Statins in the very old — primary and secondary prevention

Rationale. Atherosclerotic cardiovascular disease is the leading cause of death and disability in adults aged 75 and above, and age is the strongest single predictor of cardiovascular risk. Because absolute risk rises steeply with age, the absolute benefit of lipid lowering can be greater in older than in younger patients even though the relative risk reduction is similar. Statins act by HMG-CoA reductase inhibition, with additional plaque-stabilising and anti-inflammatory effects.

Secondary prevention — evidence is clear. In established ASCVD (previous myocardial infarction, stroke or TIA, peripheral arterial disease, or revascularisation), statins reduce major vascular events and mortality at all ages. At least moderate-intensity statin therapy is recommended regardless of age, and existing therapy should not be stopped merely because the patient has grown older. This is the strongest examination point.

Primary prevention — evidence is weaker. Older adults, particularly those over 75, were under-represented in the major trials. PROSPER (pravastatin, ages 70–82) reduced coronary events but not stroke and not mortality; ALLHAT-LLT showed no benefit in older hypertensive patients. Standard risk calculators (Pooled Cohort Equations, SCORE2) lose specificity above 75 because age dominates the score. Decisions must therefore be individualised.

Time-to-benefit and the geriatric decision. The average time to benefit is about 2.5 years for prevention of ASCVD events. A statin is inappropriate when estimated life expectancy is shorter than the time to benefit. Weigh frailty, multimorbidity, cognition, polypharmacy, functional status and patient preference, and use shared decision-making. Consider deprescribing in advanced dementia, terminal malignancy, severe frailty or when goals of care become purely palliative.

Adverse effects and interactions. Statin-associated muscle symptoms (myalgia, weakness — a cause of falls and reduced mobility; rarely rhabdomyolysis), transaminitis, and new-onset diabetes. Risk rises with CYP3A4 interactions — amiodarone, verapamil, diltiazem, macrolides, azole antifungals, ciclosporin — so avoid high-dose simvastatin. Pravastatin, rosuvastatin and pitavastatin are least CYP3A4-dependent. Evidence overall shows neutral or even protective cognitive effects; statins do not cause dementia.

Practical prescribing. Start low and go slow — moderate intensity (atorvastatin 10–20 mg or rosuvastatin 5–10 mg) is usually sufficient. Check baseline LFT and CK, exclude hypothyroidism, and repeat lipids at 6–12 weeks. If the LDL target is not met, add ezetimibe 10 mg rather than escalating the statin dose — this is better tolerated in the old. For statin intolerance, try an alternative statin, alternate-day dosing, or bempedoic acid / PCSK9 inhibitors in selected high-risk patients.

2025 National Lipid Association / American Geriatrics Society Expert Clinical Consensus (JAGS 2025) on hypercholesterolaemia in adults over 75 without ASCVD: LDL-C remains an independent predictor of ASCVD beyond age 75; it is reasonable to initiate a statin for primary prevention when LDL-C is 70–189 mg/dL in the absence of life-limiting illness; coronary artery calcium scoring can refine risk when the decision is uncertain; and deprescribing is appropriate in those with life-limiting disease. The STAREE trial (atorvastatin 40 mg versus placebo in ~10,000 Australians aged ≥ 70, co-primary endpoint disability-free survival) will settle the primary prevention question — results awaited.