One of the oldest cholesterol-lowering medications, water-soluble so it stays mostly in the liver. It lowers harmful cholesterol less than newer options but reaches muscle and nerve tissue less readily and interacts with fewer medications. Long trials show fewer heart attacks in proportion to the cholesterol drop. Best fit: moderate reduction, poor tolerance of stronger drugs, or many medications. (Full Review)
| Marker | Target | Why |
|---|---|---|
| LDL cholesterol | < 70 mg/dL with plaque; < 100 mg/dL without | The direct target of the drug |
| Apolipoprotein B (apoB) | < 80 mg/dL generally; < 60 mg/dL with established plaque | Counts atherogenic particles rather than their cholesterol; a better risk predictor than LDL |
| Lipoprotein(a) | < 30 mg/dL (< 75 nmol/L) | Genetically determined residual risk that pravastatin cannot lower and slightly raises |
| Non-HDL cholesterol | < 90 mg/dL | Captures all atherogenic particles including remnants; stands in where apolipoprotein B is unavailable |
| Triglycerides | < 80 mg/dL | Reflects metabolic health and the reliability of calculated LDL cholesterol |
| High-sensitivity C-reactive protein (hs-CRP) | < 0.5 mg/L | Residual inflammatory risk, which predicts mortality in statin users better than residual LDL |
| Alanine aminotransferase (ALT) | 10–26 U/L (men); 10–19 U/L (women) | Detects the dose-dependent transaminase elevation confirmed in blinded trials |
| Aspartate aminotransferase (AST) | 10–26 U/L | Paired with alanine aminotransferase to separate liver from muscle origin |
| Creatine kinase (CK) | 40–200 U/L (men); 30–150 U/L (women) | Separates genuine myopathy from muscle symptoms without muscle damage |
| Haemoglobin A1c (HbA1c) | 4.8–5.2% | Detects the small class-level increase in new-onset diabetes |
| Fasting insulin | 2–5 µIU/mL | Detects insulin resistance earlier than glucose or haemoglobin A1c |
| Thyroid-stimulating hormone (TSH) | 0.5–2.0 mIU/L | Thyroid underactivity raises LDL and causes myopathy that mimics statin muscle injury |
| Estimated glomerular filtration rate (eGFR) and creatinine | eGFR > 90 mL/min/1.73 m² | Reduced kidney function raises exposure, requires dose reduction, and worsens rhabdomyolysis |
| Coenzyme Q10 | 2.5–3.5 µg/mL | Depleted through the shared synthesis pathway; a candidate contributor to muscle symptoms |
Cadence: Full baseline panel before the first dose. Lipid panel and apolipoprotein B at 6–8 weeks after starting or any dose change, at 3 months once stable, then every 6–12 months. Transaminases and creatine kinase at baseline, thereafter only if clinically indicated. Glycaemic markers annually; lipoprotein(a) once in a lifetime.