title: Coronary flow velocity reserve is improved by PPAR-α agonist fenofibrate in patients with hypertriglyceridemia.
abstract: BACKGROUND
  Fenofibrate, an agonist of peroxisome proliferator-activated receptor-α (PPAR-α), has a vascular protective effect.
  
  
  OBJECTIVE
  We investigated the effect of the PPAR-α agonist on coronary artery endothelial function in patients with hypertriglyceridemia.
  
  
  METHODS
  Fifty-eight patients with hypertriglyceridemia were divided into two groups: control (no treatment; n = 23) and fenofibrate treatment (n = 35), 200 mg/d, for 6 months. The patients had undergone rest and adenosine treatment to induce hyperemia for quantification of coronary flow velocity reserve (CFVR) by noninvasive Doppler echocardiography before treatment and at 6-month follow-up. Pulse wave velocity (PWV) was measured before treatment and at 6-month follow-up.
  
  
  RESULTS
  CFVR was significantly improved with fenofibrate treatment as compared with baseline level and control group (3.14 ± 0.36 vs. 2.80 ± 0.58 and 2.79 ± 0.65, P < 0.01 and 0.05, respectively), with no difference between baseline levels and untreated controls. In addition, at 6 months, plasma level of homocysteine was significantly increased with fenofibrate treatment as compared with at baseline and control group (median 18.13 [range 14.46-22.02]μmol/L vs. 14.09 [12.01-18.81] and 13.34 [9.69-17.06]μmol/L, P < 0.001 and 0.01, respectively). Furthermore, at 6 months, PWV was significantly decreased with fenofibrate treatment as compared with control group (1446 ± 136 cm/s vs. 1570 ± 203 cm/s, P < 0.05).
  
  
  CONCLUSIONS
  Treatment with PPAR-α agonist fenofibrate significantly improved CFVR and arterial stiffness in patients with hypertriglyceridemia. This endothelial protective effect may be reduced in part by the side effect of increasing homocysteine.
authors.affiliation: Department of Endocrinology, Peking University Third Hospital, Beijing, China.
authors.forename: Guang
authors.initials: G
authors.lastname: Wang
authors.forename: Liyun
authors.initials: L
authors.lastname: He
authors.forename: Jinbo
authors.initials: J
authors.lastname: Liu
authors.forename: Jie
authors.initials: J
authors.lastname: Yu
authors.forename: Xinheng
authors.initials: X
authors.lastname: Feng
authors.forename: Fuwang
authors.initials: F
authors.lastname: Li
authors.forename: Yanting
authors.initials: Y
authors.lastname: Hao
authors.forename: Jieming
authors.initials: J
authors.lastname: Mao
authors.forename: Tianpei
authors.initials: T
authors.lastname: Hong
authors.forename: Alex F
authors.initials: AF
authors.lastname: Chen
authors.forename: Xian
authors.initials: X
authors.lastname: Wang
mesh_terms: D000328:Adult; D000368:Aged; D001783:Blood Flow Velocity / Q000187:drug effects; D018932:Chemokine CCL2 / Q000097:blood; D003326:Coronary Circulation / Q000187:drug effects* / Q000502:physiology; D005260:Female; D011345:Fenofibrate / Q000494:pharmacology / Q000627:therapeutic use*; D006710:Homocysteine / Q000097:blood; D006801:Humans; D015228:Hypertriglyceridemia / Q000188:drug therapy* / Q000503:physiopathology; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D047493:PPAR alpha / Q000819:agonists*
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D000960:Hypolipidemic Agents; D047493:PPAR alpha; D006710:Homocysteine; D011345:Fenofibrate