title: Effect of intensive compared with standard glycemia treatment strategies on mortality by baseline subgroup characteristics: the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial.
abstract: OBJECTIVE
  To determine if baseline subgroups in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial can be identified for whom intensive compared with standard glycemia treatment had different effects on all-cause mortality.
  
  
  METHODS
  Exploratory post hoc intention-to-treat comparisons were made between intensive and standard glycemia groups on all-cause mortality by subgroups defined by baseline characteristics.
  
  
  RESULTS
  There were few significant interactions between baseline characteristics and effects of intensive versus standard glycemia treatment on mortality: self-reported history of neuropathy (hazard ratio [HR] 1.95, 95% CI 1.41-2.69) versus no history of neuropathy (0.99, 0.79-1.26; P value for interaction 0.0008), higher A1C (A1C >8.5%: HR 1.64, 95% CI 1.22-2.22; A1C 7.5-8.4%: 1.00, 0.75-1.34; A1C <7.5%: 1.00, 0.67-1.50; P value for interaction 0.04), and aspirin use (HR 1.45, 95% CI 1.13-1.85, compared with 0.96, 0.72-1.27, in nonusers; P value for interaction 0.03).
  
  
  CONCLUSIONS
  We found a remarkable similarity of effect from intensive compared with standard glycemia treatment on mortality across most baseline subgroups. No differential effect was found in subgroups defined by variables anticipated to have an interaction: age, duration of diabetes, and previous history of cardiovascular disease. The three baseline characteristics that defined subgroups for which there was a differential effect on mortality may help identify patients with type 2 diabetes at higher risk of mortality from intensive regimens for glycemic control. Further research is warranted.
authors.affiliation: Department of Internal Medicine,Wake Forest UniversityHealth Sciences,Winston-Salem, North Carolina, USA. jcalles@wfubmc.edu
authors.forename: Jorge
authors.initials: J
authors.lastname: Calles-Escandón
authors.forename: Laura C
authors.initials: LC
authors.lastname: Lovato
authors.forename: Denise G
authors.initials: DG
authors.lastname: Simons-Morton
authors.forename: David M
authors.initials: DM
authors.lastname: Kendall
authors.forename: Rodica
authors.initials: R
authors.lastname: Pop-Busui
authors.forename: Robert M
authors.initials: RM
authors.lastname: Cohen
authors.forename: Denise E
authors.initials: DE
authors.lastname: Bonds
authors.forename: Vivian A
authors.initials: VA
authors.lastname: Fonseca
authors.forename: Faramarz
authors.initials: F
authors.lastname: Ismail-Beigi
authors.forename: Mary Ann
authors.initials: MA
authors.lastname: Banerji
authors.forename: Alan
authors.initials: A
authors.lastname: Failor
authors.forename: Bruce
authors.initials: B
authors.lastname: Hamilton
mesh_terms: D000368:Aged; D001786:Blood Glucose / Q000187:drug effects*; D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control*; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000401:mortality* / Q000503:physiopathology; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D008297:Male
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents