Conclusions Study -level data from this systemic review establish that different lipid lowering agents can lead to discordance between LDL-P and LDL-C , therefore , basing LDL-lowering therapy only on the achievement of cholesterol goals may result in a treatment gap .
Therefore , the use of LDL-P for monitoring lipid-lowering therapy , particularly for statins , can provide a more accurate assessment of residual cardiovascular risk
Purpose This systematic review was performed to summarize published experience using low density lipoprotein particle number ( LDL-P ) to monitor the efficacy of  lipid-lowering pharmacotherapies .
Effects of pravastatin on lipoproteins and endothelial function in patients receiving human immunodeficiency virus protease inhibitors.
BACKGROUND Although recommended as initial therapy for patients with dyslipidemia who are taking human immunodeficiency virus protease inhibitors ( HIV PIs ) , the effects of pravastatin on lipoproteins and arterial reactivity have not been eluci date d. The purpose of this study was to determine the effects of pravastatin on lipoprotein subfractions and endothelial function in patients with dyslipidemia who are receiving HIV PIs . METHODS This was a placebo-controlled , double-blind , crossover study comparing pravastatin ( 40 mg ) to placebo in 20 patients who were taking HIV PIs .  Lipoprotein subfractions were measured with nuclear magnetic resonance spectroscopic analysis . Flow-mediated vasodilation ( FMD ) of the brachial artery was evaluated with high-resolution ultrasound scanning . RESULTS At baseline , subjects had an increased concentration of low-density lipoprotein ( LDL ) particles ( 1756 + /- 180 nmol/L ) , which tended to be small ( 19.9 + /- 0.2 nm ) , a low concentration of large high-density lipoproteins ( HDL ; 0.94 + /- 0.07 mmol/L ) , and an increased concentration of large very low-density lipoproteins ( VLDL ; 1.90 + /- 0.58 mmol/L ) . FMD was impaired ( 4.5 % + /- 1.1 % ) . Compared with placebo , pravastatin result ed in a 20.8 % reduction in LDL particles ( P = .030 ) , a 26.7 % reduction in small LDL ( P = .100 ) , and a 44.9 % reduction in small VLDL ( P = .023 ) . Total and non-HDL cholesterol levels decreased by 18.3 % ( P < .001 ) and 21.7 % ( P < .001 ) , respectively . FMD tended to increase in patients receiving pravastatin ( 0.7 % + /- 0.6 % ) ; however , the difference between treatment phases was not statistically significant ( P = .080 ) . CONCLUSIONS This is the first double-blind , placebo-controlled study of the effects of statin therapy on lipids , lipoprotein subfractions , and endothelial function in patients taking HIV PIs .  Pravastatin reduced concentrations of atherogenic lipoproteins , particularly those most associated with future coronary events
Conclusions Study -level data from this systemic review establish that different lipid lowering agents can lead to discordance between LDL-P and LDL-C , therefore , basing LDL-lowering therapy only on the achievement of cholesterol goals may result in a treatment gap .
Therefore , the use of LDL-P for monitoring lipid-lowering therapy , particularly for statins , can provide a more accurate assessment of residual cardiovascular risk
Purpose This systematic review was performed to summarize published experience using low density lipoprotein particle number ( LDL-P ) to monitor the efficacy of  lipid-lowering pharmacotherapies .