This residual risk can be explained, at least partly, by subclinical endothelial dysfunction and concomitant subclinical vascular inflammation. 6 This suggests that LDL-C lowering may be a key mechanism by which vascular benefits of lipid modifying treatment are exerted.ĭespite aggressive LDL-C lowering with statins, a considerable CV risk remains both in the primary and secondary prevention settings. We have previously shown that comparable reductions of LDL-C with either simvastatin or ezetimibe resulted in similar improvements in endothelial function by significantly limiting inflammation in patients with rheumatoid arthritis. 4 5 It is still debated whether these benefits could be explained solely by LDL-C lowering. 3 Various studies have suggested that statins exert additional pleiotropic benefits, including an improvement in endothelial function, anti-inflammatory and anti-oxidant actions, as well as reduced arterial stiffness and atheromatous plaque stabilisation. 2 Statins are first-line evidence-based drugs to reduce CV morbidity and mortality in parallel with their LDL-C lowering capacity. Elevated levels of low-density lipoprotein cholesterol (LDL-C) strongly and independently predict cardiovascular (CV) events. Low-density lipoprotein (LDL) particles are highly atherogenic. There is cross-talk between vascular inflammation and endothelial dysfunction that leads to atherosclerosis, and subsequently to symptomatic CVD and atherothrombotic events secondary to rupture of inflamed lipid-rich unstable plaques. Impaired endothelial function facilitates further accumulation of atherogenic lipoproteins and attracts inflammatory cells (circulating monocytes) in the subendothelial space. 2Ītherogenesis is a chronic, subclinical inflammatory process in which apolipoprotein(apo)B-containing lipoproteins, inflammatory cells and other connective tissue cells accumulate in the subendothelial space resulting in endothelial dysfunction, vascular inflammation and arterial stiffness. The link between inflammation and atherosclerosis is firmly established, 1 and the role of cholesterol in its pathophysiology is well described. Further study is needed on the efficacy of statins.Atherosclerotic cardiovascular disease (CVD) remains a significant cause of morbidity and mortality, despite major advances in its detection and treatment. Finally, the results of our study might have been just incidental due to the small number of patients and high follow up loss of data. So, diet control for our patients might have been done improperly. That is, the previous studies on the efficacy of statin applied diet therapy first and then they enrolled the patients, but our study did not have a lead-in period because the subjects were high risk patients. Second, there is the problem in our study's protocol that diet therapy was not actively applied to the patients. 13) 26) 27) Accordingly, it is possible that our study's result was similar to that of previous studies done with high dose statin because reosuvastatin works with very high potency on Koreans. First, in the previous studies, the HDL cholesterol level tended to be reduced by high dose statin therapy. The possible reasons for the difference in results are as follows. In addition, the lipoprotein(a) level was elevated in both groups, and the elevation was particularly significant in the rosuvastatin 10 mg group(31%).

23- 25) In our study, however, the HDL cholesterol level did not change(atorvastatin 20 mg), or rather, it was reduced(rosuvastatin 10 mg).

Statins do not lower the lipoprotein(a) concentration. Statins are highly effective in reducing LDL cholesterol and they are modestly effective in raising HDL cholesterol.

High intensity statin list