title: Effects of fenofibrate treatment on cardiovascular disease risk in 9,795 individuals with type 2 diabetes and various components of the metabolic syndrome: the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study.
abstract: OBJECTIVE
  We explored whether cardiovascular disease (CVD) risk and the effects of fenofibrate differed in subjects with and without metabolic syndrome and according to various features of metabolic syndrome defined by the Adult Treatment Panel III (ATP III) in subjects with type 2 diabetes in the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study.
  
  
  METHODS
  The prevalence of metabolic syndrome and its features was calculated. Cox proportional models adjusted for age, sex, CVD status, and baseline A1C levels were used to determine the independent contributions of metabolic syndrome features to total CVD event rates and the effects of fenofibrate.
  
  
  RESULTS
  More than 80% of FIELD participants met the ATP III criteria for metabolic syndrome. Each ATP III feature of metabolic syndrome, apart from increased waist circumference, increased the absolute risk of CVD events over 5 years by at least 3%. Those with marked dyslipidemia (elevated triglycerides >or=2.3 mmol/l and low HDL cholesterol) were at the highest risk of CVD (17.8% over 5 years). Fenofibrate significantly reduced CVD events in those with low HDL cholesterol or hypertension. The largest effect of fenofibrate to reduce CVD risk was observed in subjects with marked dyslipidemia in whom a 27% relative risk reduction (95% CI 9-42, P = 0.005; number needed to treat = 23) was observed. Subjects with no prior CVD had greater risk reductions than the entire group.
  
  
  CONCLUSIONS
  Metabolic syndrome components identify higher CVD risk in individuals with type 2 diabetes, so the absolute benefits of fenofibrate are likely to be greater when metabolic syndrome features are present. The highest risk and greatest benefits of fenofibrate are seen among those with marked hypertriglyceridemia.
authors.affiliation: Lipid and Diabetes Research Group, Christchurch Hospital, Christchurch, New Zealand. fieldtrial@ctc.usyd.edu.au
authors.forename: Russell
authors.initials: R
authors.lastname: Scott
authors.forename: Richard
authors.initials: R
authors.lastname: O'Brien
authors.forename: Greg
authors.initials: G
authors.lastname: Fulcher
authors.forename: Chris
authors.initials: C
authors.lastname: Pardy
authors.forename: Michael
authors.initials: M
authors.lastname: D'Emden
authors.forename: Dana
authors.initials: D
authors.lastname: Tse
authors.forename: Marja-Riitta
authors.initials: MR
authors.lastname: Taskinen
authors.forename: Christian
authors.initials: C
authors.lastname: Ehnholm
authors.forename: Anthony
authors.initials: A
authors.lastname: Keech
mesh_terms: D002318:Cardiovascular Diseases / Q000517:prevention & control*; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy*; D050171:Dyslipidemias / Q000188:drug therapy; D005260:Female; D011345:Fenofibrate / Q000627:therapeutic use*; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008297:Male; D024821:Metabolic Syndrome / Q000188:drug therapy*
chemical_list: D000960:Hypolipidemic Agents; D011345:Fenofibrate