title: [The influence of statin therapy on circulating microRNA-92a expression in patients with coronary heart disease].
abstract: OBJECTIVE
  To investigate the modulatory function of statin therapy on circulating microRNA-92a (miR-92a) in patients with coronary heart disease (CHD), and to evaluate the possibility of miR-92a as a new target of treatment for endothelial dysfunction.
  
  
  METHODS
  A case control study was conducted. Prevalence of abnormal blood fat content, statin treatment rate, and attainment rate of low density lipoprotein-cholesterol (LDL-C) lowered to expected level in 236 patients with CHD were analyzed. Relationship between statin therapy in patients with type 2 diabetes mellitus (DM), and level of LDL-C and circulating miR-92a expression was analyzed by multivariate general linear factorial analysis. The incidence of acute coronary syndrome (ACS) was compared in patients with CHD receiving statin therapy in all groups.
  
  
  RESULTS
  Prevalence of abnormal LDL-C was 95.7% (112/117) in CHD patients of non-statin therapy group, and 47.5% (112/236) of patients with CHD who should receive statin therapy but did not. Attainment rate of lowering of LDL-C to expected level in statin therapy group was 27.7% (33/119). LDL-C level (mmol/L) was significantly lower in statin therapy group than that in non-statin therapy group (2.457 ± 0.802 vs. 3.218 ± 1.130, Z = -9.760, P = 0.001), and incidence of ACS was significantly lower in statin therapy group than that in non-statin therapy group [33.6% vs. 71.8%, χ(2) = 34.491, P = 0.001]. There was no significant difference in incidence of ACS between patients with or without attaining the expected low value of LDL-C in statin therapy group [33.3% vs. 33.7%,χ(2) = 0.002, P = 0.968]. Circulating miR-92a expression was significantly higher in patients with stable angina pectoris (SAP) complicated with DM than those without DM (0.492 vs. -0.121, Z = -3.038, P = 0.002). It was found that statin therapy could down regulate miR-92a expression in patients with SAP complicated with DM as compared with that with non-statin therapy (0.419 vs. 0.687, Z = 1.289, P = 0.072). There was no significant difference in circulating miR-92a expression between statin therapy and non-statin therapy in patients with SAP without co-existing DM (-0.032 vs. -0.198, Z = -0.614, P = 0.539). Multivariate general linear factorial analysis showed that statin therapy was the major influential factor on LDL-C level in patients with CHD (F = 22.863, P = 0.001), and complicating DM was the major influential factor on circulating miR-92a expression in patients with SAP (F = 9.641, P = 0.003).
  
  
  CONCLUSIONS
  Regulation of circulating miR-92a expression may be considered as a new clinical target for statin treating endothelial dysfunction in patients with CHD.
authors.affiliation: Department of Cardiovascular Disease, Guangxi People's Hospital, Nanning 530021, Guangxi, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Wang
authors.forename: Hong-mei
authors.initials: HM
authors.lastname: Lu
authors.forename: Wen-hui
authors.initials: WH
authors.lastname: Yang
authors.forename: Cheng
authors.initials: C
authors.lastname: Luo
authors.forename: Shan-he
authors.initials: SH
authors.lastname: Lu
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhou
authors.forename: Ying-zhong
authors.initials: YZ
authors.lastname: Lin
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000150:complications; D000368:Aged; D016022:Case-Control Studies; D008078:Cholesterol, LDL / Q000097:blood; D003327:Coronary Disease / Q000097:blood* / Q000150:complications / Q000188:drug therapy*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D035683:MicroRNAs / Q000097:blood*; D008875:Middle Aged
chemical_list: D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; C541874:MIRN92 microRNA, human; D035683:MicroRNAs