- Design
- Single-centre retrospective cohort
- Population
- 142 adults with inflammatory myopathy, 41 with statin-associated necrotising myopathy
- Primary outcome
- All-cause mortality
- Effect
- 31.7% vs 23.8%; HR 2.55 unadjusted, 1.70 (95% CI 0.71 to 4.08) fully adjusted
A US tertiary centre reviewed 142 adults with idiopathic inflammatory myopathy, 41 of whom had immune-mediated necrotising myopathy linked to recent statin exposure, usually with anti-HMGCR antibodies.
Crude mortality was 31.7% in statin-associated disease and 23.8% in other myositis (unadjusted HR 2.55, 95% CI 1.24 to 5.24). After adjusting for age, the hazard ratio fell to 1.98, and after adding diabetes and hyperlipidaemia to 1.70, no longer significant. Older patients with statin-associated disease had the lowest survival. Cardiopulmonary events and infections were the main causes of death.
The excess mortality seems to reflect who develops this condition: older people with cardiometabolic disease. The study is small and single-centre.
For clinicians, statin-associated myopathy that persists or progresses after stopping the statin needs prompt anti-HMGCR testing and referral, and these patients need careful cardiovascular and infection management.
- Suspect immune-mediated necrotising myopathy when weakness and raised CK persist after stopping a statin
- Check anti-HMGCR antibodies in that situation
- Refer early to rheumatology or neurology for immunotherapy
- Manage cardiovascular risk and infection carefully, as these drove deaths
Why it matters
It identifies a myositis subgroup with high mortality driven by cardiometabolic disease.
Don't overread it
After full adjustment the difference was not significant, and the cohort was small.
The statistics, in plain English
The hazard ratio fell from 2.55 to 1.70 as age, diabetes and lipids were accounted for, and its confidence interval then crossed 1.0. That suggests these factors, rather than the myopathy subtype, explain much of the extra mortality.
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