Document Detail


Short-term atorvastatin preload reduces levels of adhesion molecules in patients with acute coronary syndrome undergoing percutaneous coronary intervention. Results from the ARMYDA-ACS CAMs (Atorvastatin for Reduction of MYocardial Damage during Angioplasty-Cell Adhesion Molecules) substudy.
MedLine Citation:
PMID:  20613550     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: In patients with stable angina receiving percutaneous coronary intervention (PCI) prevention of periprocedural myocardial infarction by atorvastatin pretreatment was associated with reduction of endothelial activation. This mechanism was not evaluated in patients with acute coronary syndrome (ACS). The aim was to investigate effects of atorvastatin load on adhesion molecules in ACS patients undergoing PCI.
METHODS: In a planned subanalysis of the ARMYDA-ACS trial, a subgroup of 44 patients were blind-tested for measurement of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin plasma levels; 21 patients belonged to the atorvastatin (80 mg 12 h before PCI, with a further 40 mg preprocedure dose) and 23 to the placebo arm. Adhesion molecules were evaluated at randomization (12 h before intervention), immediately before PCI and after 8 and 24 h.
RESULTS: Reduction of procedural myocardial injury after statin pretreatment was confirmed in this subgroup. ICAM-1, VCAM-1 and E-selectin levels were similar at randomization and before intervention in both arms. At 8 h, ICAM-1 increase was similar in the two arms, whereas 24-h levels were lower in the atorvastatin vs. placebo group (241 ± 25 vs. 261 ± 30 ng/ml; P = 0.019). Significant attenuation of VCAM-1 elevation occurred both at 8 and 24 h in the atorvastatin group (509 ± 56 vs. 545 ± 59 ng/ml; P = 0.044 and 561 ± 58 vs. 600 ± 53 ng/ml; P = 0.025). E-selectin levels were not different at any time-point in the two arms.
CONCLUSION: In ACS patients undergoing PCI, reduction of procedural myocardial injury after atorvastatin load is associated with attenuation of endothelial inflammatory response. This may contribute to mechanisms of statin cardioprotection in this setting.
Authors:
Giuseppe Patti; Massimo Chello; Laura Gatto; Gennaro Alfano; Marco Miglionico; Elvio Covino; Germano Di Sciascio
Publication Detail:
Type:  Journal Article; Multicenter Study; Randomized Controlled Trial    
Journal Detail:
Title:  Journal of cardiovascular medicine (Hagerstown, Md.)     Volume:  11     ISSN:  1558-2035     ISO Abbreviation:  J Cardiovasc Med (Hagerstown)     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-09-30     Completed Date:  2011-01-13     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101259752     Medline TA:  J Cardiovasc Med (Hagerstown)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  795-800     Citation Subset:  IM    
Affiliation:
Department of Cardiovascular Sciences, Campus Bio-Medico University, Rome, Italy.
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MeSH Terms
Descriptor/Qualifier:
Acute Coronary Syndrome / drug therapy,  immunology,  pathology,  therapy*
Aged
Angioplasty, Balloon, Coronary* / adverse effects
Cadherins / blood
Cell Adhesion Molecules / blood*
Chi-Square Distribution
Double-Blind Method
Female
Heptanoic Acids / administration & dosage*
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use*
Inflammation Mediators / blood*
Intercellular Adhesion Molecule-1 / blood
Italy
Male
Middle Aged
Myocardial Infarction / immunology,  pathology,  prevention & control*
Myocardium / pathology*
Placebo Effect
Prospective Studies
Pyrroles / administration & dosage*
Time Factors
Treatment Outcome
Vascular Cell Adhesion Molecule-1 / blood
Chemical
Reg. No./Substance:
0/CDH1 protein, human; 0/Cadherins; 0/Cell Adhesion Molecules; 0/Heptanoic Acids; 0/Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0/Inflammation Mediators; 0/Pyrroles; 0/Vascular Cell Adhesion Molecule-1; 110862-48-1/atorvastatin; 126547-89-5/Intercellular Adhesion Molecule-1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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