Lipids, Apolipoproteins, and Their Ratios in Relation to Cardiovascular Events With Statin Treatment Should both HDL-C and LDL-C be targets for lipid therapy? A review of current evidence. Correlation of non-high-density lipoprotein cholesterol with apolipoprotein B: effect of 5 hydroxymethylglutaryl coenzyme A reductase inhibitors on non-high-density lipoprotein cholesterol levels. PREVENTION OF ATHEROSCLEROSIS WITH LDL-C LOWERING - LIPOPROTEIN CHANGES AND INTERACTIONS: THE SANDS STUDY. Is Hypertriglyceridemia a Risk Factor for Atherosclerotic Cardiovascular Disease? A Simple Question with a Complicated Answer Epidemiologic Evidence on Serum Adiponectin Level and Lipid Profile Acute effects of feeding fructose, glucose and sucrose on blood lipid levels and systemic inflammation Achieving LDL cholesterol, non-HDL cholesterol, and apolipoprotein B target levels in high-risk patients: Measuring Effective Reductions in Cholesterol Using Rosuvastatin therapY (MERCURY) II. Canadian Cardiovascular Society position statement--recommendations for the diagnosis and treatment of dyslipidemia and prevention of cardiovascular disease. Lipid, lipoprotein, and apolipoprotein profiles in active and sedentary men with tetraplegia. Lipid-modifying efficacy and tolerability of extended-release niacin/laropiprant in patients with primary hypercholesterolaemia or mixed dyslipidaemia. Beyond low-density lipoprotein cholesterol: respective contributions of non-high-density lipoprotein cholesterol levels, triglycerides, and the total cholesterol/high-density lipoprotein cholesterol ratio to coronary heart disease risk in apparently healthy men and women. Fasting insulin and apolipoprotein B levels and low-density lipoprotein particle size as risk factors for ischemic heart disease.
Background — Low-density lipoprotein ( LDL ) cholesterol is the principal target of lipid-lowering therapy , but recent evidence has suggested more appropriate targets . We compared the relationships of on-treatment levels of LDL cholesterol , non – high-density lipoprotein ( HDL ) cholesterol , and apolipoprotein B , as well as ratios of total/HDL cholesterol , LDL/HDL cholesterol , and apolipoprotein B/A-I , with the occurrence of cardiovascular events in patients receiving statin therapy .  Methods and Results — A post hoc analysis was performed that combined data from 2 prospect i ve , r and omized clinical trials in which 10 001 ( “ Treating to New Targets ” ) and 8888 ( “ Incremental Decrease in End Points through Aggressive Lipid Lowering ” ) patients with established coronary heart disease were assigned to usual-dose or high-dose statin treatment . In models with LDL cholesterol , non-HDL cholesterol and apolipoprotein B were positively associated with cardiovascular outcome , whereas a positive relationship with LDL cholesterol was lost . In a model that contained non-HDL cholesterol and apolipoprotein B , neither was significant owing to collinearity . Total/HDL cholesterol ratio and the apolipoprotein B/A-I ratio in particular were each more closely associated with outcome than any of the individual proatherogenic lipoprotein parameters . Conclusions — In patients receiving statin therapy  , on-treatment levels of non-HDL cholesterol and apolipoprotein B were more closely associated with cardiovascular outcome than levels of LDL cholesterol . Inclusion of measurements of the antiatherogenic lipoprotein fraction further strengthened the relationships . These data support the use of non-HDL cholesterol or apolipoprotein B as novel treatment targets for statin therapy . Given the absence of interventions that have been proven to consistently reduce cardiovascular disease risk through raising plasma levels of HDL cholesterol or apolipoprotein A-I , it seems premature to consider the ratio variables as clinical ly useful The current guidelines for treatment of high-risk of lipid disorders do not specify a therapeutic target level of high-density lipoprotein cholesterol ( HDL-C ) for prevention of vascular disease in high-risk population s. However , there is a substantial body of evidence from basic science and epidemiologic studies and from clinical trials , providing the strong , consistent message that raising HDL-C by therapeutic means