A Study To Evaluate The Effect Of Rosuvastatin On MRI-Derived Carotid Artery Atheroma Burden And Its Anti-inflammation Role

Objective:Atherosclerosis is the cause of ischemic cerebrovascular disease in pathophysiology. Statins have a significant benifet on prevention and treatment of atherosclerosis.ASTEROID research showed that statin therapy can reverse atherosclerotic plaques. Othervise, recent research from small samples showed that rosuvastatin may regress atherosclerotic plaques in only 1 to 3 months. Other research showed that anti-inflammatory effects of statin beside lipid-lowering,mostly in vitro, is equally important to retarding atherosclerosis. PPARs, which regulate lipid metabolism and inflammatory, probably invlved in the effects of rosuvastatin on atherosclerosis. The purposes of this study were:1. To observe the effects of rosuvastatin on carotid atherosclerotic plaque with high-resolution MRI; 2. to investigate the effects of rosuvastatin on inflammatory factors; 3. to study the relation of rosuvastatin and PPARs.Methods:1.20 patients without previous statin treatment were enrolled, with age 18 to 75 years-old, LDL-C 2.6mmol/L to 6.5mmol/L, triglyceride less than 4.0mmol/L, coratid plaques with lipid core. Rosuvastatin were given 5 to 20mg/day for 3 months. Both plaque and lipid core volume were examined with high-resolution MRI after rosuvastatin treatment and their correlation were analyzed.2. The levels of hsCRP, MCP-1 and VCAM-1 were examined in serum or plasma. The mRNA and protein expression of ICAM-1 and CCR2 were measured with RT-PCR and flow cytometry, respectively.3. The mRNA and protein expression of PPARs were detected with RT-PCR and Western blot.Result:1.Compared with the baseline, the levels of LDL-C, TC and TG were decreased after rosuvastatin treatment (P< 0.05). The levels of HDL-C is little higher with no significant (P> 0.05). Both volumes of carotid artery plaques and lipid core were decreased. The correlation between change of lipid core volume and LDL-C decrease was present as well as the reduction of the plaque volume and LDL-C, TC decrease.2. Rosuvastatin reduced hsCRP and MCP-1 levels(P< 0.05), CCR2 expression on mononuclear cells and ICAM-1 expression on lymphocyts. The effects of rosuvastatin on VCAM-1 level and ICAM-1 expression on monocyte was not be observed.3. Rosuvastatin improve mRNA and protein expression of PPARa andβ, also increase PPARy protein expression. Otherwise, its effect on PPARy mRNA expression was not significant.Conclusion:1. The study showed obviously improve on blood lipid profile by rosuvastatin. Regression of atherosclerotic plaques and lipid core also were observed in a short term, which may helpful to plaque stabilization.2. Rosuvastatin exert anti-inflammatory effects through decreasing some adhesion molecules and chemokine on mononuclear cells.3. Upregulation of PPARs levels may relate to the anti-atherosclerosis mechanisms of statin, although further study should be needed. This study may be helpful to further explore rosuvastatin anti-atherosclerosis.