Statins are the most-studied drugs in cardiovascular medicine. For someone who has already had a heart attack or is at high risk, the evidence that they save lives is about as strong as anything in medicine. All the genuine nuance — and the whole debate — is about who else should take them.
Statins block HMG-CoA reductase, the liver's cholesterol-making enzyme. The liver responds by pulling more LDL and ApoB out of the blood (it upregulates LDL receptors). They also calm inflammation and help stabilise existing plaque — the 'pleiotropic' effects. Depending on drug and dose they cut LDL ~30–55%; the high-intensity options are atorvastatin 40–80 mg and rosuvastatin 20–40 mg.
The Cholesterol Treatment Trialists' (CTT) meta-analysis of ~170,000 people found that each 1 mmol/L (~39 mg/dL) drop in LDL cuts major vascular events by about 22% per year — proportional, dose-dependent, and consistent across groups. In people who already have established disease or a prior heart attack, the absolute benefit is large and the number-needed-to-treat is excellent. This is the ground essentially no serious expert disputes. Evidence ●●●●●
In people without known heart disease, the relative risk reduction is similar, but the absolute benefit is smaller simply because there are fewer events to prevent. It's meaningful for higher-risk primary prevention and marginal for genuinely low-risk people — and that gap between relative and absolute benefit is exactly what the next section is about. Evidence ●●●●○
The real question isn't 'do they work'
Statins work — that's settled. The live question for any individual is whether your personal absolute benefit is worth it, and that depends entirely on your actual risk. A calcium score or CT angiogram can turn that abstract question into a concrete one.
The Cholesterol Guide