Rosuvastatin medicine Crestor drug information

Rosuvastatin calcium is a pharmaceutical drug prescribed along with diet for lowering high cholesterol and has been marketed to prevent heart disease, heart attacks, or strokes. Rosuvastatin is not appropriate for everyone, including women who are nursing, pregnant, or who may become pregnant, or anyone with liver problems. Rosuvastatin decreases cholesterol level and may reduce the risk for stroke and heart disease. What has not been determined yet is whether overall mortality changes with the use of rosuvastatin considering its high cost and potential side effects.

Rosuvastatin and HDL Cholesterol
Dose-dependent Effect of Rosuvastatin Treatment on HDL-subfraction Phenotype in Patients With Primary Hyperlipidemia.
J Cardiovasc Pharmacol Ther. 2009 Mar; Kostapanos MS, Milionis HJ, Filippatos TD, Christogiannis LG, Bairaktari ET, Tselepis AD, Elisaf MS. Department of Internal Medicine, University of Ioannina, Ioannina, Greece.
Although the raising effect of rosuvastatin on high-density lipoprotein cholesterol is well-established, there is a paucity of data regarding the effect of this statin on the high-density lipoprotein subfraction phenotype. A total of 150 participants without evidence of cardiovascular disease were randomized to therapeutic lifestyle modification (nonstatin-treated group) or to therapeutic lifestyle modification plus rosuvastatin at 10 mg/d (RSV10 group) or 20 mg/d (RSV20 group). We assessed the effect of rosuvastatin on the cholesterol mass of high-density lipoprotein subfractions at baseline as well as after 12 weeks post-treatment. Rosuvastatin treatment dose-dependently increased the high-density lipoprotein cholesterol (3.4% vs 5.3% in the RSV10 and RSV20 groups, respectively. A dose-related rosuvastatin-induced increase in the cholesterol concentration of large high-density lipoprotein particles was also noted (by 11% in RSV10 group vs 22% in the RSV20 group). Rosuvastatin treatment increases the high-density lipoprotein cholesterol by increasing the cholesterol mass only of the larger high-density lipoprotein particles in a dose-dependent manner.

Rosuvastating and aortic stenosis
The progression of asymptomatic aortic stenosis is slowed by treatment with rosuvastatin (Crestor), according to results of the RAAVE (Rosuvastatin Affecting Aortic Valve Endothelium) study. The risk factors for calcific aortic stenosis are similar to those for coronary heart disease, senior author Dr. Nalini M. Rajamannan and her associates note. For that reason, they hypothesized that statin treatment may slow aortic valve calcification. Dr. Rajamannan, from Northwestern University Feinberg School of Medicine in Chicago, and her team conducted a prospective study with 121 patients to determine if rosuvastatin treatment affects the hemodynamic progression of moderate to severe aortic stenosis. The subjects had asymptomatic aortic stenosis and an aortic valve area between 1.0 and 1.5 cm² (normal aortic valve area = 3-4 cm²). Sixty patients with LDL cholesterol less than 130 mg/dL received no statins, while the 61 patients with higher LDL cholesterol levels were treated with rosuvastatin at 20 mg per day. After a mean of 73 weeks, Dr. Rajamannan's group compared outcomes between groups. Adverse changes in hemodynamic markers - decrease in aortic valve area, increase in peak aortic valve velocity, peak gradient and mean gradient -- were significantly greater in the untreated group. For example, aortic valve area decreased by 0.10 cm²/year in untreated patients versus 0.05 cm²/year in those treated with rosuvastatin; peak aortic valve velocity increased by 0.24 m/s/year versus 0.04 m/s/year, respectively. Several serum markers improved significantly only in the treated group - total cholesterol, LDL cholesterol, triglycerides, and high-sensitivity C reactive protein. The research team suggests that in addition to their lipid-lowering effects, statins affect aortic stenosis by inhibiting cellular proliferation. Statins also reduce activation of the osteogenic gene program in the aortic valve myofibroblast and modulate endothelial nitric oxide synthase to improve endothelial function. In an accompanying editorial, Dr. Brian P. Griffin, from Cleveland Clinic in Ohio, points out that the result of the similar SALTIRE study indicated that statin therapy was of no benefit to patients with aortic stenosis and hyperlipidemia. J Am Coll Cardiol 2007;49:554-564.
   Comments: What has not been determined yet is whether overall mortality changes with the use of rosuvastatin considering its high cost and potential side effects.

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