will effectively and independently reduce cardiovascular risk . This review summarizes epidemiologic evidence and the results of a meta- analysis of 23 published , prospect i ve , r and omized , placebo-controlled clinical trials . It focuses on the effects of lipid therapies on coronary stenosis progression , as measured by quantitative arteriography and /or , on clinical cardiovascular endpoints . Among the seven drug/treatment classes into which individual study results were categorized and averaged , reduction in stenosis progression and reduction in clinical events are both very highly correlated with the composite lipid variable ( % ΔHDL-C - % Δ low-density lipoprotein cholesterol [ LDL-C ] ; where % Δ is percent change relative to the placebo group response ) . This holds true for all lipid drug classes or combinations of lipid drug therapy , with the exception of the unexpectedly anomalous effects of the torcetrapib-atorvastatin combination . There is a strong and consistent body of evidence that therapeutic HDL-C-raising is at least as effective as comparable percentages of LDL-C-lowering for reduction of atherosclerosis progression or clinical cardiovascular events over a broad range of risk levels . Adoption of this strategy into guidelines probably awaits results of at least one large controlled HDL-C-raising clinical trial , of which two are ongoing and one other is planned Apolipoprotein B has been shown to be a better predictor of coronary heart disease than low-density lipoprotein ( LDL ) cholesterol , and non-high-density lipoprotein ( non-HDL ) cholesterol may also be a better parameter for coronary heart disease risk assessment and as a target for therapy . Data from the Atorvastatin Comparative Cholesterol Efficacy and Safety Study ( ACCESS ) were used to assess the correlation between lipid and apolipoprotein B levels before and after lipid-lowering therapy and to examine the effects of 5 hydroxymethylglutaryl coenzyme A reductase inhibitors on lipids and apolipoprotein B. The 54-week study r and omized 3,916 hypercholesterolemic patients to atorvastatin , fluvastatin , lovastatin , pravastatin , or simvastatin , initiated at recommended starting doses with titrations as needed at weeks 6 , 12 , and 18 to achieve National Cholesterol Education Program LDL targets . Compared with LDL cholesterol , non-HDL cholesterol correlated better with apolipoprotein B levels at baseline ( r = 0.914 , p < 0.0001 ) and at week 54 ( r = 0.938 , p < 0.0001 ) , and the correlation was strong across all baseline triglyceride strata . At starting doses , atorvastatin ( 10 mg ) lowered non-HDL cholesterol by 33.3 % compared with 26.6 % with simvastatin ( 10 mg ) , 24.1 % with lovastatin ( 20 mg ) , 17.2 % with fluvastatin ( 20 mg ) , and 17.0 % with pravastatin ( 10 mg ) . Atorvastatin also provided greater reductions in non-HDL cholesterol after dose titration , and a greater percentage of patients taking atorvastatin achieved non-HDL cholesterol targets . Baseline triglyceride did not affect non-HDL cholesterol reductions with any of the 5 hydroxymethylglutaryl coenzyme A reductase inhibitors . Fewer patients achieved non-HDL cholesterol targets than LDL cholesterol targets , particularly among high-risk patients , implying that if non-HDL cholesterol was used as a target for treatment , more patients would need to be treated more aggressively than National Cholesterol Education Program guidelines require BACKGROUND : Lowering low-density lipoprotein cholesterol ( LDL-C ) with statins reduces atherosclerosis . LDL and high-density lipoprotein ( HDL ) are commonly measured by their cholesterol content , but non-HDL cholesterol , LDL particle number ( LDL-P ) , or total apolipoprotein B ( apoB ) may better predict cardiovascular risk . Few studies have examined relations among lipoprotein levels and composition before and after interventions to lower LDL-C and non-HDL-C. OBJECTIVE : To measure changes in carotid artery intimal media thickness ( CIMT ) and lipid concentration and composition during 36 months of statin therapy . METHODS : Analyses were conducted on 418 diabetic individuals , with complete data and no prior cardiovascular events , who were r and omized to aggressive ( AG ) versus st and