title: Mode of death in heart failure: findings from the ATLAS trial.
abstract: OBJECTIVE
  To investigate markers that predict modes of death in patients with chronic heart failure.
  
  
  METHODS
  Randomised, double blind, three period, comparative, parallel group study (ATLAS, assessment of treatment with lisinopril and survival).
  
  
  METHODS
  3164 patients with mild, moderate, or severe chronic heart failure (New York Heart Association functional class II-IV).
  
  
  METHODS
  High dose (32.5 or 35 mg) or low dose (2.5 or 5 mg) lisinopril once daily for a median of 46 months.
  
  
  METHODS
  All cause mortality, cardiovascular mortality, sudden death, and chronic heart failure death related to prognostic factors using competing risks analysis. Mode of death was classified by trialists and by an independent end point committee.
  
  
  RESULTS
  Age, male sex, pre-existing ischaemic heart disease, increasing heart rate, creatinine concentration, and certain drugs taken at randomisation were markers of increased risk of all cause mortality and cardiovascular death. There were risk markers for sudden death that were different from the risk markers for death from chronic heart failure. Low systolic blood pressure at baseline, raised creatinine, reduced serum sodium or haemoglobin, and increased heart rate were associated with chronic heart failure death. Use of beta blockers or antiarrhythmic agents (mainly amiodarone) was associated with a reduced risk of sudden death, whereas long acting nitrates and previous use of angiotensin converting enzyme inhibitors were markers for increased risk.
  
  
  CONCLUSIONS
  The use of competing risks analysis on the data from the ATLAS study has identified variables associated with certain modes of death in heart failure patients. This approach to analysing outcomes may make it possible to predict which patients might benefit most from particular therapeutic interventions.
authors.affiliation: Faculty of Medicial Imperial College, London, UK. p.poole-wilson@ic.ac.uk
authors.forename: P A
authors.initials: PA
authors.lastname: Poole-Wilson
authors.forename: B F
authors.initials: BF
authors.lastname: Uretsky
authors.forename: K
authors.initials: K
authors.lastname: Thygesen
authors.forename: J G F
authors.initials: JG
authors.lastname: Cleland
authors.forename: B M
authors.initials: BM
authors.lastname: Massie
authors.forename: L
authors.initials: L
authors.lastname: Rydén
mesh_terms: D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000401:mortality; D002423:Cause of Death; D003404:Creatinine / Q000097:blood; D016757:Death, Sudden, Cardiac / Q000209:etiology; D004311:Double-Blind Method; D005260:Female; D006333:Heart Failure / Q000188:drug therapy / Q000401:mortality* / Q000503:physiopathology; D006801:Humans; D017706:Lisinopril / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000401:mortality; D018570:Risk Assessment; D012307:Risk Factors; D013318:Stroke Volume / Q000502:physiology; D016896:Treatment Outcome
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents; D003404:Creatinine; D017706:Lisinopril