title: High-density lipoprotein, but not low-density lipoprotein cholesterol levels influence short-term prognosis after acute coronary syndrome: results from the MIRACL trial.
abstract: OBJECTIVE
  Patients with acute coronary syndrome (ACS) in the Myocardial Ischaemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study had diminished cardiovascular events after 16 weeks of treatment of atorvastatin 80 mg daily. We determined whether plasma lipoproteins at baseline and then at 6 weeks after randomization predicted clinical outcome.
  
  
  RESULTS
  Cox proportional hazards models were constructed to determine relations between lipoproteins and clinical endpoint events. Baseline LDL cholesterol (LDL-C) did not predict outcome. In contrast, baseline HDL-C predicted outcome with a hazard ratio of 0.986 per mg/dL increment in HDL-C, P<0.001, indicating 1.4% reduction in risk for each 1 mg/dL increase in HDL-C. Atorvastatin treatment profoundly lowered LDL-C, but had minimal effect on HDL-C. Neither Week 6 LDL-C nor absolute change of LDL-C from baseline by Week 6 had any significant impact on clinical endpoints occurring between Week 6 and Week 16 after randomization.
  
  
  CONCLUSIONS
  Plasma HDL-C, but not LDL-C, measured in the initial stage of ACS predicts the risk of recurrent cardiovascular events over the ensuing 16 weeks. LDL-C reduction does not account for the clinical risk reduction with atorvastatin treatment after ACS. This finding may suggest that the clinical benefit of atorvastatin after ACS is mediated by qualitative changes in the LDL particle and/or by non-lipid (pleiotropic) effects of the drug.
authors.affiliation: Department of Medicine and Care, Internal Medicine, University of Linköping, SE-58185 Linköping, Sweden. andol@imv.liu.se
authors.forename: Anders G
authors.initials: AG
authors.lastname: Olsson
authors.forename: Gregory G
authors.initials: GG
authors.lastname: Schwartz
authors.forename: Michael
authors.initials: M
authors.lastname: Szarek
authors.forename: William J
authors.initials: WJ
authors.lastname: Sasiela
authors.forename: Michael D
authors.initials: MD
authors.lastname: Ezekowitz
authors.forename: Peter
authors.initials: P
authors.lastname: Ganz
authors.forename: Michael F
authors.initials: MF
authors.lastname: Oliver
authors.forename: David
authors.initials: D
authors.lastname: Waters
authors.forename: Andreas
authors.initials: A
authors.lastname: Zeiher
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000097:blood / Q000188:drug therapy / Q000401:mortality; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D000069059:Atorvastatin; D008078:Cholesterol, LDL / Q000097:blood*; D004311:Double-Blind Method; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D008075:Lipoproteins, HDL / Q000097:blood*; D008297:Male; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy / Q000401:mortality; D017202:Myocardial Ischemia / Q000097:blood / Q000188:drug therapy / Q000401:mortality*; D011379:Prognosis; D016016:Proportional Hazards Models; D011758:Pyrroles / Q000627:therapeutic use*; D012008:Recurrence
chemical_list: D000924:Anticholesteremic Agents; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D008075:Lipoproteins, HDL; D011758:Pyrroles; D000069059:Atorvastatin