Abstract 12837: Effect of 10mg and 40mg Atorvastatin on Endothelial Progenitor Cells, Carotid Intima-Media Thickness, High Sensitive C Reactive Protein and Cardiac Events in Statin NaïVe Patients

Abstract

Background:Statin has been shown to retard the progression of or even reverse atherosclerosis. Besides, it has anti-inflammatory properties and reduces cardiovascular events. This study aims to assess the effect of 10mg and 40mg of statin on endothelial progenitor cells (EPCs), carotid initma-media thickness (CIMT), high-sensitivity C-reactive protein (hs-CRP) and cardiac events in statin naïve patients undergoing percutaneous coronary intervention (PCI).

Methods:Under the IVUS-Virtual Histology (VH-IVUS) study protocol, 40 Chinese patients treated by PCI were randomized to receive either atorvastatin 10mg daily or 40mg daily for 6 months. The effects on EPC, CIMT and hs-CRP and cardiac events in each arm were analyzed.

Results:Baseline demographics, low-density lipoprotein cholesterol (LDL-C), degree of coronary artery disease, baseline medications, CIMT, hs-CRP and EPCs were similar between 2 groups (p=NS) before statin treatment. Over a follow-up period of 6 months, both groups shown significantly decrease in LDL-C and hs-CRP (p<0.01). The average number of CD34⁺EPCs (21.93 versus 15.23 cells/µL, p=0.04) were significantly increased in higher dose compared with low dose group. However, there was no significant difference in CIMT changes (-0.04 versus 0.003 mm, p=0.116) between higher and low dose group. In the 10mg group, there was progression of non-culprit lesion and 4 patients had angiographic in-stent restenosis, all having percutaneous revascularization during the 6-month angiographic restudy, as compared to zero patient in 40mg group.

Conclusion:Our results demonstrated that 6 months treatment with atorvastatin (10mg and 40mg) in statin naïve patient showed substantial reduction in LDL-C and hs-CRP. Higher dose (40mg) of atorvastatin associated with elevation of CD34⁺ EPCs and better clinical outcomes. Moreover, higher dose of statin treatment appears to induce regression on CIMT. The mediating mechanism, whether by pure lipid-lowering effects or by other pleiotropic effects, warrants further investigation.