title: Low triglyceride, not low cholesterol concentration, independently predicts poor outcome following acute stroke.
abstract: BACKGROUND
  Recent data have shown an unexpected association between poor outcome after acute stroke and lower serum cholesterol. Triglyceride concentration has been linked to coronary heart disease and stroke; however, there are currently no data on the relationship between triglyceride and stroke outcome. Such information may yield further mechanistic information on the relationship between lipids and stroke outcome.
  
  
  METHODS
  We studied 1,310 nondiabetic patients presenting to our acute stroke unit with computed tomography-confirmed acute stroke. Fasting blood samples were drawn within 24 h of admission for glucose, lipids and a standard battery of biochemistry and hematological tests. Information on age, stroke type, admission blood pressure, smoking status, presence of atrial fibrillation, resolution time of symptoms and Oxfordshire Community Stroke Project clinical classification was collated. Stepwise proportional hazards regression was used to estimate the effect of the above variables on survival following stroke.
  
  
  RESULTS
  Increased age (p < 0.0001), presence of atrial fibrillation (p = 0.009), hyperglycemia (p = 0.0005) and lower triglyceride level (p < 0.0001) independently predicted higher mortality; early resolution of symptoms (p = 0.005) independently predicted lower mortality. Although serum cholesterol level predicted outcome after adjusting for other prognostic factors, it did not remain significant when triglyceride level was entered into the model. The relative hazard per additional quartile of triglyceride was 0.84 (95% confidence interval 0.77-0.91).
  
  
  CONCLUSIONS
  Low triglyceride concentration strongly predicts higher mortality following stroke, whereas serum cholesterol level is not an independent predictor. Outcome following stroke is thus related more strongly to triglyceride-rich than to cholesterol-rich lipoprotein concentrations. The mechanisms explaining this require further investigation.
authors.affiliation: Acute Stroke Unit, University Department of Medicine and Therapeutics, Gardiner Institute, Western Infirmary, Glasgow, UK.
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Weir
authors.forename: Naveed
authors.initials: N
authors.lastname: Sattar
authors.forename: Matthew R
authors.initials: MR
authors.lastname: Walters
authors.forename: Kennedy R
authors.initials: KR
authors.lastname: Lees
mesh_terms: D000208:Acute Disease; D000368:Aged; D001281:Atrial Fibrillation / Q000503:physiopathology; D001786:Blood Glucose / Q000378:metabolism; D002784:Cholesterol / Q000097:blood*; D005260:Female; D006801:Humans; D008297:Male; D011237:Predictive Value of Tests; D011379:Prognosis; D016016:Proportional Hazards Models; D012606:Scotland; D012907:Smoking / Q000503:physiopathology; D020521:Stroke / Q000097:blood* / Q000503:physiopathology*; D016019:Survival Analysis; D014057:Tomography, X-Ray Computed; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood*
chemical_list: D001786:Blood Glucose; D014280:Triglycerides; D002784:Cholesterol