***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Human plasma platelet-activating factor acetylhydrolase ( PAF-AH ) is a phospholipase A2 that is primarily associated with low density lipoprotein ( LDL ) . PAF-AH activity has also been found in high density lipoprotein ( HDL ) , although it has recently been indicated that there is no PAF-AH protein in HDL . Plasma paraoxonase 1 ( PON1 ) is an HDL-associated esterase , which also exhibits PAF-AH – like activity . The effect of atorvastatin ( 20 mg per day for 4 months ) on PAF-AH and PON1 activities in patients with dyslipidemia of type IIA ( n=55 ) or type IIB ( n=21 ) was studied . In both patient groups , atorvastatin significantly reduced plasma PAF-AH activity because of the decrease in LDL plasma levels and the preferential decrease in PAF-AH activity on dense LDL subfractions ( LDL-4 and LDL-5 ) . Drug therapy did not affect HDL-associated PAF-AH activity or serum PON1 activities toward paraoxon and phenylacetate in either patient group . However , because of the reduction in LDL cholesterol levels , the ratios of HDL-associated PAF-AH and serum PON1 activities to LDL cholesterol levels were significantly increased after drug administration . The reduction of the LDL-associated PAF-AH activity and the elevation in the ratios of HDL-associated PAF-AH and PON1 activities to LDL plasma levels may represent a new dimension in the antiatherogenic effect of atorvastatin Objective — Lipoprotein-associated phospholipase A2 ( Lp-PLA2 ) is a predictor for incident atherosclerotic disease . We investigated the effect of 3 hypolipidemic drugs that exert their action through different mechanisms on plasma and lipoprotein-associated Lp-PLA2 activity and mass . Methods and Results — In 50 patients with Type IIA dyslipidemia were administered rosuvastatin ( 10 mg daily ) , whereas in 50 Type IIA dyslipidemic patients exhibiting intolerance to previous statin therapy were administered ezetimibe as monotherapy ( 10 mg daily ) . Fifty patients with Type IV dyslipidemia were given micronised fenofibrate ( 200 mg daily ) . Low- and high-density lipoprotein ( LDL and HDL , respectively ) subclass analysis was performed electrophoretically , whereas lipoprotein subfractions were isolated by ultracentrifugation . Ezetimibe reduced plasma Lp-PLA2 activity and mass attributable to the reduction in plasma levels of all LDL subfractions . Rosuvastatin reduced enzyme activity and mass because of the decrease in plasma levels of all LDL subfractions and especially the Lp-PLA2 on dense LDL subfraction ( LDL-5 ) . Fenofibrate preferentially reduced the Lp-PLA2 activity and mass associated with the VLDL+IDL and LDL-5 subfractions . Among studied drugs only fenofibrate increased HDL-associated Lp-PLA2 ( HDL-Lp-PLA2 ) activity and mass attributable to a preferential increase in Lp-PLA2 associated with the HDL-3c subfraction . Conclusion — Ezetimibe , rosuvastatin , and fenofibrate reduce Lp-PLA2 activity and mass associated with the atherogenic apoB-lipoproteins . Furthermore , fenofibrate improves the enzyme specific activity on apoB-lipoproteins and induces the HDL-Lp-PLA2 . The clinical implication s of these effects remain to be established Background —Lipoprotein-associated phospholipase A2 ( Lp-PLA2 ) has been proposed as an inflammatory marker of cardiovascular disease . In the present study , we investigated whether Lp-PLA2 is an independent predictor of coronary heart disease and ischemic stroke . Methods and Results —The Rotterdam Study is a population -based follow-up study in 7983 subjects ≥55 years of age . We performed a case-cohort  study , including 308 coronary heart disease cases , 110 ischemic stroke cases , and a r and om sample of 1820 subjects . We used Cox proportional-hazard models with modification of the st and ard errors based on robust variance estimates to compute hazard ratios adjusted for age , sex , body mass index , systolic blood pressure , non-HDL cholesterol , HDL cholesterol , diabetes , smoking , alcohol consumption , cholesterol-lowering medication , white blood cell count , and C-reactive protein . Compared with the first quartile of Lp-PLA2 activity , multivariate-adjusted hazard ratios for coronary heart disease for the second , third , and fourth quartiles were 1.39 ( 95 % CI , 0.92 to 2.10 ) , 1.99 ( 95 % CI , 1.32 to 3.00 ) , and 1.97 ( 95 % CI , 1.28 to 3.02 ) , respectively ( P for trend=0.01 ) . Corresponding multivariate-adjusted hazard ratios for ischemic stroke were 1.08 ( 95 % CI , 0.55 to 2.11 ) , 1.58 ( 95 % CI , 0.82 to 3.04 ) , and 1.97 ( 95 % CI , 1.03 to 3.79 ) ( P for trend=0.03 ) . The relation between Lp-PLA2 and coronary heart disease was present in both subjects with non-HDL cholesterol levels below the median and those with non-HDL cholesterol levels above the median . Conclusions —This study shows that Lp-PLA2 activity is an independent predictor of coronary heart disease and ischemic stroke in the general population BACKGROUND Statins lower the levels of low-density lipoprotein ( LDL ) cholesterol and C-reactive protein ( CRP ) . Whether this latter property affects clinical outcomes is unknown . METHODS We evaluated relationships between the LDL cholesterol and CRP levels achieved after treatment with 80 mg of atorvastatin or 40 mg of pravastatin per day and the risk of recurrent myocardial infa rct ion or death from coronary causes among 3745 patients with acute coronary syndromes . RESULTS Patients in whom statin therapy result ed in LDL cholesterol levels  of less than 70 mg per deciliter ( 1.8 mmol per liter ) had lower event rates than those with higher levels ( 2.7 vs. 4.0 events per 100 person-years , P=0.008 ) . However , a virtually identical difference was observed between those who had CRP levels of less than 2 mg per liter after statin therapy and those who had higher levels ( 2.8 vs. 3.9 events per 100 person-years , P=0.006 ) , an effect present at all levels of LDL cholesterol achieved . For patients with post-treatment LDL cholesterol levels  of more than 70 mg per deciliter , the rates of recurrent events were 4.6 per 100 person-years among those with CRP levels of more than 2 mg per liter and 3.2 events per 100 person-years among those with CRP levels of less than 2 mg per liter ; the respective rates among those with LDL cholesterol levels of less than 70 mg per deciliter were 3.1 and 2.4 events per 100 person-years ( P<0.001 ) . Although atorvastatin was more likely than pravastatin to result in low levels of LDL cholesterol and CRP , meeting these targets was more important in determining the outcomes than was the specific choice of therapy . Patients who had LDL cholesterol levels of less than 70 mg per deciliter and CRP levels of less than 1 mg per liter after statin therapy had the lowest rate of recurrent events ( 1.9 per 100 person-years ) . CONCLUSIONS Patients who have low CRP levels after statin therapy  have better clinical outcomes than those with higher CRP levels , regardless of the result ant level of LDL cholesterol . Strategies to lower cardiovascular risk with statins should include monitoring CRP as well as cholesterol BACKGROUND Measurement of inflammatory markers has been reported to identify individuals at increased risk for ischemic stroke .  Lipoprotein-associated phospholipase A2 ( Lp-PLA2 ) is a proinflammatory enzyme secreted by macrophages . We assessed Lp-PLA2 and C-reactive protein ( CRP ) levels along with traditional risk factors to examine their relation to ischemic stroke . METHODS A proportional hazards model was used in a prospect i ve case-cohort study of 12,762 apparently healthy middle-aged men and women in the Atherosclerosis Risk in Communities ( ARIC ) study who were observed for about 6 years . RESULTS Mean Lp-PLA2 and CRP levels adjusted for sex , race , and age were higher in the 194 stroke cases than the 766 noncases , whereas low-density