====== Pravastatin (Pravachol®) ======

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<WRAP infobox>
^ Drug Overview | {{ :cardio:lipids:pravastatin.svg |}}|
| Drug Class | [[cardio:lipids:start|Statins]] |
| Mechanism | HMG-CoA Reductase Inhibitor |
| Primary Uses | [[cardio:lipids:hyperlipidemia|Hyperlipidemia]]; [[cardio:lipids:ascvd|ASCVD Prevention]] |
| Route | Oral |
| Dose Range | 10–80 mg daily |
| Intensity | Low–Moderate |
| LDL Reduction | 20–40% |
| Metabolism | Minimal CYP (non-CYP metabolism) |
| Half-life | ~1.5–2 hours |
| Elimination | Hepatic + Renal |
| Renal Adjustment | Yes (severe CKD) |
| Black Box Warning | No |
| FDA Approval | 1991 |
</WRAP>
</WRAP>

===== Overview =====

Pravastatin is a hydrophilic [[cardio:lipids:start|statin]] with lower drug–drug interaction potential compared to CYP-metabolized statins.

It is less potent than [[cardio:lipids:atorvastatin|Atorvastatin]] and [[cardio:lipids:rosuvastatin|Rosuvastatin]], but is often selected in patients with polypharmacy or high interaction risk.

It is considered a safer option in complex medication regimens.

<WRAP clear></WRAP>

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===== Mechanism of Action =====

Primary Target:
  * HMG-CoA reductase (rate-limiting enzyme in hepatic cholesterol synthesis)

Physiologic Effects:
  * ↓ Hepatic cholesterol synthesis
  * ↑ LDL receptor expression
  * ↑ LDL clearance

Net Effect:
  * Mild-to-moderate LDL reduction
  * Reduced ASCVD risk

LDL lowering is dose-dependent.

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===== Indications =====

  * [[cardio:lipids:hyperlipidemia|Hyperlipidemia]]
  * [[cardio:lipids:ascvd|ASCVD prevention]]
  * Secondary prevention after:
      *