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.
OBJECTIVE
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.


CONCLUSIONS
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.
Patti
Giuseppe
G
Department of Cardiovascular Sciences, Campus Bio-Medico University, Rome, Italy.
Chello
Massimo
M
Gatto
Laura
L
Alfano
Gennaro
G
Miglionico
Marco
M
Covino
Elvio
E
Di Sciascio
Germano
G
D054058:Acute Coronary Syndrome / Q000188:drug therapy / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D015703:Antigens, CD; D000069059:Atorvastatin; D015820:Cadherins / Q000097:blood; D015815:Cell Adhesion Molecules / Q000097:blood*; D016009:Chi-Square Distribution; D004311:Double-Blind Method; D005260:Female; D006538:Heptanoic Acids / Q000008:administration & dosage*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D007558:Italy; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D009206:Myocardium / Q000473:pathology*; D015990:Placebo Effect; D011446:Prospective Studies; D011758:Pyrroles / Q000008:administration & dosage*; D013997:Time Factors; D016896:Treatment Outcome; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
D015703:Antigens, CD; C513384:CDH1 protein, human; D015820:Cadherins; D015815:Cell Adhesion Molecules; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018836:Inflammation Mediators; D011758:Pyrroles; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D000069059:Atorvastatin