Generic Name

Crestor

Mechanism

• Rosuvastatin is a highly potent, selective inhibitor of 3‑hydroxy‑3‑methyl‑glutaryl‑CoA (HMG‑CoA) reductase, the rate‑limiting enzyme in hepatic cholesterol synthesis.
• By blocking this step, *Crestor* reduces intracellular cholesterol, up‑regulates LDL‑receptor expression, and increases clearance of low‑density lipoprotein particles (LDL‑C).
• The drug’s lipophilic nature allows good hepatocyte distribution and a strong, dose‑responsive plaque‑stabilizing effect in atherosclerotic lesions.

Pharmacokinetics

• Absorption: ~80 % bioavailability; peak plasma concentration (Tmax) 2–4 h post‑dose.
• Distribution: Tissue half‑life ~15 h; high plasma protein binding (~95 %); predominantly binds to albumin.
• Metabolism: Minimal hepatic oxidation; metabolized mainly via SULT2A1 (sulfation) and SULT1A1; phase‑II glucuronidation negligible.
• Elimination: Primarily excreted unchanged in bile (~85 %); renal excretion (~15 %).
• Half‑life: Terminal (T½) ~19 h; steady state achieved in 5–7 days.

Indications

• Primary: Secondary prevention of coronary heart disease and stroke in patients with elevated LDL‑C or mixed dyslipidemia.
• Secondary: Primary prevention of atherosclerotic cardiovascular disease (ASCVD) in adults ≥40 y with LDL‑C >70 mg/dL and additional risk factors (diabetes, hypertension, smoking).
• Tertiary: treatment of familial hypercholesterolemia (heterozygous) and mixed dyslipidemia when dietary measures alone are inadequate.

Contraindications

• Absolute Contraindications:
• Known hypersensitivity to rosuvastatin.
• Active myopathy with unexplained muscle symptoms (e.g., rhabdomyolysis).
• Warning:
• Concomitant use with garlic supplements, caffeine, or nitrates may increase myopathy risk.
• Pregnancy and lactation: Category X; avoid.
• Severe hepatic impairment (Child‑Pugh C) contraindicated.
• Monitor for liver dysfunction (ALT/AST ≥3× ULN) and creatine kinase (CK) for signs of myopathy.

Dosing

• Take once daily with or without food; absorption is superior when taken with meals.
• Avoid concomitant use with strong CYP3A4 inhibitors (e.g., clarithromycin) or potent inducers (e.g., rifampin).

Adverse Effects

• Common (≤2 %):
• Headache, myalgia, dizziness, nasopharyngitis, constipation.
• Less common (≤0.5 %):
• Elevated liver enzymes (≥3× ULN), arthralgia, fatigue.
• Serious (rare):
• Rhabdomyolysis (CK ≥10,000 U/L + myalgia).
• Severe hepatotoxicity (acute liver failure).
• Allergic dermatitis, anaphylaxis.

Monitoring

Clinical Pearls

1. High‑potency, low‑dose approach: Rosuvastatin’s potency allows minimal effective dosing (10 mg) while meeting 40 % LDL‑C reduction, reducing polypharmacy risk.

2. Rapid lipid lowering: Peak LDL‑C reduction occurs within 2–3 weeks; optimal therapy is usually achieved by 8 weeks—prompt reassessment is key.

3. Non‑lipid benefits: Statin therapy with *Crestor* decreases vascular inflammation and improves endothelial function, providing extra protection when LDL‑C targets are met.

4. Drug‑drug interaction vigilance: No CYP3A4 metabolism lowers interaction risk, but nitrates and garlic can potentiate myopathy; caution with coenzyme Q10 supplements—potential influence on muscle symptoms.

5. Patient adherence: Create a simple administration routine (same time each day). Use “pill organizer” or smartphone reminders; improved compliance >20 % correlates with LDL‑C control.

6. Pregnancy precaution: Offer safety counseling and explore statin‑free alternatives for women of childbearing age; consider an early pregnancy test before initiation.

7. Special populations: In elderly ≥75 y, begin low (5 mg) and monitor for myopathy; dose escalation may be slower.

8. Efficacy confirmation: If LDL‑C >100 mg/dL after 12 weeks on *Crestor* 20 mg/day, increase dose or add ezetimibe or PCSK9 inhibitor.

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• *This drug card serves as a concise reference for medical students and clinicians, integrating current pharmacologic science with practical patient care insights.*