El tratamiento con dosis altas de atorvastatina disminuye la inflamación en la aterosclerosis carotídea humana

  1. J.L. Martín-Ventura 1
  2. L.M. Blanco-Colio 1
  3. A. Gómez-Hernández 1
  4. B. Muñoz-García 1
  5. M. Vega 2
  6. J. Serrano 2
  7. L. Ortega 3
  8. G. Hernández 4
  9. J. Egido 1
  10. J. Tuñón 5
  1. 1 Laboratorio de Patología Vascular. Fundación Jiménez Díaz y Universidad Autónoma de Madrid. Madrid. España
  2. 2 Servicio de Cirugía Vascular. Hospital Clínico San Carlos. Universidad Complutense. Madrid. España
  3. 3 Servicio de Anatomía Patológica. Hospital Clínico San Carlos. Universidad Complutense. Madrid. España
  4. 4 Laboratorios Pfizer. Madrid. España
  5. 5 Servicio de Cardiología. Fundación Jiménez Díaz y Universidad Autónoma de Madrid. Madrid. España
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Journal:
Clínica e investigación en arteriosclerosis

ISSN: 0214-9168,  1578-1879

Year of publication: 2006

Volume: 18

Issue: 1

Pages: 18-23

Type: Article

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More publications in: Clínica e investigación en arteriosclerosis

Abstract

Introduction Statins improve plaque stability by diminishing inflammatory activity. We analyzed the effect of short-term high-dose atorvastatin on plaque inflammation in human carotid atherosclerosis. Materials and methods Twenty patients scheduled to undergo elective carotid endarterectomy without previous statin treatment were randomized at the time of surgical indication to receive either atorvastatin 80 mg/day (n = 11) or no statins (n = 9) until surgery (1 month later). Atherosclerotic plaques were analyzed by immunohistochemistry to investigate macrophage infiltrate, and expression of monocyte chemoattractant protein-1 (MCP-1) and cyclooxygenase-2 (COX-2). In addition, nuclear factor-κB (NF-κB) activity was studied by Southwestern histochemistry. Results Atorvastatin decreased serum levels of total cholesterol (118 ± 10 versus 191 ± 10 mg/dl; p = 0.016) and low-density lipoprotein (63 ± 9 versus 125 ± 9 mg/dl; p = 0.038), while no changes were noted in the control group. Triglycerides and highdensity lipoprotein showed no significant changes in either of the two groups. Carotid atherosclerotic plaques from the atorvastatin group demonstrated a significant reduction in macrophage infiltration (2.5 ± 1% versus 9.3 ± 2.4%; p < 0.05) and expression of MCP-1 (11 ± 1% versus 24 ± 4%; p < 0.05) and COX-2 (16 ± 2.3% versus 34 ± 4.4%; p < 0.05). The number of nuclei active for NF-?B was lower in plaques from patients that received atorvastatin than in those from the non-treated group (5,706 ± 1,260 versus 8063 ± 1,308; p < 0.05). Conclusions Intensive atorvastatin therapy decreases inflammatory activity in human carotid atherosclerotic plaques in as little as 1 month.

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