title: The influence of statin-fibrate combination therapy on lipids profile and apolipoprotein A5 in patients with acute coronary syndrome.
abstract: BACKGROUND
  Statin-fibrate combination therapy has been used to treat patients with acute coronary syndrome (ACS) complicated by elevated triglycerides (TG) and decreased high density lipoprotein cholesterol (HDL-C). The purpose of this study was to evaluate the influence of the combination therapy on lipids profile and apolipoprotein A5 (apoA5) level in patients with ACS.
  
  
  METHODS
  One hundred and four patients with ACS were recruited and randomly assigned into two groups: one was statin group (n = 52), given atorvastatin (20 mg QN) or other statins with equivalent dosages; the other was combination group (n = 52), given the same dose of statin plus bezafibrate (200 mg BID). Follow-up visits were scheduled at the end of 6 and 12 weeks post treatment. Serum apoA5 levels were determined using a commercial available ELISA kit.
  
  
  RESULTS
  (1) Compared with that of statin monotherapy, statin-bezafibrate combination treatment not only resulted in a significant reduction of TG, TC and LDL-C levels, (all p < 0.05), but also led to increases in HDL-C and apoA5 levels (p < 0.05).(2) The percentage changes of TC, TG, LDL-C and apoA5 levels in both groups were even bigger at 12 weeks after treatment than that at 6 weeks (all p < 0.05). Similarly, the rates of achieving lipid-control target were higher in statin-bezafibrate combination treatment group than those in statin monotherapy group (all p < 0.05).(3) Spearman rank correlation analysis showed that the pre-treatment apoA5 level was positively correlated with TG (r = 0.359, p = 0.009). However, a negative correlation was observed between apoA5 and TG (r = -0.329, p = 0.017) after 12 weeks treatment.
  
  
  CONCLUSIONS
  Statin and fibrate combination therapy is more effective than statin alone in achieving a comprehensive lipid control for ACS patients. Serum apoA5 elevation after statin and fibrate combination treatment could be due to the synergistic effect of both drugs on hypertriglyceridemia control.
authors.affiliation: Department of Cardiology, The Second Xiang Ya Hospital, Central South University, No, 139, Renmin Zhonglu, Changsha, Hunan 410011, China. zhaosp@medmail.com.cn.
authors.forename: Xiang-ping
authors.initials: XP
authors.lastname: Li
authors.forename: Hai-rong
authors.initials: HR
authors.lastname: Gong
authors.forename: Xian-sheng
authors.initials: XS
authors.lastname: Huang
authors.forename: Wen-yu
authors.initials: WY
authors.lastname: Huang
authors.forename: Shui-ping
authors.initials: SP
authors.lastname: Zhao
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D000368:Aged; D000072040:Apolipoprotein A-V; D001054:Apolipoproteins A / Q000097:blood; D000069059:Atorvastatin; D001629:Bezafibrate / Q000627:therapeutic use*; D008076:Cholesterol, HDL / Q000097:blood; D004357:Drug Synergism; D004359:Drug Therapy, Combination; D005260:Female; D005464:Fluorobenzenes / Q000627:therapeutic use*; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011743:Pyrimidines / Q000627:therapeutic use*; D011758:Pyrroles / Q000627:therapeutic use*; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000627:therapeutic use*; D014280:Triglycerides / Q000097:blood
chemical_list: C437704:APOA5 protein, human; D000072040:Apolipoprotein A-V; D001054:Apolipoproteins A; D008076:Cholesterol, HDL; D005464:Fluorobenzenes; D006538:Heptanoic Acids; D000960:Hypolipidemic Agents; D011743:Pyrimidines; D011758:Pyrroles; D013449:Sulfonamides; D014280:Triglycerides; D000068718:Rosuvastatin Calcium; D000069059:Atorvastatin; D001629:Bezafibrate
references.citation: J Biol Chem. 2003 Jul 11;278(28):25468-80
references.pmid: 12709436
references.citation: J Am Coll Cardiol. 2005 Oct 4;46(7):1225-8
references.pmid: 16198835
references.citation: J Infect Dis. 2000 Jun;181 Suppl 3:S462-72
references.pmid: 10839741
references.citation: N Engl J Med. 2010 Apr 29;362(17):1563-74
references.pmid: 20228404
references.citation: Atherosclerosis. 2009 Jun;204(2):e99-102
references.pmid: 19150068
references.citation: Atherosclerosis. 2007 Jul;193(1):129-34
references.pmid: 16777114
references.citation: N Engl J Med. 1999 Jan 14;340(2):115-26
references.pmid: 9887164
references.citation: Atherosclerosis. 2004 Sep;176(1):37-44
references.pmid: 15306172
references.citation: Diabetologia. 2006 Jul;49(7):1505-11
references.pmid: 16752169
references.citation: J Am Coll Cardiol. 2008 Feb 19;51(7):724-30
references.pmid: 18279736
references.citation: N Engl J Med. 2005 Jan 6;352(1):29-38
references.pmid: 15635110
references.citation: Br J Pharmacol. 2009 Oct;158(3):706-12
references.pmid: 19694729
references.citation: J Biol Chem. 2001 Nov 30;276(48):44512-20
references.pmid: 11577099
references.citation: J Biol Chem. 2003 May 16;278(20):17982-5
references.pmid: 12637506
references.citation: Science. 2001 Oct 5;294(5540):169-73
references.pmid: 11588264
references.citation: Atherosclerosis. 2011 Dec;219(2):737-42
references.pmid: 21889769
references.citation: Clin Chim Acta. 2007 Feb;376(1-2):68-71
references.pmid: 16962087
references.citation: J Lipid Res. 2006 Sep;47(9):2064-70
references.pmid: 16769999