***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: BACKGROUND The natural history of atherosclerosis progression following revascularization procedures ( PTCA or CABG )  limits the long-term benefits of these procedures and requires continuation of risk management . MATERIAL / METHODS Of 392 patients with multivessel disease r and omized to an initial strategy of PTCA or CABG in the Emory Angioplasty Versus Surgery Trial ( EAST ) , 298 patients ( 152 PTCA and 146 CABG ) completed 3-year angiographic follow-up . Native coronary artery disease progression was defined as lesions with < 50 % diameter stenosis ( % S ) at baseline , measured by QCA , that increased at least 10%S to become > or=50%S during the 3-year follow-up . Major ischemic events ( new Q-wave myocardial infa rct ion , a large reversible thallium defect or additional revascularization procedures ) attributed to these new lesions were determined based on the ECG ischemic changes and /or the details of the coronary anatomy . RESULTS Of 298 patients , 53 ( 18 % ) ( 15 % of PTCA and 21 % of CABG ) developed at least one significant new native coronary artery lesion . Of 136 patients with events , 19 ( 14 % ) had such events due to progression . In multivariate analysis , native coronary disease progression was independently correlated with hypertension ( OR=2.4 , p=0.03 ) , ST segment depression = 1 mm on baseline ETT ( OR=2.7 , p=0.01 ) , and percent of small LDL particles ( LDL IIIa-IVb ) ( OR=1.2 for every 5 % increase , p=0.01 ) . CONCLUSIONS In EAST , the native CAD progression accounted for one in seven major ischemic episodes over a 3-year follow-up . Patients with metabolic atherogenic risk profiles were more likely to have disease progression . These findings indicate the importance of more aggressive risk factor modification following revascularization AIMS To evaluate the association of  low-density lipoprotein cholesterol ( LDL-C )  levels in small and large LDL particles with risk of incident coronary heart disease ( CHD ) .  METHODS AND RESULTS We performed a prospect i ve case-control study nested in the EPIC-Norfolk cohort . Cases were apparently healthy men and women aged 45 - 79 years who developed fatal or non-fatal CHD ( n = 1035 ) , and who were matched by age , gender , and enrollment time to 1920 controls who remained free of CHD .  Electrophoretic characteristics of LDL particles were measured using 2 - 16 % polyacrylamide gradient gel electrophoresis .  Concentrations of LDL-C(<255 A ) were higher in cases than controls in men ( 1.34 + /- 0.88 vs. 1.15 + /- 0.80 mmol/L , P < 0.001 ) as well as in women ( 1.12 + /- 0.84 vs. 0.94 + /- 0.74 mmol/L , P < 0.001 ) . The unadjusted odds ratio ( OR ) for future CHD in men of the top tertile of LDL-C(<255 A ) was 1.68 ( 95 % CI , 1.33 - 2.13 ; P < 0.001 ) whereas in women the unadjusted OR was 1.53 ( 95 % CI , 1.13 - 2.07 ; P < 0.001 ) . However , after further adjustments for confounding variables , the association between LDL-C(<255 A ) and CHD was no longer significant in men and in women . CONCLUSION Cholesterol concentrations in different LDL subclasses show different relationships with CHD risk in this European cohort Background — Changes in conventional lipid risk factors with gemfibrozil treatment only partially explain the reductions in coronary heart disease ( CHD ) events experienced by men in the Veterans Affairs High-Density Lipoprotein Intervention Trial ( VA-HIT ) . We examined whether measurement of low-density lipoprotein ( LDL ) and high-density lipoprotein ( HDL ) particle subclasses provides additional information relative to CHD risk reduction . Methods and Results — This is a prospect i ve nested case-control study of 364 men with a new CHD event ( nonfatal myocardial infa rct ion or cardiac death ) during a 5.1-year ( median ) follow-up and 697 age-matched controls .  