title: Greater remnant lipoprotein cholesterol reduction with pitavastatin compared with pravastatin in HIV-infected patients.
abstract: Cardiovascular disease (CVD) is a leading cause of morbidity and mortality in those with HIV. An emerging CVD risk factor is triglyceride-rich remnant lipoprotein cholesterol (RLP-C: the sum of intermediate-density lipoprotein and very low-density lipoprotein cholesterol). The effects of statin therapy on lipoprotein subfractions, including RLP-C, in HIV dyslipidemia are unknown.
  
  
  
  This is a post hoc analysis of the randomized INTREPID trial (NCT 01301066) comparing pitavastatin 4 mg daily vs. pravastatin 40 mg daily in study participants with HIV. We measured apolipoproteins AI and B and lipoprotein cholesterol subfractions separated by density gradient ultracentrifugation at baseline and 12 weeks. We compared changes in atherogenic subfractions over 12 weeks in INTREPID participants using analysis of covariance.
  
  
  
  Lipoprotein subfraction data were available for 213 study participants (pitavastatin n = 104, pravastatin n = 109). Baseline characteristics were similar between treatment groups. Reductions in RLP-C were significantly greater in the pitavastatin group compared with pravastatin group (-11.6 mg/dl vs. -8.5 mg/dl; P = 0.01). Similarly, ratios of risk [apolipoproteins B/apolipoproteins AI, total cholesterol/high-density lipoprotein cholesterol (HDL-C)] showed greater reductions with pitavastatin (P < 0.05). There were no differences in changes in HDL-C, HDL-C subfractions or lipoprotein(a) cholesterol levels.
  
  
  
  In patients with HIV, pitavastatin 4 mg/dl lowered both RLP-C and established apolipoprotein and lipid risk ratios more so than pravastatin 40 mg/dl. The impact of RLP-C reduction on CVD in HIV dyslipidemic patients merits further study.
authors.affiliation: aDivision of Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas bJohns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore cDepartment of Critical Care Medicine, National Institutes of Health, Bethesda, Maryland dDepartment of Biostatistics, Boston University School of Public Health, Boston, Massachusetts eAtherotech Diagnostics Laboratory, Birmingham fKowa Pharmaceuticals America, Inc., Montgomery, Alabama gCGH Medical Center, University of Illinois School of Medicine, Peoria, Illinois, USA.
authors.forename: Parag H
authors.initials: PH
authors.lastname: Joshi
authors.forename: P Elliott
authors.initials: PE
authors.lastname: Miller
authors.forename: Seth S
authors.initials: SS
authors.lastname: Martin
authors.forename: Steven R
authors.initials: SR
authors.lastname: Jones
authors.forename: Joseph M
authors.initials: JM
authors.lastname: Massaro
authors.forename: Ralph B
authors.initials: RB
authors.lastname: D'Agostino
authors.forename: Krishnaji R
authors.initials: KR
authors.lastname: Kulkarni
authors.forename: Craig
authors.initials: C
authors.lastname: Sponseller
authors.forename: Peter P
authors.initials: PP
authors.lastname: Toth
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D002784:Cholesterol / Q000097:blood*; D004311:Double-Blind Method; D050171:Dyslipidemias / Q000188:drug therapy*; D005260:Female; D015658:HIV Infections / Q000150:complications*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D017035:Pravastatin / Q000627:therapeutic use*; D011804:Quinolines / Q000627:therapeutic use*; D016896:Treatment Outcome; D014461:Ultracentrifugation; D055815:Young Adult
chemical_list: D000924:Anticholesteremic Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008074:Lipoproteins; D011804:Quinolines; C030104:lipoprotein cholesterol; D002784:Cholesterol; D017035:Pravastatin; C108475:pitavastatin