- Clinical science
Statins are the lipid-lowering drugs of choice. Statins reduce hepatic cholesterol synthesis by inhibiting enzyme HMG-CoA reductase. This leads to a consequent upregulation of LDL receptors on hepatocytes, which, in turn, lowers LDL cholesterol levels and triglycerides while raising HDL cholesterol. Headache and gastrointestinal side-effects are common. Statins carry a risk of hepatic and muscle toxicity. Mucle toxicity may rarely manifest with rhabdomyolysis.
|Statin||Half-life in hours||CYP-450||Bioavailability|
|Simvastatin||2–3||CYP3A4, CYP3A5||∼ 5%|
|Pravastatin||∼ 2||-||∼ 20%|
|Pitavastatin||12||Limited CYP2C9||∼ 50%|
|Rosuvastatin||19||Limited CYP2C9||∼ 20%|
- ↓↓ LDL cholesterol (by ∼ 21–63%)
- ↑ HDL cholesterol (by ∼ 5–10%)
- ↓ triglyceride level (by ∼ 10–20%)
- Pleiotropic effect: ↓ C-reactive protein, ↑ plaque stabilization; , ↑ anti-inflammatory effect, antioxidant effect and improved endothelial function of coronary arteries
- General (common): headache and gastrointestinal symptoms (e.g., constipation, diarrhea, flatulence)
- Hepatic (<1% of patients): ↑ LFTs due to the involvement of cytochrome P450 systems (CYP3A4 and CYP2C9) in the breakdown of statins
- Muscular: Statins decrease the synthesis of coenzyme Q10 and impair energy production within the muscle.
Treatment must be discontinued if myopathy/rhabdomyolysis occurs!
Interaction with certain drugs (see below) can increase the risk of myopathy!
We list the most important adverse effects. The selection is not exhaustive.
- Patients with LDL cholesterol elevated ≥ 190 mg/dL
- Patients with a clinical atherosclerotic cardiovascular disease (includes (CHD), , and )
- Patients aged 40–75 with diabetes and LDL levels of 70–189 mg/dL
- Patients aged 40–75 with an estimated 10-year ASCVD risk ≥ 7.5% and LDL levels 70–189 mg/dL
→ For details seeand
Statins are the first-line therapy for hypercholesterolemia!
- Other lipid-lowering agents
- CYP3A4 inhibitors