Hypertriglyceridemia is not always adequately managed with statin monotherapyLiterature - Karlson BW, et al. Am J Cardiol 2016
A VOYAGER Meta-Analysis of the Impact of Statin Therapy on Low-Density Lipoprotein Cholesterol and Triglyceride Levels in Patients with Hypertriglyceridaemia
Karlson BW, Palmer MK, Nicholls SJ, et al.
The American Journal of Cardiology 2016; published online ahead of print
BackgroundElevated plasma triglyceride levels have been shown to be independent predictors of cardiovascular risk, even in patients who have achieved their LDL-C treatment goals with statin therapy [1,2]. LDL-C reduction with statins remains the primary treatment goal for these patients, although previous analyses have found no clear relationship between statin-mediated reductions in LDL-C and reductions in TG .
For severe hypertriglyceridemia, defined as a TG level of >885 mg/dL [>10.0 mmol/L]), which is also a risk factor for pancreatitis, clear management guidance exists, using agents that target mainly elevated TG levels [3,4]. However, it is not very clear how to treat mild to moderate hypertriglyceridemia (defined as a TG level of 177–885 mg/dL [2.0–10.0 mmol/L]) for which, according to guidelines, a TG level of <150 mg/dL (<1.7 mmol/L) is desirable [5,6].
In this analysis, LDL-C and TG reductions were evaluated in 15,800 patients with TG ≥177 mg/dL (≥2.0 mmol/L) who were receiving treatment with different statins and doses in randomised direct comparison studies. The source of patient data is the indiVidual patient meta-analysis Of statin therapY in At risk Groups: Effects of Rosuvastatin, atorvastatin and simvastatin (VOYAGER) database .
Main results• Reductions in LDL-C: There was a clear relationship between increasing statin dose and reduction in LDL-C. Across all statins and doses, the mean percent reduction (±SEM) in LDL-C ranged from –26.9% (2.0%) to –55.5% (0.8%)
- the LDL-C reductions with rosuvastatin 10, 20, and 40 mg were significantly greater than those with equal or double mg doses of atorvastatin and simvastatin (P<0.05 for all comparisons)
- the LDL-C reductions in with atorvastatin 80 mg were significantly greater than those with rosuvastatin 5 and 10 mg (P<0.05)
- the LDL-C reductions with rosuvastatin 5, 10 and 20 mg were greater than those with simvastatin 20, 40 and 80 mg, respectively (P<0.05)
- rosuvastatin 10 mg resulted in a significantly greater reduction in TG compared with atorvastatin 10 mg (P<0.001)
- TG reductions with rosuvastatin 20 and 40 mg were similar to those observed with equal doses of atorvastatin
- atorvastatin 80 mg resulted in significantly greater reductions in TG than rosuvastatin 10 mg (P<0.05)
- rosuvastatin 10–40 mg resulted in significantly greater TG reductions compared with equal or double doses of simvastatin (P<0.05)
- for atorvastatin 10, 20, 40, and 80 mg: 30.3%, 38.5%, 44.8%, and 54.8% respectively
- for rosuvastatin 5, 10, 20, and 40 mg: 28.3%, 35.0%, 38.3%, and 48.9% respectively
- for simvastatin 10, 20, 40, and 80 mg: 22.6%, 25.4%, 25.9%, and 35.7% respectively
ConclusionIn patients with hypertriglyceridemia, statin monotherapy resulted in TG reductions, however, a substantial number of patients did not achieve the recommended TG level of <150 mg/dL (<1.7 mmol/L). Additional TG-lowering therapy should be considered to further reduce the residual cardiovascular risk in patients with persisting high TG levels, even if LDL-C goals are met with statin therapy.
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