lipoprotein cholesterol ( LDL-C ) level was not significantly different . Both Lp-PLA2 and CRP levels were associated with ischemic stroke after adjustment for age , sex , and race : hazard ratios were 2.23 for the highest vs the lowest tertile of Lp-PLA2 and 2.70 for CRP level higher than 3 vs lower than 1 mg/L. In a model that included smoking , systolic hypertension , lipid levels , and diabetes , Lp-PLA2 and CRP levels in the highest category were associated with hazard ratios of 1.91 ( 95 % confidence interval , 1.15 - 3.18 ; P = .01 ) and 1.87 ( 95 % confidence interval , 1.13 - 3.10 ; P = .02 ) , respectively . Individuals with high levels of both CRP and Lp-PLA2 were at the highest risk after adjusting for traditional risk factors compared with individuals with low levels of both , whereas others were at intermediate risk . CONCLUSION Levels of Lp-PLA2 and CRP may be complementary beyond traditional risk factors in identifying middle-aged individuals at increased risk for ischemic stroke OBJECTIVES The aim of this study was to determine the effects of pravastatin and atorvastatin on markers of oxidative stress in plasma . BACKGROUND Hydroxymethylglutaryl coenzyme A reductase inhibitors reduce low-density lipoprotein cholesterol ( LDL-C ) and cardiovascular risk , but their effects on circulating biomarkers of oxidative stress are not well-defined . METHODS Hypercholesterolemic subjects ( n = 120 , ages 21 to 80 years with LDL-C 130 to 220 mg/dl ) were r and omized in a double-blind , parallel design to pravastatin 40 mg/day ( prava40 ) , atorvastatin 10 mg/day ( atorva10 ) , atorvastatin 80 mg/day ( atorva80 ) , or placebo . At baseline and 16 weeks , urinary isoprostanes ( 8 , 12-iso-iPF(2 alpha)-VI isoform ) , plasma lipoprotein-associated phospholipase A2 ( Lp-PLA2 ) , Mercodia oxidized LDL ( OxLDL ) with antibody 4E6 , oxidized phospholipids/apolipoprotein B-100 particle ( OxPL/apoB ) with antibody E06 , immunoglobulin (Ig)G/IgM autoantibodies to malondialdehyde (MDA)-LDL , and apolipoprotein B (apoB)-immune complexes ( IC ) were measured . RESULTS After 16 weeks , there were no significant changes in urinary 8 , 12-iso-iPF(2 alpha)-VI . The Lp-PLA2 and OxLDL were reduced in statin-treated groups , but after adjusting for apoB , only prava40 led to a reduction in Lp-PLA2 ( -15 % , p = 0.008 ) and atorva10 to a decrease in OxLDL ( -12.9 % , p = 0.01 ) . The OxPL/apoB increased 25.8 % ( p < 0.01 ) with prava40 and 20.2 % ( p < 0.05 ) with atorva80 . There were no changes in MDA-LDL autoantibodies , but significant decreases in IC were noted . CONCLUSIONS This study suggests that statin therapy results in variable effects on oxidative stress markers in hypercholesterolemic subjects . Future outcome studies should collectively assess various oxidative markers to define clinical utility Background —Inflammation may be a causative factor in congestive heart failure ( CHF ) .  Lipoprotein-associated phospholipase A2 ( Lp-PLA2 ) is an inflammation marker associated with vascular risk . One previous study showed an association of Lp-PLA2 activity with CHF risk , but there were only 94 CHF cases and Lp-PLA2 antigen , which is available clinical ly in the United States , was not measured . Methods and Results —We measured baseline Lp-PLA2 antigen and activity  in 3991 men and women without baseline CHF or cardiovascular disease who were participating in the Cardiovascular Health Study , a prospect i ve observational study of adults 65 
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The association was consistent across a wide variety of subjects of both sexes and different ethnic background s. CONCLUSIONS The role of Lp-PLA2 as a significant biomarker of vascular inflammation was confirmed , and Lp-PLA2 seems to be closely correlated to cardiovascular events .
It may be an important therapeutic target and may have an important role in prevention , risk stratification and personalised medicine