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J Am Coll Cardiol, 2006; 48:1560-1566, doi:10.1016/j.jacc.2006.06.061 (Published online 25 September 2006).
© 2006 by the American College of Cardiology Foundation
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CLINICAL RESEARCH: INTERVENTIONAL CARDIOLOGY

Protection From Procedural Myocardial Injury by Atorvastatin Is Associated With Lower Levels of Adhesion Molecules After Percutaneous Coronary Intervention

Results From the ARMYDA-CAMs (Atorvastatin for Reduction of MYocardial Damage during Angioplasty-Cell Adhesion Molecules) Substudy

Giuseppe Patti, MD*, Massimo Chello, MD*, Vincenzo Pasceri, MD, PhD, FACC{dagger}, Diego Colonna, MD{ddagger}, Annunziata Nusca, MD*, Marco Miglionico, MD*, Andrea D’Ambrosio, MD*, Elvio Covino, MD* and Germano Di Sciascio, MD, FACC*,*

* Department of Cardiovascular Sciences, Campus Bio-Medico University, Rome, Rome, Italy
{dagger} Interventional Cardiology Unit, San Filippo Neri Hospital of Rome, Rome, Italy
{ddagger} Second University of Naples, Naples, Italy

Manuscript received May 10, 2006; revised manuscript received June 19, 2006, accepted June 26, 2006.

* Reprint requests and correspondence: Dr. Germano Di Sciascio, Department of Cardiovascular Sciences, Campus Bio-Medico University, Via E. Longoni, 83, 00155 Rome, Italy (Email: g.disciascio{at}unicampus.it).

OBJECTIVES: The goal of this work was to investigate whether protection from myocardial injury during percutaneous coronary intervention (PCI) by atorvastatin is related to reduction of endothelial inflammatory response.

BACKGROUND: In the randomized ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) trial, 7-day pre-treatment with atorvastatin before PCI significantly reduced procedural myocardial injury; mechanisms underlying this effect are not characterized.

METHODS: In a planned subanalysis of the ARMYDA trial, a subgroup of 76 patients was blind-tested for measurement of plasma levels of vascular cell adhesion molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1), and E-selectin: 38 patients belonged to atorvastatin (40 mg/day) and 38 to the placebo arm. Adhesion molecules were evaluated 7 days before intervention, immediately before PCI, and after 8 and 24 h.

RESULTS: Reduction of procedural myocardial injury after statin pre-treatment was also confirmed in this subgroup. Intercellular cell adhesion molecule-1, E-selectin, and VCAM-1 levels were not different at randomization and before intervention in either arm. At 8 h, increase of ICAM-1 levels was similar in the 2 arms, whereas 24-h levels were significantly lower in the atorvastatin versus placebo group (282 ± 56 vs. 325 ± 70 ng/ml; p = 0.007). Attenuation of E-selectin elevation occurred at 8 h in the atorvastatin group (50 ± 8 vs. 59 ± 13 ng/ml; p = 0.002) and became even more significant at 24 h (57 ± 9 vs. 73 ± 18 ng/ml; p = 0.0008). Vascular cell adhesion molecule-1 levels were not different at any time point in the 2 arms.

CONCLUSIONS: In patients undergoing PCI, reduction of procedural myocardial injury after 7-day pre-treatment with atorvastatin is paralleled by concomitant attenuation of post-procedural increase of ICAM-1 and E-selectin levels; thus, reduction of endothelial inflammatory response may explain this protective effect of statins.

Abbreviations and Acronyms
  ARMYDA = Atorvastatin for Reduction of MYocardial Damage during Angioplasty
  ARMYDA-CAMs = Atorvastatin for Reduction of MYocardial Damage during Angioplasty-Cell Adhesion Molecules substudy
  CRP = C-reactive protein
  ICAM-1 = intercellular cell adhesion molecule-1
  VCAM-1 = vascular cell adhesion molecule-1


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