Pravastatin, an inexpensive prescription oral medication from the statin family that slows the liver's cholesterol production, is used to lower the cholesterol that builds artery plaque. Strong, consistent evidence shows a moderate effect rising with dose, short of stronger statins or drug combinations. Large trials tie it to fewer heart attacks and heart-disease deaths. Drawbacks: a small rise in diabetes diagnoses, mostly temporary liver-test changes; serious muscle injury is rare. (Full Review)
| Marker | Target | Why |
|---|---|---|
| LDL cholesterol | Below 55 mg/dL at very high risk, below 70 mg/dL at high risk, plus at least 50% reduction | Primary efficacy marker |
| ApoB | Below 65 mg/dL at very high risk, below 80 mg/dL at high risk | Counts plaque-forming particles |
| Triglycerides | Below 150 mg/dL | Falls modestly |
| ALT | 7–56 U/L | Liver injury safety check |
| CK | About 30–200 U/L, sex-specific | Myopathy safety check |
| HbA1c | 4.0–5.6% | Statins nudge glucose upward |
| Fasting glucose | 70–99 mg/dL | Pairs with HbA1c |
| Creatinine | Not specified in the ER | Basis for eGFR |
| eGFR | 60 mL/min/1.73 m² or higher | Severe impairment caps dose at 40 mg |
| TSH | About 0.4–4.5 mIU/L | Untreated hypothyroidism raises myopathy risk |
| Lp(a) | No established target; change from own baseline | Statins can raise it |
Cadence: Baseline panel before starting; lipids at 4–12 weeks after starting or changing dose, then every 3–12 months; HbA1c yearly; eGFR yearly when kidney function is reduced; ALT and CK only when symptoms suggest liver or muscle injury; Lp(a) once