ard ( STD ) treatment for LDL-C , non-HDL-C , and systolic blood pressure ( SBP ) as part of the Stop Atherosclerosis in Native Diabetics Study ( S AND S ) . RESULTS : The AG group achieved average LDL-C and non-HDL-C of 71mg/dL and 100mg/dL and a decrease in CIMT . No significant interactions were observed between treatment effect and initial levels of LDL-C , non-HDL-C , HDL-C , triglycerides , apoB , or LDL-P. Decreases in LDL-C ( p<.005 ) and non-HDL-C ( p<.001 ) were independently correlated with CIMT regression in the AG group . Changes in apoB and LDL-P showed borderline correlations with CIMT regression ( p=.07 and p=.09 ) . CONCLUSIONS : In diabetic adults with no prior cardiovascular events , treatment to current targets for lipids and SBP reduces atherosclerosis progression and when more aggressive targets are met , atherosclerosis regresses . The aggressive targets for LDL-C and non-HDL-C appeared to be the main determinants of CIMT regression and were more predictive of this outcome than changes in LDL-P or The role of hypertriglyceridemia in the pathogenesis of atherosclerotic cardiovascular disease has been controversial for many years [ 1 , 2 ] . It remains so despite extensive investigation by basic scientists , clinicians , and epidemiologists . The lack of resolution of this issue derives mainly from the complexity inherent in the lipoprotein transport system [ 3 ] . Although it is not possible to either unravel all of this complexity or resolve the controversy here , I attempt to provide a balanced review of the relevant literature , concluding with a suggested approach to the evaluation and treatment of the many patients who have elevated plasma triglyceride levels . I focus on the lipid aspects of this issue , but it should not be forgotten that elevated triglyceride levels have been associated with several abnormalities of the clotting-fibrinolytic systems [ 4 ] . Triglyceride does not accumulate in the vessel wall . Its atherogenicity must be based , therefore , on the association , within lipoproteins , between triglyceride and cholesterol , the lipid that does accumulate in atherosclerotic plaque . Thus , proponents of an association between hypertriglyceridemia and atherosclerotic cardiovascular disease must postulate that disordered metabolism of the triglyceride-rich lipoproteins-very low density lipoprotein ( VLDL ) or chylomicron or both-is proatherogenic . This concept is not extreme : Even the well-accepted link between cholesterol and atherosclerotic cardiovascular disease relies on the accumulation of low-density lipoprotein ( LDL ) cholesterol , not simply plasma cholesterol , in lesions . The concept that several lipoprotein species can contribute cholesterol to lesion formation is not , therefore , unreasonable . Indeed , ample studies have shown that chylomicron remnants ( the lipoprotein formed from chylomicrons after removal of much , but not all , of the chylomicron triglyceride ) and VLDL ( or its remnants ) enter the subendothelial space of the vessel wall [ 5 , 6 ] . These lipoproteins can also be internalized by monocyte macrophages , result ing in formation of foam cells . Recent studies in transgenic mice dramatically demonstrated the atherogenic potential of VLDL and chylomicron remnants , even when the mice were consuming normal chow diets [ 7 ] . If the delivery of cholesterol to the vessel wall by triglyceride-rich lipoproteins is , in fact , involved in the pathophysiology of atherosclerotic cardiovascular disease , epidemiologic data should show links between hypertriglyceridemia and this disease . When examining the role of triglyceride by univariate analyses , most prospect i ve cohort studies have shown a positive relation between triglyceride levels and risk [ 2 ] . In multivariate analyses , however , triglyceride has often been shown to no longer be significantly associated with risk . Important exceptions may be seen in women with hypertriglyceridemia and patients with diabetes . I focus here only on three potential confounders of this statistical approach : the inverse relation between plasma levels of triglyceride and high-density lipoprotein ( HDL ) cholesterol , the potential atherogenicity of postpr and ial hypertriglyceridemia , and the