
The following table compares the side-effects of drugs used in hyperlipidaemia:
| Drugs | Mechanism of action | Adverse effects |
|---|---|---|
| Statins | HMG CoA reductase inhibitors | Myositis, deranged LFTs |
| Ezetimibe | Decreases cholesterol absorption in the small intestine by inhibiting NPC1L1 (Niemann-Pick 1 like 1) transmembrane protein | Headache |
| Nicotinic acid | Decreases hepatic VLDL secretion | Flushing, myositis |
| Fibrates | Agonist of PPAR-alpha therefore increases lipoprotein lipase expression | Myositis, pruritus, cholestasis |
| Cholestyramine | Decreases bile acid reabsorption in the small intestine, upregulating the amount of cholesterol that is converted to bile acid | GI side-effects |
Statins enhance hepatic LDL receptor recycling and increased LDL clearance form the circulation
The statins have a greater effect on lowering mortality compared with the other lipid lowering agents.
All patients with CVD should be taking a statin in the absence of any contraindication.
Atorvastatin 80mg should be offered first-line.
Note the downstream synthesis of CoQ which is important for electron transport chain. Once you inhibits HMG CoA reductase, it interferes with CoQ synthesis --> mitochondrial energy production --> muscle pain (myositis and myopathy)
So, consider adding CoQ10 supplement when giving Statins.
Follow-up of people started on statins
NICE recommend we follow-up patients at 3 months