There are very good reasons to use rosuvastatin over atorvastatin. Crestor is not a CYP3A4 substrate (Lipitor is), Crestor has only minor actitive metabolites (Lipitor has several very active metabolites), and Crestor is hydrophilic whereas Lipitor is not; hydrophilicity appears to minimize entry into muscles and minimizes muscle pain complaints.
Lipitor differs from simvastatin only in efficacy. If you don't like simva you shouldn't like Lipitor. Pravastatin, although the least potent, is not a 3A4 suThere are very good reasons to use rosuvastatin over atorvastatin. Crestor is not a CYP3A4 substrate (Lipitor is), Crestor has only minor acbstrate and is hydrophilic. It is a good first choice for many.
with all the publicity over rhabdomyolysis at the 80 mg dose, the fact that simvastatin is markedly inferior to atorvastatin (both in hard endpoint trials like IDEAL and in 'softer' surrogate marker studies), and that simvastatin is by far and away the most prone to drug interactions through CYP3A4 of all the statins (witness the labelling revisions for amiodarone, verapamil, diltiazem on top of the previous litany of azole antifungals, antivirals, etc). Quite simply, this statin sucks! It is also the most myopathic of all the statins and the dose-response curve and renal clearance are worrisome. More than 40% of patients in SHARP discontinued it.
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