title: A VOYAGER Meta-Analysis of the Impact of Statin Therapy on Low-Density Lipoprotein Cholesterol and Triglyceride Levels in Patients With Hypertriglyceridemia.
abstract: Elevated triglyceride (TG) levels are associated with increased cardiovascular disease risk. In patients with mild-to-moderate hypertriglyceridemia, defined by the European Atherosclerosis Society Consensus Panel as a TG level of 177 to 885 mg/dl (2.0 to 10.0 mmol/L), low-density lipoprotein cholesterol (LDL-C) reduction remains the primary treatment goal. Using data from the indiVidual patient meta-analysis Of statin therapY in At risk Groups: Effects of Rosuvastatin, atorvastatin and simvastatin (VOYAGER) meta-analysis, we analyzed LDL-C and TG reductions in patients with baseline TG ≥177 mg/dl (≥2.0 mmol/L). Least squares mean percentage change from baseline in LDL-C and TG was compared using 15,800 patient exposures to rosuvastatin 5 to 40 mg, atorvastatin 10 to 80 mg, and simvastatin 10 to 80 mg in patients with baseline TG ≥177 mg/dl (≥2.0 mmol/L). Comparisons were made using mixed-effects models with data only from studies directly comparing treatments by randomized design. Mean LDL-C reductions ranged from -26.9% to -55.5%. Rosuvastatin 10 to 40 mg resulted in significantly greater LDL-C reductions than equal or double doses of atorvastatin and simvastatin (p <0.05). Mean TG reductions ranged from -15.1% to -31.3%. Rosuvastatin 10 mg resulted in significantly greater TG reductions than atorvastatin 10 mg (p <0.05). Rosuvastatin 20 and 40 mg resulted in TG reductions similar to those with equal doses of atorvastatin. Rosuvastatin 10 to 40 mg resulted in significantly greater TG reductions than equal or double doses of simvastatin (p <0.05). In conclusion, in patients with hypertriglyceridemia, LDL-C reduction was substantial and dependent on the choice and dose of statin. TG reduction was numerically less than for LDL-C, and additional TG-lowering therapy may be considered to further reduce residual cardiovascular risk.
authors.affiliation: AstraZeneca, Gothenburg, Mölndal, Sweden; Department of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Electronic address: Bjorn.W.Karlson@astrazeneca.com.
authors.forename: Björn W
authors.initials: BW
authors.lastname: Karlson
authors.affiliation: School of Healthcare Science, Manchester Metropolitan University, Manchester, United Kingdom.
authors.forename: Michael K
authors.initials: MK
authors.lastname: Palmer
authors.affiliation: South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia.
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Nicholls
authors.affiliation: Department of Clinical Sciences, Danderyd Hospital, Karolinska Institute, Stockholm, Sweden.
authors.forename: Pia
authors.initials: P
authors.lastname: Lundman
authors.affiliation: Centre for Vascular Research, University of New South Wales, Sydney, Australia.
authors.forename: Philip J
authors.initials: PJ
authors.lastname: Barter
mesh_terms: D000368:Aged; D000069059:Atorvastatin / Q000627:therapeutic use; D008078:Cholesterol, LDL / Q000097:blood*; D016208:Databases, Factual; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D015228:Hypertriglyceridemia / Q000097:blood* / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D000068718:Rosuvastatin Calcium / Q000627:therapeutic use; D019821:Simvastatin / Q000627:therapeutic use; D014280:Triglycerides / Q000097:blood*
chemical_list: D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D014280:Triglycerides; D000068718:Rosuvastatin Calcium; D000069059:Atorvastatin; D019821:Simvastatin