title: Effects of lowering elevated LDL cholesterol on the cardiovascular risk of lipoprotein(a).
abstract: OBJECTIVE
  To determine if lowering elevated low-density lipoprotein cholesterol (LDL-C) levels offsets the adverse effect of raised lipoprotein(a) (Lp[a]) levels on coronary artery disease (CAC) in men.
  
  
  METHODS
  Randomized, double-blind, placebo-controlled trial of lipid lowering for CAD.
  
  
  METHODS
  Post hoc analysis of the Familial Atherosclerosis Treatment Study.
  
  
  METHODS
  A total of 146 men aged 62 years or younger with CAD and apolipoprotein B levels of at least 125 mg/dL.
  
  
  METHODS
  Patients received a Step II Diet and lovastatin (40 mg daily) plus colestipol (30 g daily), niacin (4 g daily) plus colestipol, or placebo (plus colestipol if LDL-C > 90th percentile) for 2.5 years. They were grouped by their LDL-C responses: "minimal" if LDL-C decreased by 10% or less from baseline (mean [SD] change, +6% [13%]) and "substantial" if LDL-C decreased more than 10% (mean [SD] change, -40% [16%]).
  
  
  METHODS
  Impact of lowering elevated LDL-C on the cardiac event rate (death, myocardial infarction, and revascularization for refractory ischemia) and CAD change associated with elevated Lp(a).
  
  
  RESULTS
  In multivariate analyses, the best correlate of baseline CAD severity was Lp(a) (r = 0.30; P < .001). For 36 patients with minimal LDL-C reduction, CAD progression correlated only with in-treatment Lp(a) levels (r = 0.45; P < .01), but for 84 patients with substantial LDL-C reduction, disease regressed and its change correlated with in-treatment LDL-C (r = 0.24; P < .05) but not with Lp(a) (r = -0.05). Lipoprotein(a) levels were not significantly altered in either group. For 40 patients with Lp(a) at the 90th percentile or higher, events were frequent (39%) if reduction of LDL-C was minimal, but were few (9%) if reduction was substantial (relative risk, 0.23; 95% confidence interval, 0.06 to 0.99).
  
  
  CONCLUSIONS
  In men with CAD and elevated LDL-C, Lp(a) levels were dominant correlates of baseline disease severity, its progression, and event rate over 2.5 years. However, with substantial LDL-C reductions, persistent elevations of Lp(a) were no longer atherogenic or clinically threatening. This provides a possible direction for treatment in such patients with elevated Lp(a) and LDL-C.
mesh_terms: D000328:Adult; D008078:Cholesterol, LDL / Q000097:blood*; D003327:Coronary Disease / Q000150:complications / Q000401:mortality / Q000503:physiopathology*; D018450:Disease Progression; D004311:Double-Blind Method; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology; D012086:Reoperation; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: D008078:Cholesterol, LDL; D017270:Lipoprotein(a)