Low-density Lipoprotein Cholesterol Subfractions Research Articles

CYP2C19 metabolizer phenotypes may affect the efficacy of statins on lowering small dense low-density lipoprotein cholesterol of patients with coronary artery disease.

Dyslipidemia is a major cause of arteriosclerotic cardiovascular disease (ASCVD), and low-density lipoprotein cholesterol (LDL-C) is the profile to be reduced to prevent disease progression. Small dense low-density lipoprotein cholesterol (sdLDL-C) has been proven to be a more effective biomarker than LDL-C for ASCVD primary and secondary prevention. CYP2C19 is an important drug metabolism gene. This study aimed to investigate the relationship between sdLDL-C and coronary artery disease (CAD) risk factors and explore the influence of CYP2C19 metabolizer phenotypes on the sdLDL-C lowering efficacy of statins. This study recruited 182 patients with CAD and 200 non-CAD controls. Baseline laboratory indices of fasting blood were detected, including blood lipids, glucose, and creatinine. In addition, LDL-C subfractions were separated and quantified. Gene polymorphisms of SLCO1B1 and CYP2C19 were detected in patients with CAD. The LDL-C subfractions levels of patients with CAD were followed up after statin drug treatment. Total cholesterol, LDL-C, LDLC-2, LDLC-3, LDLC-4, LDLC-5, LDLC-6, LDLC-7, and sdLDL-C levels of patients with CAD were significantly higher than those in non-CAD controls. Meanwhile, sdLDL-C (AUC = 0.838) and LDLC-4 (AUC = 0.835) performed outstandingly in distinguishing patients with CAD from controls. Based on CYP2C19 metabolizer phenotypes, 113 patients with CAD were divided into the extensive metabolizer (EM, n = 49), intermediate metabolizer (IM, n = 52), and poor metabolizer (PM, n = 12) groups. The patients with IM and PM metabolizer phenotypes had better sdLDL-C lowering efficacy after taking statin drugs than patients with EM phenotype (P = 0.0268, FDR = 0.0536). The SLCO1B1 genotype had no significant impact on the efficacy of statins (P = 0.1611, FDR = 0.1611). sdLDL-C and LDLC-4 outperformed other blood lipids such as LDL-C for CAD risk screening. CYP2C19 metabolizer phenotypes had the potential to predict the efficacy of statins in lowering sdLDL-C.

A Ketogenic Low-Carbohydrate High-Fat Diet Increases LDL Cholesterol in Healthy, Young, Normal-Weight Women: A Randomized Controlled Feeding Trial.

Ketogenic low-carbohydrate high-fat (LCHF) diets are popular among young, healthy, normal-weight individuals for various reasons. We aimed to investigate the effect of a ketogenic LCHF diet on low-density lipoprotein (LDL) cholesterol (primary outcome), LDL cholesterol subfractions and conventional cardiovascular risk factors in the blood of healthy, young, and normal-weight women. The study was a randomized, controlled, feeding trial with crossover design. Twenty-four women were assigned to a 4 week ketogenic LCHF diet (4% carbohydrates; 77% fat; 19% protein) followed by a 4 week National Food Agency recommended control diet (44% carbohydrates; 33% fat; 19% protein), or the reverse sequence due to the crossover design. Treatment periods were separated by a 15 week washout period. Seventeen women completed the study and treatment effects were evaluated using mixed models. The LCHF diet increased LDL cholesterol in every woman with a treatment effect of 1.82 mM (p < 0.001). In addition, Apolipoprotein B-100 (ApoB), small, dense LDL cholesterol as well as large, buoyant LDL cholesterol increased (p < 0.001, p < 0.01, and p < 0.001, respectively). The data suggest that feeding healthy, young, normal-weight women a ketogenic LCHF diet induces a deleterious blood lipid profile. The elevated LDL cholesterol should be a cause for concern in young, healthy, normal-weight women following this kind of LCHF diet.

Effects of RG7652, a Monoclonal Antibody Against PCSK9, on LDL-C, LDL-C Subfractions, and Inflammatory Biomarkers in Patients at High Risk of or With Established Coronary Heart Disease (from the Phase 2 EQUATOR Study)

