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Percentage low-density lipoprotein-cholesterol response to a given statin dose is not fixed across the pre-treatment range: Real world evidence from clinical practice: Data from the ESC-EORP EUROASPIRE V Study.

  • Bacquer, Dirk De1
  • Smedt, Delphine De1
  • Reiner, Željko2
  • Tokgözoğlu, Lale3
  • Clays, Els1
  • Kotseva, Kornelia4, 5
  • Rydén, Lars6
  • Wood, David4, 5
  • Backer, Guy De1
  • 1 Department of Public Health and Primary Care, Ghent University, Belgium. , (Belgium)
  • 2 Department of Internal Medicine, University Hospital Center Zagreb, Croatia. , (Croatia)
  • 3 Department of Cardiology, Hacettepe University, Turkey. , (Turkey)
  • 4 National Institute for Prevention and Cardiovascular Health, National University of Ireland-Galway, Republic of Ireland. , (Ireland)
  • 5 National Heart and Lung Institute, Imperial College London, UK.
  • 6 Department of Medicine Solna, Karolinska Institutet, Sweden. , (Sweden)
Published Article
European Journal of Preventive Cardiology
SAGE Publications
Publication Date
Oct 01, 2020
DOI: 10.1177/2047487319874898
PMID: 31500460


Recent European guidelines recommend in patients with atherosclerotic cardiovascular disease to achieve a reduction of low-density lipoprotein-cholesterol of at least 50% if the baseline low-density lipoprotein-cholesterol level is between 1.8 and 3.5 mmol/L. Systematic reviews have associated a given statin/dose combination with a fixed percentage low-density lipoprotein-cholesterol response. Algorithms for detecting cases and estimating the prevalence of familial hypercholesterolaemia often rely on such fixed percentage reductions. We used data from 915 coronary patients participating in the EUROASPIRE V study in whom atorvastatin or rosuvastatin therapy was initiated at hospital discharge and who were still using these drugs at the same dose at a follow-up visit 6 or more months later. Pre and on-treatment low-density lipoprotein-cholesterol levels were compared across the full low-density lipoprotein-cholesterol range. The prevalence of FH was estimated using the Dutch Lipid Clinic Network criteria, once using observed pre-treatment low-density lipoprotein-cholesterol and once using imputed pre-treatment low-density lipoprotein-cholesterol by following the common strategy of applying fixed correction factors to on-treatment low-density lipoprotein-cholesterol. Inter-individual variation in the low-density lipoprotein-cholesterol response to a fixed statin and dose was considerable, with a strong inverse relation of percentage reductions to pre-treatment low-density lipoprotein-cholesterol. The percentage low-density lipoprotein-cholesterol response was markedly lower at the left end of the pre-treatment low-density lipoprotein-cholesterol range especially for levels less than 3 mmol/L. The estimated prevalence of familial hypercholesterolaemia was 2% if using observed pre-treatment low-density lipoprotein-cholesterol and 10% when using imputed low-density lipoprotein-cholesterol. The inter-individual variation in the percentage low-density lipoprotein-cholesterol response to a given dose of a statin is largely dependent on the pre-treatment level: the lower the pre-treatment low-density lipoprotein-cholesterol level the smaller the percentage low-density lipoprotein-cholesterol reduction. The use of uniform correction factors to estimate pre-treatment low-density lipoprotein-cholesterol is not justified.

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