VSMC, MCP-1 expression and NF-B activity induced by tumor necrosis factor alpha were downregulated by atorvastatin.
Conclusions. In a rabbit atherosclerosis model, atorvastatin diminishes the neointimal inflammation, and this could contribute to the stabilization of the atherosclerotic plaque. This may be an additional explanation for the reduction of acute ischemic events in patients treated with statins.
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