Nuclear magnetic resonance ( NMR ) spectroscopy was used to quantify levels of LDL and HDL particle subclasses and mean particle sizes in plasma obtained at baseline and after 7 months of treatment with gemfibrozil or placebo . Odds ratios for a 1-SD increment of each lipoprotein variable were calculated with adjusted logistic regression models . Gemfibrozil treatment increased LDL size and lowered numbers of LDL particles ( −5 % ) while raising numbers of HDL particles ( 10 % ) and small HDL subclass particles ( 21 % ) . Concentrations of these LDL and HDL particles achieved with gemfibrozil were significant , independent predictors of new CHD events . For total LDL and HDL particles , odds ratios predicting CHD benefit were 1.28 ( 95 % CI , 1.12 to 1.47 ) and 0.71 ( 95 % CI , 0.61 to 0.81 ) , respectively . Mean LDL and HDL particle sizes were not associated with CHD events . Conclusions — The effects of gemfibrozil on NMR-measured LDL and HDL particle subclasses , which are not reflected by conventional lipoprotein cholesterol measures , help to explain the demonstrated benefit of this therapy in patients with low HDL cholesterol Abstract Objective To examine the extent and nature of outcome reporting bias in a broad cohort of published r and omised trials . Design Retrospective review of publications and follow up survey of authors . Cohort All journal articles of r and omised trials indexed in PubMed whose primary publication appeared in December 2000 . Main outcome measures Prevalence of incompletely reported outcomes per trial ; reasons for not reporting outcomes ; association between completeness of reporting and statistical significance . Results 519 trials with 553 publications and 10 557 outcomes were identified . Survey responders ( response rate 69 % ) provided information on unreported outcomes but were often unreliable — for 32 % of those who denied the existence of such outcomes there was evidence to the contrary in their publications . On average , over 20 % of the outcomes measured in a parallel group trial were incompletely reported . Within a trial , such outcomes had a higher odds of being statistically non-significant compared with fully reported outcomes ( odds ratio 2.0 ( 95 % confidence interval 1.6 to 2.7 ) for efficacy outcomes ; 1.9 ( 1.1 to 3.5 ) for harm outcomes ) . The most commonly reported reasons for omitting efficacy outcomes included space constraints , lack of clinical importance , and lack of statistical significance . Conclusions Incomplete reporting of outcomes within published articles of r and omised trials is common and is associated with statistical non- significance . The medical literature therefore represents a selective and biased subset of study outcomes , and trial protocol s should be made publicly available OBJECTIVES To investigate the mechanisms by which bezafibrate retarded the progression of coronary lesions in the Bezafibrate Coronary Atherosclerosis Intervention Trial ( BECAIT ) , we examined the relationships of on-trial lipoproteins and lipoprotein subfractions to the angiographic outcome measurements . BACKGROUND BECAIT , the first double-blind , placebo-controlled , r and omized serial angiographic trial of a fibrate compound , showed that progression of focal coronary atherosclerosis in young survivors of myocardial infa rct ion could be retarded by bezafibrate treatment . METHODS A total of 92 dyslipoproteinemic men who had survived a first myocardial infa rct ion before the age of 45 years were r and omly assigned to treatment for 5 years with bezafibrate ( 200 mg three times daily ) or placebo ; 81 patients underwent baseline and at least one post-treatment coronary angiography .  RESULTS In addition to the decrease in very low density lipoprotein ( VLDL ) cholesterol ( -53 % ) and triglyceride ( -46 % ) and plasma apolipoprotein ( apo ) B ( -9 % ) levels , bezafibrate treatment result ed in a significant increase in high density lipoprotein-3 ( HDL3 ) cholesterol ( + 9 % ) level and a shift in the low density lipoprotein ( LDL ) subclass distribution toward larger particle species ( peak particle diameter + 032 nm ) . The on-trial HDL3 cholesterol and plasma apo B concentrations were found to be independent predictors of the changes in mean minimum lumen diameter ( r=-0.23 , p < 0.05 ) , and percent ( % ) stenosis ( r = 0.30 , p < 0.01 ) , respectively . Decreases in small dense LDL and /or VLDL lipid concentrations were unrelated to disease progression . CONCLUSIONS Our results suggest that the effect of bezafibrate on progression of focal coronary atherosclerosis could be at least partly attributed to a rise in HDL3 cholesterol and a decrease in the total number of apo B-containing lipoproteins Background —The Diabetes Atherosclerosis Intervention Study showed that treatment with fenofibrate