biochemical and physical heterogeneity of triglyceride-rich lipoproteins . High-density lipoprotein cholesterol is widely accepted as being protective against atherosclerotic cardiovascular disease [ 8 ] . The evidence has primarily been derived from prospect i ve cohort studies and from secondary analyses of intervention trials in which lowering LDL cholesterol levels was the primary goal . The leading theory invokes a role for HDL in the reverse cholesterol transport pathway , whereby cellular cholesterol can associate with HDL ; in turn , the latter delivers cellular cholesterol to the liver for excretion . In most population s , triglyceride and HDL cholesterol levels are inversely related . Thus , analyses of triglyceride as a risk factor that use HDL cholesterol as a covariate will be confounded by the lack of independence of the two variables ; both of these variables affect risk for atherosclerotic cardiovascular disease , but in opposite directions . Although recent studies in gene-knockout and transgenic mice support direct antiatherogenic roles for HDL [ 9 , 10 ] , the physiologic basis for the inverse relation between plasma levels of triglyceride and HDL cholesterol suggests that low HDL cholesterol levels may simply reflect proatherogenic disorders of triglyceride-rich lipoproteins . Increased levels of VLDL and chylomicrons stimulate the exchange of their triglyceride for cholesterol in HDL . Although this exchange , which is mediated in plasma by cholesteryl ester transfer protein [ 11 ] , may be an alternate pathway for reverse cholesterol transport ( with delivery of the cholesterol to the liver by VLDL and chylomicron remnants ) , movement of HDL cholesterol into triglyceride-rich lipoproteins could also result in the delivery of some cholesterol back to peripheral cells . Over time , such short-circuiting of the reverse cholesterol transport system could result in accumulation of cholesterol in tissues , including the arterial wall . Essentially all of the epidemiologic data linking lipids and lipoproteins to risk for atherosclerotic cardiovascular disease are based on fasting levels [ 2 ] . Plasma levels of triglycerides vary widely throughout the day , however , because we absorb many grams of dietary fat after each meal . In the past decade , evidence for the atherogenicity of postpr and ial triglyceride-rich lipoproteins has increased . Several recent studies have indicated that postpr and ial levels of triglyceride and chylomicron remnants are predictive of the presence of atherosclerotic cardiovascular disease even when other risk factors , including HDL cholesterol , are considered [ 12 , 13 ] . The role of triglyceride in atherogenesis might have been more readily demonstrated if epidemiologic studies had used nonfasting blood levels . Another important reason for the difficulty in linking triglyceride levels to risk for atherosclerotic cardiovascular disease is the physical and biochemical heterogeneity of VLDL and chylomicrons . In particular , the size , number , and cholesterol content of these lipoproteins can vary greatly among individual persons . Size is important because very large particles can not easily pass into the subendothelial space , the site of initiation of the atherogenic process . The number of triglyceride-rich particles in the bloodstream is also crucial , in part because the presence of more particles increases the probability that they will enter and be retained in the vessel wall , and in part because for any triglyceride level , more particles mean smaller , more atherogenic particles . Finally , the cholesterol content of the triglyceride-rich lipoproteins can vary significantly , and persons with more cholesterol-enriched particles will be at greater risk . Because of differences in the size , number , and cholesterol content of triglyceride-rich particles , patients with similar levels of plasma triglyceride may have very different risks for atherosclerotic cardiovascular disease . So what is the clinician to do with the not uncommon , middle-aged patient who has hypertriglyceridemia ? The National Cholesterol Education Program ( NCEP ) has not developed precise guidelines on which to base therapy [ 14 ] . Moreover , neither of the reports