Atorvastatin
HMG-CoA reductase inhibitor · “The post-MI powerhouse”
The Clinical Case
Male, 58 yo. Admitted with NSTEMI, PCI performed on LAD. LDL 3.8 mmol/L, TG normal, no prior statin therapy. Cardiologist targets LDL <1.4 mmol/L and starts high-intensity therapy before discharge. The chosen statin achieves ~51% LDL reduction at 80 mg, has a 14-hour half-life allowing any-time dosing, and has the best overall safety profile in primary prevention trials.
The Answer
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Clinical Pearl
Mechanism: ~51% LDL reduction at 80 mg — high-intensity; second most potent statin after rosuvastatin; most prescribed globally; inhibits hepatic HMG-CoA reductase
All Hints
Mechanism: ~51% LDL reduction at 80 mg — high-intensity; second most potent statin after rosuvastatin; most prescribed globally; inhibits hepatic HMG-CoA reductase
Pharmacokinetics: Half-life ~14 h → any time of day dosing; unlike short-acting statins (pravastatin, simvastatin, fluvastatin) that require evening administration
Pleiotropic: Reduces CRP and stabilises atherosclerotic plaques independently of LDL — critical in acute coronary syndrome
Interactions: CYP3A4 substrate — caution with azoles, macrolides, ARTs; avoid grapefruit juice
Evidence: TNT "trial": 80 mg vs 10 mg → further MACE reduction in stable CAD; ASCOT-"LLA": 36% RRR in hypertensives
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