Rosuvastatin has a stronger lipid-lowering effect compared to atorvastatin. Rosuvastatin effectively lowers blood lipids at lower doses of 5 to 10 mg, while atorvastatin requires doses of 10 to 20 mg to achieve similar effects.
In terms of hydrophilicity and lipophilicity, rosuvastatin is hydrophilic, whereas atorvastatin is lipophilic. Lipophilic drugs more easily cross the blood-brain barrier, which may lead to central nervous system adverse effects.
Regarding metabolic pathways, atorvastatin is primarily metabolized by the CYP3A4 enzyme, while rosuvastatin is mainly metabolized by the CYP2C9 and CYP2C19 enzymes. This difference may affect drug interactions with other medications or foods and may necessitate dosage adjustments when needed.
In terms of liver damage risk, atorvastatin may cause elevated transaminase levels, whereas rosuvastatin is less likely to cause this. Therefore, for patients with impaired liver function, rosuvastatin may be a more suitable choice.
Atorvastatin has 2% of its components metabolized through the kidneys, whereas rosuvastatin has 10% metabolized through the kidneys. This means that for patients with renal insufficiency, atorvastatin may be more suitable.
While both drugs are very effective in lipid-lowering intensity, rosuvastatin slightly outperforms atorvastatin in this aspect.
In terms of reversing atherosclerotic plaques, studies have shown that taking 10 mg of rosuvastatin or 20 mg of atorvastatin daily for six months can significantly reverse plaque development, with rosuvastatin appearing to be more effective in this regard.