Latest research on Rosuvastatin

Rosuvastatin is an antilipemic agent that competitively inhibits hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. HMG-CoA reducuase catalyzes the conversion of HMG-CoA to mevalonic acid, the rate-limiting step in cholesterol biosynthesis. Rosuvastatin belongs to a class of medications called statins and is used to reduce plasma cholesterol levels and prevent cardiovascular disease.

Rosuvastatin indications

The available studies have also shown that the effectiveness of statin therapy, especially high-intensive regimens with Rosuvastatin 20–40 mg and Atorvastatin 40–80 mg, could be very high, and even in >90 % of patients we might achieve lipid goals [14]. [source, 2016]
The dose of Rosuvastatin was chosen to elicit pleiotropic effects in the absence of lipid lowering as previously reported [23,24]. [source, 2016]
Likewise, in the TAA model in rats both Atorvastatin and Rosuvastatin failed to inhibit liver cirrhosis or oxidative stress formation and had no effect of HSC proliferation (Shirin et al., 2013). [source, 2016]
A recent study investigating the short-term (13 days) effect of statins on the urinary protein concentration and proteome in healthy volunteers found that either Rosuvastatin (40 mg/day) or Pravastatin (80 mg/day) did not induce major changes in the urinary protein concentration/proteome (on a background of high variability in the baseline urinary proteome/proteins among volunteers 191). [source, 2015]
Such reduction in carotid intima media thickness was comparable to or greater than the effects observed from some statins: pitavastatin decreased carotid intima media thickness by 0.024 mm/year in patients with known atherosclerosis,[46] while Rosuvastatin decreased carotid intima media thickness by 0.0014 mm/year among low-risk individuals. [source, 2015]
This study evaluated these hypotheses by investigating the in vivo time-dependent and dose-dependent effects of daily Atorvastatin or Rosuvastatin oral therapy initiated either 1 day or 3 days after venous thrombosis (VT) formation, in established, already formed stasis or nonstasis chemical-induced murine VT. [source, 2015]
To assess the individual and potential additive effects of statin therapy and clinically-employed anticoagulant low molecular weight heparin (LMWH) therapy [34] on established DVT, daily enoxaparin (10 mg/kg) starting at day 1 after DVT formation, without and with daily Atorvastatin or Rosuvastatin therapy, was studied at day 4 after stasis DVT induction (S2 Fig.). [source, 2015]
Other statins may improve the resolution of established VT; Atorvastatin and Rosuvastatin were chosen for this study given their high potency and established effectiveness in other clinical conditions. [source, 2015]
Possible heterogeneity in the effects of statin therapy across biomarker tertiles was evaluated in a proportional hazards model that included tertile indicators, an indicator of Rosuvastatin assignment, and an interaction term combining statin assignment and biomarker tertile. [source, 2015]
Rosuvastatin was equally effective in preventing the occurrence of the primary end point across different baseline concentrations of either hsTnI or BNP (Table 3 and Figure II in the online-only Data Supplement). [source, 2015]