Preventive CardiologyA VOYAGER Meta-Analysis of the Impact of Statin Therapy on Low-Density Lipoprotein Cholesterol and Triglyceride Levels in Patients With Hypertriglyceridemia
Section snippets
Methods
Data for this analysis were obtained from the VOYAGER database. Detailed patient demographics and methods from the VOYAGER meta-analysis have been reported previously.10 In brief, VOYAGER comprises results from 32,258 patients in 37 randomized, fixed-dose trials directly comparing (by randomized design) the changes in lipid levels observed during treatment with rosuvastatin, atorvastatin, and simvastatin. The present analysis includes the results of 15,800 patients with baseline TG levels of
Results
Baseline patient demographic data are presented in Table 1. A clear relationship between increasing statin dose and reduction in LDL-C was observed (Figure 1). Across all statins and doses, the mean percent reduction (±SEM) in LDL-C ranged from −26.9% (2.0%) to −55.5% (0.8%; Figure 1). The differences in LSM percent change in LDL-C between rosuvastatin and equal or higher milligram doses of atorvastatin and simvastatin are shown in Figure 2. The reductions in LDL-C observed with rosuvastatin
Discussion
It is well known that residual cardiovascular risk often persists despite the use of high-intensity statin therapy to reduce LDL-C.11, 12, 13 A component of this residual risk may relate to the persistence of elevated TG or non–high-density lipoprotein cholesterol (non–HDL-C) levels. Elevated TG levels have been shown to be independently associated with an increased incidence of cardiovascular events, even in patients who have achieved LDL-C treatment goals with statin therapy,5, 14 and TG-rich
Disclosures
Dr. Karlson is an employee of AstraZeneca; Dr. Palmer has received fees for statistical analysis from AstraZeneca; Dr. Nicholls has received research support from AstraZeneca; Dr. Lundman has received speaker fees from AstraZeneca; and Dr. Barter has received research support and speaker fees from AstraZeneca.
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Cited by (0)
This study was funded by AstraZeneca. Editorial support was provided by Alex Mellors, Prime Medica, Knutsford, Cheshire, UK, funded by AstraZeneca. Statistical analyses were funded by AstraZeneca and performed by Michael. K. Palmer, a former employee of AstraZeneca.
See page 1447 for disclosure information.