title: Changes in HDL cholesterol and cardiovascular outcomes after lipid modification therapy.
abstract: BACKGROUND
  Lipid modification therapy (LMT) produces cardiovascular benefits principally through reductions in low density lipoprotein cholesterol. While recent evidence, using data from 454 participants in the Framingham Offspring Study, has suggested that increases in high density lipoprotein cholesterol (HDL-C) are also associated with a reduction in cardiovascular outcomes, independently of changes in low density lipoprotein cholesterol, replication of this finding is important. The authors therefore present further results using data from the EPIC-Norfolk (UK) and Rotterdam (The Netherlands) prospective cohort studies.
  
  
  METHODS
  A total of 1148 participants, 446 from the EPIC-Norfolk and 702 from the Rotterdam study, were assessed for lipids before and after starting LMT. Subsequent risk of cardiovascular events, ascertained through linkage with mortality records and hospital databases, was investigated using Cox proportional hazards regression. Random effects meta-analysis was used to combine results across studies.
  
  
  RESULTS
  Based on combined data from the EPIC-Norfolk and Rotterdam studies there was some evidence that change in HDL-C resulting from LMT was associated with reduced cardiovascular risk (HR per pooled SD (=0.34 mmol/l) increase=0.74, 95% CI 0.56 to 0.99, adjusted for age, sex and baseline HDL-C). However, this association was attenuated and was not (statistically) significant with further adjustments for non-HDL-C and for cigarette smoking history, prevalent diabetes, systolic blood pressure, body mass index, use of antihypertensive medication, previous myocardial infarction, prevalent angina and previous stroke (0.92, 0.701.20).
  
  
  CONCLUSIONS
  Following adjustment for conventional non-lipid risk factors of cardiovascular disease, this study provides no evidence to support a significant benefit from increasing HDL-C independent of the effect of lowering non-HDL-C.
authors.affiliation: Division of Clinical Sciences, St George's University of London, Cranmer Terrace, London, UK. kray@sgul.ac.uk
authors.forename: Kausik
authors.initials: K
authors.lastname: Ray
authors.forename: Nick W J
authors.initials: NW
authors.lastname: Wainwright
authors.forename: Loes
authors.initials: L
authors.lastname: Visser
authors.forename: Jacqueline
authors.initials: J
authors.lastname: Witteman
authors.forename: Monique
authors.initials: M
authors.lastname: Breteler
authors.forename: Baishali
authors.initials: B
authors.lastname: Ambegaonkar
authors.forename: Albert
authors.initials: A
authors.lastname: Hofman
authors.forename: Bruno
authors.initials: B
authors.lastname: Stricker
authors.forename: Nick
authors.initials: N
authors.lastname: Wareham
authors.forename: Kay Tee
authors.initials: KT
authors.lastname: Khaw
authors.forename: Manjinder
authors.initials: M
authors.lastname: Sandhu
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002318:Cardiovascular Diseases / Q000097:blood / Q000150:complications / Q000453:epidemiology*; D008076:Cholesterol, HDL / Q000097:blood*; D050171:Dyslipidemias / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009017:Morbidity / Q000639:trends; D009426:Netherlands / Q000453:epidemiology; D019339:Port-Wine Stain; D012042:Registries; D012307:Risk Factors; D015996:Survival Rate / Q000639:trends; D006113:United Kingdom / Q000453:epidemiology
chemical_list: D008076:Cholesterol, HDL; D000960:Hypolipidemic Agents