title: Risk reductions for cardiovascular disease with pravastatin treatment by dyslipidemia phenotype: a post hoc analysis of the MEGA Study.
abstract: BACKGROUND
  The beneficial effect of statins for cardiovascular disease (CVD) prevention has been well established. However, the effectiveness among different phenotypes of dyslipidemia has not been confirmed.
  
  
  OBJECTIVE
  We evaluated the effect of pravastatin on the incidence of CVD in relation to the phenotype of dyslipidemia.
  
  
  METHODS
  The MEGA Study evaluated the effect of low-dose pravastatin on primary prevention of CVD in 7832 Japanese patients, who were randomized to diet alone or diet plus pravastatin and followed for more than 5 years. These patients were classified into phenotype IIa (n=5589) and IIb (n=2041) based on the electrophoretic pattern for this post hoc analysis.
  
  
  RESULTS
  In the diet group there was no significant difference in the incidence of coronary heart disease (CHD), stroke, CVD, and total mortality between the two phenotypes. Phenotype IIb patients, compared to phenotype IIa, had lower levels of high-density lipoprotein cholesterol (HDL-C) and a significantly higher incidence of CVD in relation to a low HDL-C level (<47.5mg/dL; p=0.02). Furthermore, pravastatin decreased the relative risk for each major endpoint in both type IIa and type IIb dyslipidemia. Significant risk reductions were observed for CHD by 38% (p=0.04) and CVD by 31% (p=0.02) in type IIa dyslipidemia but not in phenotype IIb.
  
  
  CONCLUSIONS
  Pravastatin therapy provided significant risk reductions for CHD and CVD in patients with phenotype IIa dyslipidemia, but not in those with phenotype IIb dyslipidemia.
authors.affiliation: Keyaki Naika Clinic, 3-1-7-102 Namiki, Tokorozawa, Saitama, Japan. masato@hi-ho.ne.jp
authors.forename: Masato
authors.initials: M
authors.lastname: Nishiwaki
authors.forename: Katsunori
authors.initials: K
authors.lastname: Ikewaki
authors.forename: Makoto
authors.initials: M
authors.lastname: Ayaori
authors.forename: Kyoichi
authors.initials: K
authors.lastname: Mizuno
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Ohashi
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Ohsuzu
authors.forename: Toshitsugu
authors.initials: T
authors.lastname: Ishikawa
authors.forename: Haruo
authors.initials: H
authors.lastname: Nakamura
mesh_terms: D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000008:administration & dosage*; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000209:etiology / Q000517:prevention & control*; D008076:Cholesterol, HDL; D050171:Dyslipidemias / Q000145:classification / Q000150:complications / Q000188:drug therapy* / Q000235:genetics*; D004586:Electrophoresis; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D017035:Pravastatin / Q000008:administration & dosage*; D016032:Randomized Controlled Trials as Topic; D012044:Regression Analysis; D040242:Risk Reduction Behavior; D013997:Time Factors
chemical_list: D000924:Anticholesteremic Agents; D008076:Cholesterol, HDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D017035:Pravastatin