of two intervention trials gives a clearcut answer . The Helsinki Heart Study subgroup analysis [ 15 ] indicated that patients who had pure hypertriglyceridemia and were receiving  gemfibrozil had a risk reduction similar to that of patients with either pure hypercholesterolemia or combined hyperlipidemia ; however , the size of the subgroup was small . In the Stockholm Ischemic Heart Disease Study [ 16 ] , the reductions in the rate of coronary events seen in patients treated with clofibrate and niacin correlated with reductions in triglyceride levels , but neither HDL nor LDL cholesterol levels were measured . In the face of these suggestive but incomplete data , one approach would be to use the NCEP guidelines , particularly focusing on the presence of other risk factors commonly associated with hypertriglyceridemia ( hypertension , diabetes , low HDL cholesterol levels ) to guide the intensity of therapy focused on LDL cholesterol . Thus , if the patient is a man older than 45 years of age or a postmenopausal woman , it is likely that he or she will have two or more of the risk factors listed in the NCEP guidelines [ 14 ] and will require an LDL cholesterol level less than 130 mg/dL. If the patient has clinical atherosclerotic cardiovascular disease , an LDL cholesterol level less than 100 mg/dL would be the goal . When a patient with hypertriglyceridemia but not clinical atherosclerotic cardiovascular disease has an LDL cholesterol  less than 130 mg/dL , however , the NCEP guidelines do not provide clear direction for therapy , regardless of the number of additional risk factors . Here , the LDL : HDL ratio might be helpful ; both the Helsinki Study [ 17 ] and the Procam Study [ 18 ] indicated that patients with ratios exceeding 5.0 and triglyceride levels exceeding 200 mg/dL had markedly increased risk . It must be understood , however , that no data support the value of further lowering LDL cholesterol levels that are already less than 130 mg/dL in patients without clinical atherosclerotic cardiovascular disease . Measurement of apoprotein B levels ( when st and ardization programs are widely available ) might be of particular benefit in these patients [ 19 ] . Because of the multiple links between elevated triglyceride levels and risk for atherosclerotic cardiovascular disease , it seems prudent to screen for the presence of hypertriglyceridemia when determining a patient 's risk for atherosclerotic cardiovascular disease . A therapeutic program for hypertriglyceridemia should obviously include diet , exercise , and weight loss programs : These are even more important in patients with hypertriglyceridemia than in persons with The concentration of adiponectin , a hormone which is secreted from adipose tissue , is inversely correlated with body fat mass . This hormone has anti inflammatory and anti atherogenic properties . Its concentration reduces in metabolic syndrome and cardiovascular diseases . This study review s the evidence on the relationship between serum  adiponectin concentration and lipid profile .  In this study former clinical trials , cross sectional and prospect i ve studies have been review ed . The PubMed search engine has been used to find related research for the topic by considering dyslipidemia , total cholesterol ( TC ) , high and low density protein ( HDL and LDL ) , triglyceride ( TG ) , lipid profile ( LP ) and adiponectin as the key words . Finally , 25 articles were recruited to review in the present article . Serum adiponectin level was positively correlated with plasma HDL cholestrol concentrations . There was a significant inverse relationship between plasma triglyceride and serum adiponectin . An inverse correlation between very low density lipoprotein ( VLDL ) and LDL levels and adiponectin was reported from the studies . So , Adiponectin has an important role in the metabolism of lipid profile including HDLc Background Recent studies have demonstrated a relationship between fructose consumption and risk of developing metabolic syndrome . Mechanisms by which dietary fructose mediates metabolic changes are poorly understood . This study compared the effects of fructose , glucose and sucrose consumption on post-postpr and ial lipemia and low grade inflammation measured as hs-CRP . Methods This was a r and omized , single blinded , cross-over trial involving healthy subjects ( n = 14 ) . After an overnight fast , participants were given one of 3 different isocaloric drinks , containing 50 g of either fructose or glucose or sucrose dissolved in water .  