title: Association Between Very Low Levels of High-Density Lipoprotein Cholesterol and Long-term Outcomes of Patients With Acute Coronary Syndrome Treated Without Revascularization: Insights From the TRILOGY ACS Trial.
abstract: BACKGROUND
  Low levels of high-density lipoprotein cholesterol (HDL-C; <40 mg/dL) are associated with increased risk of cardiovascular events, but it is unclear whether lower thresholds (<30 mg/dL) are associated with increased hazard.
  
  
  OBJECTIVE
  Very low levels of HDL-C may provide prognostic information in acute coronary syndrome (ACS) patients treated medically without revascularization.
  
  
  METHODS
  We examined data from 9064/9326 ACS patients enrolled in the TRILOGY ACS trial. Participants were randomized to clopidogrel or prasugrel plus aspirin. Study treatments continued for 6 to 30 months. Relationships between baseline HDL-C and the composite of cardiovascular death, myocardial infarction (MI), or stroke, and individual endpoints of death (cardiovascular and all-cause), MI, and stroke, adjusted for baseline characteristics through 30 months, were analyzed. The HDL-C was evaluated as a dichotomous variable-very low (<30 mg/dL) vs higher (≥30 mg/dL)-and continuously.
  
  
  RESULTS
  Median baseline HDL-C was 42 mg/dL (interquartile range, 34-49 mg/dL) with little variation over time. Frequency of the composite endpoint was similar for very low vs higher baseline HDL-C, with no risk difference between groups (hazard ratio [HR]: 1.13, 95% confidence interval [CI]: 0.95-1.34). Similar findings were seen for MI and stroke. However, risks for cardiovascular (HR: 1.42, 95% CI: 1.13-1.78) and all-cause death (HR: 1.36, 95% CI: 1.11-1.67) were higher in patients with very low baseline HDL-C.
  
  
  CONCLUSIONS
  Medically managed ACS patients with very low baseline HDL-C levels have higher risk of long-term cardiovascular and all-cause death but similar risks for nonfatal ischemic outcomes vs patients with higher baseline HDL-C.
authors.affiliation: Department of Medical Sciences, Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.
authors.forename: Emil
authors.initials: E
authors.lastname: Hagström
authors.affiliation: Division of Cardiovascular Medicine, Duke Clinical Research Institute, Duke University School of Medicine, Durham, North Carolina.
authors.forename: Matthew T
authors.initials: MT
authors.lastname: Roe
authors.affiliation: Department of Statistics, Duke Clinical Research Institute, Duke University School of Medicine, Durham, North Carolina.
authors.forename: Gail
authors.initials: G
authors.lastname: Hafley
authors.affiliation: Department of Statistics, Duke Clinical Research Institute, Duke University School of Medicine, Durham, North Carolina.
authors.forename: Megan L
authors.initials: ML
authors.lastname: Neely
authors.affiliation: Department of Medicine, Albany Stratton VA Medical Center and Albany Medical Center, Albany Medical College, Albany, New York.
authors.forename: Mandeep S
authors.initials: MS
authors.lastname: Sidhu
authors.affiliation: Eli Lilly and Company (Winters), Indianapolis, Indiana.
authors.forename: Kenneth J
authors.initials: KJ
authors.lastname: Winters
authors.affiliation: Centre for Chronic Disease Control and Public Health Foundation of India, New Delhi, India.
authors.forename: Dorairaj
authors.initials: D
authors.lastname: Prabhakaran
authors.affiliation: Green Lane Cardiovascular Service, Auckland City Hospital, Auckland, New Zealand.
authors.forename: Harvey D
authors.initials: HD
authors.lastname: White
authors.affiliation: Division of Cardiology, Department of Medicine/Canadian VIGOUR Centre, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: Paul W
authors.initials: PW
authors.lastname: Armstrong
authors.affiliation: Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, Scotland, United Kingdom.
authors.forename: Keith A A
authors.initials: KA
authors.lastname: Fox
authors.affiliation: Division of Cardiovascular Medicine, Duke Clinical Research Institute, Duke University School of Medicine, Durham, North Carolina.
authors.forename: E Magnus
authors.initials: EM
authors.lastname: Ohman
authors.affiliation: Department of Medicine, Albany Stratton VA Medical Center and Albany Medical Center, Albany Medical College, Albany, New York.
authors.forename: William E
authors.initials: WE
authors.lastname: Boden
mesh_terms: D054058:Acute Coronary Syndrome / Q000175:diagnosis / Q000188:drug therapy* / Q000209:etiology / Q000401:mortality; D000368:Aged; D000789:Angina, Unstable / Q000175:diagnosis / Q000188:drug therapy* / Q000209:etiology / Q000401:mortality; D001241:Aspirin / Q000009:adverse effects / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood*; D000077144:Clopidogrel; D015536:Down-Regulation; D004359:Drug Therapy, Combination; D050171:Dyslipidemias / Q000097:blood* / Q000150:complications / Q000175:diagnosis / Q000401:mortality; D005260:Female; D006801:Humans; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology / Q000401:mortality; D000072658:Non-ST Elevated Myocardial Infarction / Q000175:diagnosis / Q000188:drug therapy* / Q000209:etiology / Q000401:mortality; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D000068799:Prasugrel Hydrochloride / Q000009:adverse effects / Q000627:therapeutic use*; D018570:Risk Assessment; D012307:Risk Factors; D020521:Stroke / Q000209:etiology / Q000401:mortality; D013988:Ticlopidine / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D008076:Cholesterol, HDL; D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D000068799:Prasugrel Hydrochloride; D013988:Ticlopidine; D001241:Aspirin