***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: CONTEXT High levels of lipoprotein(a ) are associated with increased risk of myocardial infa rct ion ( MI ) . OBJECTIVE To assess whether genetic data are consistent with this association being causal . DESIGN , SETTING , AND PARTICIPANTS Three studies of white individuals from Copenhagen , Denmark , were used : the Copenhagen City Heart Study ( CCHS ) , a prospect i ve general population study with 16 years of follow-up ( 1991 - 2007 , n = 8637 , 599 MI events ) ; the Copenhagen General Population Study ( CGPS ) , a cross-sectional general population study ( 2003 - 2006 , n = 29 388 , 994 MI events ) ; and the Copenhagen Ischemic Heart Disease Study ( CIHDS ) , a case-control study ( 1991 - 2004 , n = 2461 , 1231 MI events ) . MAIN OUTCOME MEASURES Plasma lipoprotein(a ) levels , lipoprotein(a ) kringle IV type 2 ( KIV-2 ) size polymorphism genotype , and MIs recorded from 1976 through July 2007 for all participants . RESULTS In the CCHS , multivariable-adjusted hazard ratios ( HRs ) for MI for elevated lipoprotein(a ) levels were 1.2 ( 95 % confidence interval [ CI ] , 0.9 - 1.6 ; events/10,000 person-years , 59 ) for levels between the 22nd and 66th percentile , 1.6 ( 95 % CI , 1.1 - 2.2 ; events/10,000 person-years , 75 ) for the 67th to 89th percentile , 1.9 ( 95 % CI , 1.2 - 3.0 ; events/10,000 person-years , 84 ) for the 90th to 95th percentile , and 2.6 ( 95 % CI , 1.6 - 4.1 ; events/10,000 person-years , 108 ) for levels greater than the 95th percentile , respectively , vs levels less than the 22nd percentile ( events/10,000 person-years , 55 ) ( trend P < .001 ) . Numbers of KIV-2 repeats ( sum of repeats on both alleles ) ranged from 6 to 99 and on analysis of variance explained 21 % and 27 % of all variation in plasma lipoprotein(a ) levels in the CCHS and CGPS , respectively . Mean lipoprotein(a ) levels were 56 , 31 , 20 , and 15 mg/dL for the first , second , third , and fourth quartiles of KIV-2 repeats in the CCHS , respectively ( trend P < .001 ) ; corresponding values in the CGPS were 60 , 34 , 22 , and 19 mg/dL ( trend P < .001 ) . In the CCHS , multivariable-adjusted HRs for MI were 1.5 ( 95 % CI , 1.2 - 1.9 ; events/10,000 person-years , 75 ) , 1.3 ( 95 % CI , 1.0 - 1.6 ; events/10,000 person-years , 66 ) , and 1.1 ( 95 % CI , 0.9 - 1.4 ; events/10,000 person-years , 57 ) for individuals in the first , second , and third quartiles , respectively , as compared with individuals in the fourth quartile of KIV-2 repeats ( events/10,000 person-years , 51 ) ( trend P < .001 ) . Corresponding odds ratios were 1.3 ( 95 % CI , 1.1 - 1.5 ) , 1.1 ( 95 % CI , 0.9 - 1.3 ) , and 0.9 ( 95 % CI , 0.8 - 1.1 ) in the CGPS ( trend P = .005 ) , and 1.4 ( 95 % CI , 1.1 - 1.7 ) , 1.2 ( 95 % CI , 1.0 - 1.6 ) , and 1.3 ( 95 % CI , 1.0 - 1.6 ) in the CIHDS ( trend P = .01 ) . Genetically elevated lipoprotein(a ) was associated with an HR of 1.22 ( 95 % CI , 1.09 - 1.37 ) per doubling of lipoprotein(a ) level on instrumental variable analysis , while the corresponding value for plasma lipoprotein(a ) levels on Cox regression was 1.08 ( 95 % CI , 1.03 - 1.12 ) . CONCLUSION These data are consistent with a causal association between elevated lipoprotein(a ) levels and increased risk of MI Background Elevated lipoprotein(a ) [ Lp(a ) ] levels predict cardiovascular events incidence in patients with coronary artery disease ( CAD ) . Genetic variants in the rs3798220 , rs10455872 and rs6415084 single-nucleotide polymorphisms ( SNPs ) in the Lp(a ) gene ( LPA ) correlate with elevated Lp(a ) levels , but whether these SNPs have prognostic value for CAD patients is unknown . The present study evaluated the association of LPA SNPs with incidence of subsequent cardiovascular events in CAD patients after percutaneous coronary intervention ( PCI ) .  