A long-established, low-cost statin that reliably lowers artery-clogging cholesterol by slowing the liver's cholesterol production. Decades of large trials show fewer heart attacks, strokes, and—in higher-risk people—deaths. It is moderate-strength with dose limits and notable drug and grapefruit interactions. Main downsides are muscle complaints and, less often, liver-enzyme changes and slightly higher diabetes risk. (Full Review)
| Marker | Target | Why |
|---|---|---|
| LDL-C | <70 mg/dL (high risk); <100 mg/dL otherwise | Primary treatment target |
| ApoB | <80 mg/dL (lower if high risk) | Best single measure of atherogenic particle number |
| Non-HDL-C | <100 mg/dL (high risk) | Captures all atherogenic particles incl. triglyceride-rich |
| ALT/AST (transaminases) | Within or below conventional reference range | Detect dose-dependent liver-enzyme effect |
| Creatine kinase (CK) | Within reference range | Reference point for muscle symptoms |
| HbA1c | <5.7% | Detect statin-related glucose rise |
| Lp(a) | <30 mg/dL (or <75 nmol/L) | Independent residual risk; statins may raise it slightly |
Cadence: Baseline lipid panel and liver enzymes (plus CK and glucose/HbA1c if higher-risk) before the first dose; recheck lipid panel at 6–12 weeks after starting or changing dose, then every 6–12 months once stable; liver enzymes if symptoms or risk factors warrant; CK only if muscle symptoms occur; glucose/HbA1c periodically (e.g., annually) near the diabetes threshold.