Rosuvastatin: A Review of the Pharmacology and Clinical Effectiveness in Cardiovascular Disease

Abstract

Rosuvastatin is a new generation HMG-CoA reductase inhibitor which exhibits some unique pharmacologic and pharmacokinetic properties. It has low extrahepatic tissue penetration, low potential for CYP3A4 interactions and substantial LDL-C lowering capacity and therefore has distinct advantages. We conducted a Medline literature search to identify rosuvastatin papers published in English. In this review, we outline the pharmacology of rosuvastatin, highlighting its efficacy and safety. We also review the major clinical trials with reference to primary and secondary prevention, familial hypercholesterolaemia and comparison with other statins. Finally we address its place in clinical practice.

Impact of combined treatment with rosuvastatin and antidepressants on liver and kidney function in rats

“…However, the administration of rosuvastatin for 14 days did not significantly influence the serum activity levels of the enzymes compared with the control group. Previous studies demonstrated that rosuvastatin may occasionally induce alterations in hepatic enzyme activity levels; however, these changes infrequently caused liver failure (4,6). In the controlled clinical trials of rosuvastatin, the incidence of clinically significant ALT increases was low, and similar across all doses (0.1-0.5%), and these elevations were dose-dependent (24,25).…”

“…In short-term placebo-controlled trials, transient proteinuria was detected in 0.1% patients receiving rosuvastatin at a dose of 40 mg. Patient elevated proteinuria levels during rosuvastatin therapy were generally resolved spontaneously later during the trial (4,6,9). In addition, long-term data indicates that rosuvastatin appears to marginally improve renal function (6).…”

“…The differences between combined treatment with rosuvastatin and amitriptyline or fluoxetine and the experimental marker activity levels and concentrations may be a result of the metabolism of these drugs. Rosuvastatin and fluoxetine are biotransformed in the liver by cytochrome P450 izoenzyme CYP2C9, although this izoenzyme is not involved in the metabolism of amitriptyline (4,29).…”

“…The most effective and commonly used drugs to lower the levels of low-density lipoprotein lipids are statins; 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors (4,5). Rosuvastatin induces the most potent reduction of LDL and elevation of high-density lipoprotein in its class of drug (6).…”

“…Rosuvastatin induces the most potent reduction of LDL and elevation of high-density lipoprotein in its class of drug (6). Rosuvastatin effectively reduces the concentration of C-reactive protein by ~37%, and diminishes the risk of myocardial infarction, stroke and other cardiovascular events among individuals with established coronary heart disease (4,7). Severe adverse effects during this drug therapy are rare and include myopathy and rhabdomyolysis (8,9).…”