One of the original statins, pravastatin lowers the harmful cholesterol tied to clogged arteries by roughly a fifth to a third and, backed by strong long-term evidence, cuts heart attacks and major heart events. Water-soluble and gentle, it causes fewer drug interactions and less muscle and blood-sugar trouble than other statins, but lowers cholesterol less than newer, stronger ones. (Full Review)
| Marker | Target | Why |
|---|---|---|
| LDL cholesterol (LDL-C) | Risk-dependent; often <100 mg/dL, <70 mg/dL for high risk | Primary target of therapy |
| Apolipoprotein B (apoB) | <90 mg/dL (lower for high risk) | Counts atherogenic particles; often tracks risk better than LDL-C alone |
| Triglycerides | <100 mg/dL (functional); <150 mg/dL conventional | Secondary lipid affected by pravastatin; metabolic marker |
| Liver enzymes (ALT/AST) | Within normal limits (ALT often <25–30 U/L functional) | Detects hepatic stress from the drug |
| Creatine kinase (CK) | Within normal limits | Flags muscle injury (myopathy) |
| Fasting glucose / HbA1c | Glucose <90 mg/dL; HbA1c <5.4% (functional) | Screens for the small statin-related diabetes risk |
| Lipoprotein(a) [Lp(a)] | <30 mg/dL (<75 nmol/L) | Independent genetic risk marker that refines overall risk |
Cadence: Baseline lipid panel and liver enzymes before starting; lipid panel repeated at ~6–12 weeks, then every 6–12 months once stable; liver enzymes and creatine kinase checked as prompted by symptoms.