Methods TaqMan SNP genotyping assays were performed to detect the rs6415084 , rs3798220 and rs10455872 genotypes in 517 Chinese Han patients with CAD after PCI .  We later assessed whether there was an association of these SNPs with incidence of major adverse cardiovascular events ( MACE : cardiac death , nonfatal myocardial infa rct ion , ischemic stroke and coronary revascularization ) . Serum lipid profiles were also determined using biochemical methods . Results Only the rs6415084 variant allele was associated with higher Lp(a ) levels [ 41.3 ( 20.8 , 74.6 ) vs. 18.6 ( 10.3 , 40.9 ) mg/dl , p < 0.001 ] . During a 2-year follow-up period , 102 patients suffered MACE , and Cox regression analysis demonstrated that elevated Lp(a ) ( ≥30 mg/dl ) levels correlated with increased MACE ( adjusted HR , 1.69 ; 95 % CI 1.13 - 2.53 ) , but there was no association between LPA genetic variants ( rs6415084 and rs3798220 ) and MACE incidence ( p > 0.05 ) . Conclusions Our data did not support a relationship between genetic LPA variants ( rs6415084 and rs3798220 ) and subsequent cardiovascular events after PCI in Chinese Han CAD patients Background Many patients with coronary heart disease do not achieve recommended LDL-cholesterol levels , due to either intolerance or inadequate response to available lipid-lowering therapy . Microsomal triglyceride transfer protein ( MTP ) inhibitors might provide an alternative way to lower LDL-cholesterol levels . We tested the safety and LDL-cholesterol-lowering efficacy of an MTP inhibitor , AEGR-733 ( Aegerion Pharmaceuticals Inc. , Bridgewater , NJ ) , alone and in combination with ezetimibe . Methods We performed a multicenter , double-blind , 12-week trial , which included 84 patients with hypercholesterolemia . Patients were r and omly assigned ezetimibe 10 mg daily ( n = 29 ) ; AEGR-733 5.0 mg daily for the first 4 weeks , 7.5 mg daily for the second 4 weeks and 10 mg daily for the last 4 weeks ( n = 28 ) ; or ezetimibe 10 mg daily and AEGR-733 administered with the dose titration described above ( n = 28 ) . Results Ezetimibe monotherapy led to a 20–22 % decrease in LDL-cholesterol concentrations .  AEGR-733 monotherapy led to a dose-dependent decrease in LDL-cholesterol concentration : 19 % at 5.0 mg , 26 % at 7.5 mg and 30 % at 10 mg . Combined therapy produced similar but larger dose-dependent decreases ( 35 % , 38 % and 46 % , respectively ) . The number of patients who discontinued study drugs owing to adverse events was five with ezetimibe alone , nine with AEGR-733 alone , and four with combined ezetimibe and AEGR-733 . Discontinuations from AEGR-733 were due primarily to mild transaminase elevations . Conclusions Inhibition of LDL production with low-dose AEGR-733 , either alone or in combination with ezetimibe , could be an effective therapeutic option for patients unable to reach target LDL-cholesterol levels OBJECTIVE A minor allele variant ( rs3798220 ) of apolipoprotein(a ) has been reported to be associated with elevated plasma lipoprotein(a ) [ Lp(a ) ] and increased cardiovascular risk . We investigated whether this allele was associated with elevated Lp(a ) and cardiovascular risk in the Women 's Health Study , a r and omized trial of low-dose aspirin , and whether aspirin reduced cardiovascular risk in minor allele carriers . METHODS AND RESULTS Genotypes of rs3798220 were determined for 25,131 initially healthy Caucasian participants .  