An Overview of the Extra-Lipid Effects of Rosuvastatin

Abstract

Statins, in addition to their beneficial lipid modulation effects, exert a variety of several so-called "pleiotropic" actions that may result in clinical benefits. Rosuvastatin, the last agent of the class to be introduced, has proved remarkably potent in reducing low-density lipoprotein cholesterol levels. At present, no large-scale primary or secondary prevention clinical trials document either its long-term safety or its effectiveness in preventing cardiovascular events. A substantial number of experimental and clinical studies have indicate favorable effects of rosuvastatin on endothelial function, oxidized low-density lipoprotein, inflammation, plaque stability, vascular remodeling, hemostasis, cardiac muscle, and components of the nervous system. Available data regarding the effects of rosuvastatin on renal function and urine protein excretion do not seem to raise any safety concerns. Whether the established "pleiotropy" and/or lipid-lowering efficacy of rosuvastatin may translate into reduced morbidity and mortality remains to be shown in ongoing clinical outcome trials.

Effect of Switch to the Highest Dose of Rosuvastatin Versus Add‐on‐Statin Fenofibrate Versus Add‐on‐Statin Nicotinic Acid/Laropiprant on Oxidative Stress Markers in Patients with Mixed Dyslipidemia

“…In fact, titer of autoantibodies to ox-LDL was an independent predictor of the progression of carotid atherosclerosis in Finnish men [26]. In the previous studies, both rosuvastatin and fenofibrate have been associated with reduced ox-LDL levels [3,12,14,27]. Specifically, in a previous study, fenofibrate-associated ox-LDL reduction was greater in patients with high baseline ox-LDL levels, which was also the case in our study [14].…”

“…Treatment with statins has been associated with improved outcomes either in the primary or in the secondary prevention of CVD [2]. This benefit has been attributed not only to the lipid-lowering potency, but also to various pleiotropic antiatherosclerotic properties of these drugs (namely antiinflammatory, antioxidative and antithrombotic) [3]. Oxidative stress, mostly by giving rise to endothelial dysfunction and pro-inflammatory processes, plays a major role in atherogenesis [4].…”

“…We recently showed that both switch to the highest dose of rosuvastatin monotherapy (40 mg) and add-on-current-statin extended release nicotinic acid (ER-NA)/laropiprant (LRPT) were associated with marked reductions in non-HDL-C and LDL-C levels and with beneficial modifications of emerging cardiovascular risk factors compared with add-on fenofibrate in patients with mixed dyslipidemia not on goal with a standard statin dose [7][8][9]. Rosuvastatin has a known favorable effect on oxidative stress markers, while both NA and fenofibrate have been also associated with reduced oxidative stress [3,[10][11][12][13][14]. We now report the results of a prespecified analysis on the effect of these 3 treatment strategies on oxidative stress markers.…”

The methyl ester of rosuvastatin elicited an endothelium-independent and 3-hydroxy-3-methylglutaryl coenzyme A reductase-independent relaxant effect in rat aorta

“…Rosuvastatin-elicited vasodilatation was mediated by the production of NO and the opening of Ca 2+ -dependent K + channels of the Slow subfamily (7). Several protective effects of this statin related to its vascular effects have been demonstrated, including the prevention of inflammation and endothelial glycocalyx damage elicited by metalloproteinases, the inhibition of smooth muscle cell proliferation, the production of oxidized low-density lipoprotein, and an increase in plaque stability (13,14).…”

Hypoglycemic and Anticoagulant Effects of Tetrapeptide Pro-Gly-Pro-Leu in Hypercholesterolemia

“…It was found that some amino acids can prevent deposition of pre-atherogenic cholesterol in the arterial wall and reduce the risk of atherothrombosis, diabetes, and atherosclerosis [6]. Thus, amino acid leucine stimulates the production of insulin by the pancreas, which leads to normoglycemia in the blood of diabetic patients [5].…”