Telomere erosion of EPCs (endothelial progenitor cells) may be a key factor in 
endothelial cell senescence and is highly dependent on cellular oxidative 
damage. The aim of the present study was to investigate whether LLT 
(lipid-lowering therapy) with statins could attenuate EPC telomere erosion in 
patients with CAD (coronary artery disease). The study included 100 patients 
with stable CAD and 25 subjects without CAD as controls. CAD patients were 
randomized to 12 months of intensive LLT with atorvastatin or moderate LLT with 
pravastatin. EPCs were obtained from peripheral blood at baseline and after 12 
months of statin therapy. Telomere length in EPCs was measured by FISH 
(fluorescence in situ hybridization) and oxidative DNA damage by flow cytometry 
of oxidized DNA bases. EPC telomere length was shorter in the CAD group than in 
the controls, and oxidative DNA damage to EPCs was higher in the CAD group 
compared with controls. After 12 months of therapy, changes in lipid profiles 
were greater in the intensive LLT group than in the moderate LLT group. 
Intensive LLT markedly increased EPC number and decreased oxidative DNA damage 
in EPCs (both P<0.05), with no change in telomere length. In contrast, moderate 
LLT did not change EPC counts or oxidative DNA damage, but showed telomere 
shortening (P<0.05). There was a weak negative correlation between changes in 
EPC number and LDL (low-density lipoprotein)-cholesterol levels after intensive 
LLT, whereas there was no correlation between them after moderate LLT. With in 
vitro culturing of EPCs subjected to oxidative stress, atorvastatin led to the 
prevention of EPC telomere shortening compared with pravastatin. In conclusion, 
the present study has demonstrated that intensive LLT may prevent EPC telomere 
erosion in patients with CAD, possibly contributing to the beneficial effects of 
intensive LLT in this disorder.