Median Lp(a ) levels at baseline were 10.0 , 79.5 , and 153.9mg/dL for major allele homozygotes , heterozygotes , and minor allele homozygotes , respectively ( P<0.0001 ) . During the 9.9 years of follow-up , minor allele carriers ( 3.7 % ) in the placebo group had twofold higher risk of major cardiovascular events than non-carriers ( age-adjusted hazard ratio (HR)=2.21 , 95 % CI : 1.39 - 3.52 ) . Among carriers , risk was reduced more than twofold by aspirin : for aspirin compared with placebo the age-adjusted HR was 0.44 ( 95 % CI : 0.20 - 0.94 ) ; risk was not significantly reduced among non-carriers ( age-adjusted HR=0.91 , 95 % CI : 0.77 - 1.08 ) . This interaction between carrier status and aspirin allocation was significant ( P=0.048 ) . CONCLUSIONS In the Women 's Health Study , carriers of an apolipoprotein(a ) variant had elevated Lp(a ) , doubled cardiovascular risk , and appeared to benefit more from aspirin than non-carriers Background —Oxidized phospholipids ( OxPL ) circulate on apolipoprotein B-100 particles ( OxPL/apoB ) , and primarily on Lp(a ) lipoprotein ( a ) [ Lp(a ) ] . The relationship of OxPL/apoB levels to future cardiovascular events is not known . Methods and Results —The Bruneck study is a prospect i ve population -based survey of 40- to 79-year-old men and women recruited in 1990 .  Plasma levels of OxPL/apoB and lipoprotein ( a ) [ Lp(a ) ]  were measured in 765 subjects in 1995 and incident cardiovascular disease ( CVD ) , defined as cardiovascular death , myocardial infa rct ion , stroke , and transient ischemic attack , was assessed from 1995 to 2005 . During the follow-up period , 82 subjects developed CVD . In multivariable analysis , which included traditional risk factors , high sensitivity C-reactive protein ( hsCRP ) , and lipoprotein-associated phospholipase A2 ( Lp-PLA2 ) activity , subjects in the highest tertile of OxPL/apoB had a significantly higher risk of cardiovascular events than those in the lowest tertile ( hazard ratio[95 % CI ] 2.4[1.3 to 4.3 ] , P=0.004 ) . The strength of the association between OxPL/apoB and CVD risk was amplified with increasing Lp-PLA2 activity ( P=0.018 for interaction ) . Moreover , OxPL/apoB levels predicted future cardiovascular events beyond the information provided by the Framingham Risk Score ( FRS ) . The effects of OxPL/apoB and Lp(a ) were not independent of each other but they were independent of all other measured risk factors . Conclusions —This study demonstrates that OxPL/apoB levels predict 10-year CVD event rates independently of traditional risk factors , hsCRP , and FRS . Increasing Lp-PLA2 activity further amplifies the risk of CVD mediated by BACKGROUND Low-density lipoprotein ( LDL ) particle ( P , or molar ) concentration has been shown to be a more sensitive marker 
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The present article is aim ed at outlining the current state of knowledge regarding the clinical value of lipoprotein(a )  ( Lp(a ) ) as a marker of cardiovascular disease ( CVD ) risk by summarizing the results of recent clinical studies , meta-analyses and systematic review s. The literature supports the predictive value of Lp(a ) on CVD outcomes , although the effect size is modest .
Lp(a ) would also appear to have an effect on cerebrovascular outcomes , however the effect appears even smaller than that for CVD outcomes .