decreases progression of coronary atherosclerosis in subjects with type 2 diabetes . We determined whether on-treatment plasma lipid concentrations and LDL particle size contribute to the favorable effect of fenofibrate on the progression of coronary artery disease ( CAD ) . Methods and Results —A total of 418 subjects with type 2 diabetes were r and omly assigned to 200 mg micronized fenofibrate daily or placebo . The mean follow-up time was 39.6 months . LDL peak particle diameter ( LDL size ) was determined by polyacrylamide gradient gel electrophoresis from 405 subjects at baseline and at the end of the study . Progression of CAD was measured with quantitative coronary angiography . LDL size increased significantly more in the fenofibrate group than in the placebo group ( 0.98±1.04 versus 0.32±0.92 nm , P < 0.001 ) . In the combined group , small LDL size was significantly associated with progression of CAD measured as the increase of percentage diameter stenosis ( r = −0.16 , P = 0.002 ) and decreases in minimum ( r = −0.11 , P = 0.030 ) and mean ( r = −0.10 , P = 0.045 ) lumen diameter . High on-treatment LDL cholesterol , apolipoprotein B , and triglyceride concentrations were also associated with the progression of CAD . In regression analyses , small LDL size added to the effect of LDL cholesterol and apolipoprotein B on the progression of CAD . Similar associations were observed in the fenofibrate group , whereas in the placebo group , lipoprotein variables were not significantly correlated with the progression of CAD . Conclusions —Changes in LDL size and plasma lipid levels account for part of the antiatherogenic effect of fenofibrate in type 2 diabetes Accumulating evidence suggests that triglyceride-rich lipoproteins contribute to coronary artery disease . Using data from the Monitored Atherosclerosis Regression Study , an angiographic trial of middle-aged men and women r and omized to lovastatin or placebo  , we investigated relationships between lipoprotein subclasses and progression of coronary artery atherosclerosis . Coronary artery lesion progression was determined by quantitative coronary angiography in low- grade ( < 50 % diameter stenosis ) , high- grade ( > or = 50 % diameter stenosis ) , and all coronary artery lesions in 220 baseline/2-year angiogram pairs .  Analytical ultracentrifugation was used to measure lipoprotein masses that were statistically evaluated for treatment group differences and relationships to progression of coronary artery atherosclerosis . All low density lipoprotein ( LDL ) , intermediate density lipoprotein ( IDL ) , and very low density lipoprotein ( VLDL ) masses were significantly lowered and all high density lipoprotein ( HDL ) masses were significantly raised with lovastatin therapy . The mass of smallest LDL ( Svedberg flotation rate [ Sf ] 0 to 3 ) , IDL ( Sf 12 to 20 ) , all VLDL subclasses ( Sf 20 to 60 , Sf 60 to 100 , and Sf 100 to 400 ) , and peak LDL flotation rate were significantly related to the progression of coronary artery lesions , specifically low- grade lesions . Greater baseline levels of HDL3 , were related to a lower likelihood of coronary artery lesion progression . In multivariate analyses , small VLDL ( Sf 20 to 60 ) and HDL3 mass were the most important correlates of coronary artery lesion progression . These results provide further evidence for the importance of triglyceride-rich lipoproteins in the progression of coronary artery disease . In addition , these results present new evidence for the possible protective role of HDL3 in the progression of coronary artery lesions . More specific information on coronary artery lesion progression may be obtained through the study of specific apolipoprotein B-containing lipoproteins OB 
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Commonly Used LDL Subfraction Tests and Terms If LDL subfractions are predictive of cardiovascular risk and are of incremental value when added to established cardiovascular risk factors , it remains to be determined whether the different characteristics of the LDL subfractions assessed by various methods would result in similar predictive abilities for estimating cardiovascular risk .
Lipid research ers have proposed that small , dense LDL particles confer greater atherogenic risk than larger , less dense LDL particles ( 6 , 7 ) .