Blood sample s were collected at baseline , 30 , 60 and 120 minutes post intervention for the analysis of blood lipids , glucose , insulin and high sensitivity C-reactive protein ( hs-CRP ) . Results Glucose and sucrose supplementation initially result ed in a significant increase in glucose and insulin levels compared to fructose supplementation and returned to near baseline values within 2 hours . Change in plasma cholesterol , LDL and HDL-cholesterol ( measured as area under curve , AUC ) was significantly higher when participants consumed fructose compared with glucose or sucrose ( P < 0.05 ) . AUC for plasma triglyceride levels however remained unchanged regardless of the dietary intervention . Change in AUC for hs-CRP was also significantly higher in subjects consuming fructose compared with those consuming glucose ( P < 0.05 ) , but not sucrose ( P = 0.07 ) . Conclusion This study demonstrates that fructose as a sole source of energy modulates plasma lipids and hsCRP levels in healthy individuals . The significance of increase in HDL-cholesterol with a concurrent increase in LDL-cholesterol and elevated hs-CRP levels remains to be delineated when considering health effects of feeding fructose-rich diets . Registration number for clinical BACKGROUND National Cholesterol Education Program Adult Treatment Panel III guidelines for patients at a high risk of coronary heart disease set a low-density lipoprotein cholesterol ( LDL-C ) target of < 100 mg/dL. This target can be difficult to attain with diet and current therapy . METHODS In a 16-week multinational trial , 1993 high-risk patients were r and omized to rosuvastatin 20 mg , atorvastatin 10 mg , atorvastatin 20 mg , simvastatin 20 mg , or simvastatin 40 mg for 8 weeks . Patients either remained on starting treatment or switched to lower or milligram-equivalent doses of rosuvastatin for 8 more weeks . RESULTS At 16 weeks , more patients achieved their LDL-C target by switching to rosuvastatin 10 mg than staying on atorvastatin 10 mg ( 66 % vs 42 % , P < .001 ) or simvastatin 20 mg ( 73 % vs 32 % , P < .001 ) . Changing to rosuvastatin 20 mg brought more patients to their LDL-C target than staying on atorvastatin 20 mg ( 79 % vs 64 % , P < .001 ) or simvastatin 40 mg ( 84 % vs 56 % , P < .001 ) . More very high risk patients achieved an LDL-C target of < 70 mg/dL when changed to rosuvastatin from atorvastatin or simvastatin ( within-arm comparisons P < .01 ) . More hypertriglyceridemic patients ( triglycerides > or = 200 mg/dL ) met LDL-C , non-high-density lipoprotein cholesterol ( non-HDL-C ) , and apolipoprotein B targets by changing to rosuvastatin . Switching to rosuvastatin produced greater reductions in LDL-C , total cholesterol , non-HDL-C , apolipoprotein B , and lipid ratios . All treatments were well tolerated , with no differences among treatment groups in skeletal muscle , hepatic , or renal toxicity . CONCLUSION Rosuvastatin 10 or 20 mg is an effective and safe therapeutic option for high-risk patients to achieve their lipid and apolipoprotein targets Since the last publication of the recommendations for the management and treatment of dyslipidemia , new clinical trial data have emerged that support a more vigorous approach to lipid lowering in specific patient groups . The decision was made to up date the lipid guidelines in collaboration with the Canadian Cardiovascular Society . A systematic electronic search of medical literature for original research consisting of blinded , r and omized controlled trials was performed . Meta-analyses of studies of the efficacy and safety of lipid-lowering therapies , and of the predictive value of established and emerging risk factors were also review ed . All recommendations are evidence -based , and have been review ed in detail by primary and secondary review panels . Major changes include a lower low-density lipoprotein cholesterol ( LDL-C ) treatment target ( lower than 2.0 mmol/L ) for high-risk patients , a slightly higher intervention point for the initiation of drug therapy in most low-risk individuals ( LDL-C of 5.0 mmol/L or a total cholesterol to high-density lipoprotein cholesterol ratio of 6.0 ) and recommendations regarding additional investigations of potential use in the further evaluation of coronary artery disease risk in subjects in the moderate-risk category OBJECTIVE To investigate whether the risk profile of coronary heart disease ( CHD ) is more favorable in physically active men with tetraplegia compared with sedentary men with tetraplegia . DESIGN Using a cross-sectional design , the lipid and (apo)lipoprotein concentrations of 11 active and 13 sedentary men with tetraplegia were compared . Regression analysis was applied to investigate the influence of subject characteristics and behavioral factors on the risk profile of CHD . MAIN OUTCOME MEASURES Total plasma cholesterol ( TC ) , high-density lipoprotein cholesterol ( HDL-C ) , triglycerides , apolipoprotein-A1 ( ApoA1 ) , and apolipoprotein-B ( ApoB ) concentrations were determined . Low-density lipoprotein cholesterol ( LDL-C ) and the ratios TC/HDL-C , LDL-C/HDL-C , ApoA1/ApoB , and HDL-C/ApoA1 were calculated . RESULTS A significantly higher HDL-C and ApoA1/ApoB and lower TC/HDL-C were found in the active group . Age and body mass index were important determinants of the lipids and (apo)lipoproteins .  Sport activity was the only significant determinant of HDL-C. CONCLUSIONS Results suggest a positive influence of sport activity on HDL-C in men with tetraplegia , which may reduce the risk of CHD BACKGROUND Improving lipids beyond low-density lipoprotein cholesterol ( LDL-C ) lowering with statin monotherapy may further reduce cardiovascular risk . Niacin has complementary lipid-modifying efficacy to statins and cardiovascular benefit , but is underutilised because of flushing , mediated primarily by prostagl and in D(2 ) ( PGD(2 ) ) . Laropiprant ( LRPT ) , a PGD(2 ) receptor ( DP1 ) antagonist that reduces niacin-induced flushing has been combined with extended-release niacin ( ERN ) into a fixed-dose tablet . METHODS AND RESULTS Dyslipidaemic patients were r and omised to ERN/LRPT 1 g ( n = 800 ) , ERN 1 g ( n = 543 ) or placebo ( n = 270 ) for 4 weeks . Doses were doubled ( 2 tablets/day ; i.e. 2 g for active treatments ) for 20 weeks . ERN/LRPT 2 g produced significant changes vs. placebo in LDL-C ( -18.4 % ) , high-density lipoprotein cholesterol ( HDL-C ; 20.0 % ) , LDL-C : HDL-C ( -31.2 % ) , non-HDL-C ( -19.8 % ) , triglycerides ( TG ; -25.8 % ) , apolipoprotein ( Apo ) B ( -18.8 % ) , Apo A-I ( 6.9 % ) , total cholesterol ( TC ; -8.5 % ) , TC : HDL-C ( -23.1 % ) and lipoprotein(a ) ( -20.8 % ) across weeks 12 - 24 . ERN/LRPT produced significantly less flushing than ERN during initiation ( week 1 ) and maintenance ( weeks 2 - 24 ) for all prespecified flushing end-points ( incidence , intensity and discontinuation because of flushing ) . Except for flushing , ERN/LRPT had a safety/tolerability profile comparable with ERN . CONCLUSION Extended-release niacin/LRPT 2 g produced significant , durable improvements in multiple lipid/lipoprotein parameters . The improved tolerability of ERN/LRPT supports a simplified 1 g-->2 g dosing regimen of niacin , a therapy proven to reduce cardiovascular risk OBJECTIVES This study was design ed to test the hypothesis that at any low-density lipoprotein cholesterol ( LDL-C ) level , other lipid parameters such as non-high-density lipoprotein cholesterol ( HDL-C ) levels , triglyceride ( TG ) levels , and the total cholesterol (TC)/HDL-C are still associated with an increased coronary heart disease ( CHD ) risk . BACKGROUND Although LDL-C is considered to be the primary target of lipid-lowering therapy , other parameters of the lipoprotein-lipid profile may more closely associated with CHD risk . METHODS In the EPIC ( European Prospect i ve Investigation Into Cancer and Nutrition)-Norfolk prospect i ve population study , 21,448 participants without diabetes or CHD between age 45 and 79 years were followed for 11.0 years . A total of 2,086 participants developed CHD during follow-up . RESULTS Among individuals with low LDL-C levels ( < 100 mg/dl ) , after adjustment for age , sex , smoking , systolic blood pressure , waist circumference , physical activity , and hormone replacement therapy ( in women ) , those with non-HDL-C > 130 mg/dl had a hazard ratio ( HR ) for future CHD of 1.84 ( 95 % confidence interval [ CI ] : 1.12 to 3.04 ) when compared with those with non-HDL-C levels < 130 mg/dl . In a similar model , individuals with TG levels > 150 mg/dl had an HR of 1.63 ( 95 % CI : 1.02 to 2.59 ) when compared with those with TG levels < 150 mg/dl , and individuals with a TC/HDL-C ratio > 5 had an HR of 2.19 ( 95 % CI : 1.22 to 3.93 ) when compared with those with a TC/HDL-C ratio < 5 . CONCLUSIONS In this prospect i ve study , independently of their plasma LDL-C levels , participants with high non-HDL-C levels , high TG levels , or with an elevated TC/HDL-C ratio were at increased CHD risk . CHD risk assessment algorithms as well as lipid targets of lipid-lowering trials may also need to consider other easily available parameters such as CONTEXT Epidemiological studies have established a relationship between cholesterol and low-density lipoprotein cholesterol ( LDL-C ) concentrations and the risk of ischemic heart disease ( IHD ) , but up to half of patients with IHD may have cholesterol levels in the normal range . OBJECTIVE To assess the ability to predict the risk of IHD using a cluster of nontraditional metabolic risk factors that includes elevated fasting insulin and apolipoprotein B levels as well as small , dense LDL particles . DESIGN Nested case-control study . SETTING Cases and controls were identified from the population -based cohort of the Quebec Cardiovascular Study , a prospect i ve study conducted in men free of IHD in 1985 and followed up for 5 years . PARTICIPANTS Incident IHD cases were matched with controls selected from among the sample of men who remained IHD free during follow-up . Matching variables were age , smoking habits , body mass index , and alcohol consumption . The sample included 85 complete pairs of nondiabetic IHD cases and controls . MAIN OUTCOME MEASURES Ability of fasting insulin level , apolipoprotein B level , and LDL particle diameter to predict IHD events , defined as angina , coronary insufficiency , nonfatal myocardial infa rct ion , and coronary death . RESULTS The risk of IHD was significantly increased in men who had elevated fasting plasma insulin and apolipoprotein B levels and small , dense LDL particles , compared with men who had normal levels for 2 of these 3 risk factors ( odds ratio [ OR ] , 5.9 ; 95 % confidence interval [ CI ] , 2.3 - 15.4 ) . Multivariate adjustment for LDL-C , triglycerides , and high-density lipoprotein cholesterol ( HDL-C ) did not attenuate the relationship between the cluster of nontraditional risk factors and IHD ( OR , 5.2 ; 95 % CI , 1.7 - 15.7 ) . On the other h and , the risk of IHD in men having a combination of elevated LDL-C and triglyceride levels and reduced HDL-C levels was no longer significant ( OR , 1.4 ; 95 % CI , 0.5 - 3.5 ) after multivariate adjustment for fasting plasma insulin level , apolipoprotein B level , and LDL particle size . CONCLUSION Results from this prospect i ve study suggest that the measurement of fasting plasma insulin level , apolipoprotein B level , and LDL particle size may provide further information on the risk of IHD compared with the information provided by conventional lipid variables
Fructose had no effect on LDL-C , non-HDL-C , apolipoprotein B , triglycerides , or HDL-C in isocaloric trials .
Conclusions Pooled analyses showed that fructose only had an adverse effect on established lipid targets when added to existing diets so as to provide excess calories ( + 21 % to 35 % energy ) .
When isocalorically exchanged for other carbohydrates , fructose had no adverse effects on blood lipids .
Background Debate over the role of fructose in mediating  cardiovascular  risk remains active .
To up date the evidence on the effect of fructose on established therapeutic lipid targets for cardiovascular disease ( low-density lipoprotein cholesterol [LDL]-C , apolipoprotein B , non-high-density lipoprotein cholesterol [ HDL-C ] ) , and metabolic syndrome ( triglycerides and HDL-C ) , we conducted a systematic review and meta- analysis of controlled feeding trials .