Restenosis after successful revascularization by percutaneous transluminal
coronary angioplasty (PTCA) represents a major problem limiting the clinica
l efficacy of this procedure.(1) Although coronary artery stenting has defi
nitely been proved to improve results of PTCA in a large number of patients
, in-stent restenosis remains a significant clinical problem.(2) Coronary s
tent implantation is invariably accompanied by a certain degree of endothel
ium damage. This may be induced by ischemia/reperfusion because of the shor
t periods of blood flow reduction during the procedures, or by plaque ruptu
re.(3,4) Both events trigger endothelium to express adhesion molecules at h
igh density. Thereafter, circulating leukocytes up-regulating the appropria
te counter receptors can roll on the injured endothelium, tightly adhere to
it, and finally transmigrate to the site of lesion.(5) Vessel-infiltrating
leukocytes may promote neointimal hyperplasia through the release of sever
al proinflammatory cytokines, chemokines, and growth-promoting factors.(6-8
) The aim of this study was to analyze the expression of adhesion molecules
very late antigen (VLA)-2, intercellular adhesion molecule (ICAM)-1, leuko
cyte functional antigen (LFA)-1, and Mac-1 on lymphocytes circulating withi
n the coronary sinus compared with aortic root in coronary artery disease p
atients who underwent coronary stent placement.