RG7652 (MPSK3169A), a fully human immunoglobulin G1 (IgG1) monoclonal antibody directed against proprotein convertase subtilisin/kexin type 9 (PCSK9), blocks the interaction between PCSK9 and low-density lipoprotein (LDL) receptor. EQUATOR (ClinicalTrials.govNCT01609140), a randomized, double-blind, and dose-ranging phase 2 study, evaluated RG7652 in patients (1) at high risk for or (2) with coronary heart disease (CHD). The primary end point was change in LDL cholesterol (LDL-C) from baseline to day 169. Patients (n= 248; median age, 64years; 57% men; 52% with established CHD; 82% on statins) with baseline LDL-C levels of 90 to 250mg/dl (mean, 126mg/dl) continuing on standard-of-care therapy were randomized to receive 1 of 5 RG7652 doses or placebo, subcutaneously every 4, 8, or 12weeks for 24weeks. Significant dose-dependent reductions in LDL-C levels from baseline to nadir (56 to 74mg/dl [48% to 60%]) were observed in all RG7652-dosed patients; effects persisted to day 169 with the highest doses (reduction vs placebo up to 62mg/dl [51%]) with no unexpected safety signals. RG7652 reduced apolipoprotein B and lipoprotein(a) levels. LDL-C subfraction analysis by nuclear magnetic resonance spectroscopy revealed a prominent decrease in large LDL-C and some decrease in small LDL particles. There was significant reduction in mean particle size of LDL-C on day 169 but no significant reductions in systemic markers of inflammation (high-sensitivity C-reactive protein, interleukin-6, and tumor necrosis factor-alpha). RG7652 reduced LDL-C levels and was well tolerated in patients at high risk for or with CHD on standard-of-care therapy. In conclusion, RG7562 treatment affected large LDL-C and, to a lesser extent, small LDL-C particles; RG7562 did not affect systemic circulating pro-inflammatory cytokines or high-sensitivity C-reactive protein.

Pitavastatin 4 mg Provides Significantly Greater Reduction in Remnant Lipoprotein Cholesterol Compared With Pravastatin 40 mg: Results from the Short-term Phase IV PREVAIL US Trial in Patients With Primary Hyperlipidemia or Mixed Dyslipidemia

PurposeRemnants are partially hydrolyzed, triglyceride-rich lipoproteins that are implicated in atherosclerosis. We assessed the adequacy of pitavastatin 4 mg and pravastatin 40 mg in reducing atherogenic lipid parameters beyond LDL-C, in particular remnant lipoprotein cholesterol (RLP-C). MethodsFrom the Phase IV, multicenter, randomized, double-blind PREVAIL US (A Study of Pitavastatin 4 mg Vs. Pravastatin 40 mg in Patients With Primary Hyperlipidemia or Mixed Dyslipidemia) trial, we examined lipoprotein cholesterol subfractions using Vertical Auto Profile testing and apolipoproteins B and A-I at baseline and 12 weeks. Participants with primary hyperlipidemia or mixed dyslipidemia had LDL-C levels of 130 to 220 mg/dL and triglyceride levels ≤400 mg/dL. In this post hoc analysis, changes in lipid parameters were compared by using ANCOVA. FindingsLipoprotein subfraction data were available in 312 patients (pitavastatin, n = 157; pravastatin, n = 155). Pitavastatin promoted a greater reduction in RLP-C than pravastatin (–13.6 [8.7] vs –9.3 [9.5] mg/dL). Furthermore, the pitavastatin group reported greater reductions in both components of RLP-C (both, P < 0.001): intermediate-density lipoprotein cholesterol (–9.5 [6.3] vs –6.4 [6.6] mg/dL) and very low-density lipoprotein cholesterol subfraction 3 (–4.1 [3.5] vs –2.9 [3.8] mg/dL). There were also greater reductions in the major ratios of risk (apolipoprotein B/apolipoprotein A-I and total cholesterol/HDL-C) (both, P < 0.001). There were no significant changes in HDL-C, its subfractions, or natural log lipoprotein(a)-cholesterol. The mean age was 58.8 ± 8.9 years in the pitavastatin group and 57.0 ± 10.2 years in the pravastatin group. ImplicationsCompared with pravastatin 40 mg daily, pitavastatin 4 mg provided superior reductions in atherogenic lipid parameters beyond LDL-C, including RLP-C. Future studies are needed investigate the clinical implications of lowering directly measured RLP-C as the principal target. ClinicalTrials.gov identifier: NCT01256476.

Relationship of the triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio to the remainder of the lipid profile: The Very Large Database of Lipids-4 (VLDL-4) study.

High levels of the triglycerides to high-density lipoprotein cholesterol (TG/HDL-C) ratio are associated with obesity, metabolic syndrome, and insulin resistance. We evaluated variability in the remaining lipid profile, especially remnant lipoprotein particle cholesterol (RLP-C) and its components (very low-density lipoprotein cholesterol subfraction 3 and intermediate-density lipoprotein cholesterol), with variability in the TG/HDL-C ratio in a very large study cohort representative of the general U.S. We examined data from 1,350,908 US individuals who were clinically referred for lipoprotein cholesterol ultracentrifugation (Atherotech, Birmingham, AL) from 2009 to 2011. Demographic information other than age and sex was not available. Changes to the remaining lipid profile across percentiles of the TG/HDL-C ratio were quantified, as well as by three TG/HDL-C cut-off points previously proposed in the literature: 2.5 (male) and 2 (female), 3.75 (male) and 3 (female), and 3.5 (male and female). The mean age of our study population was 58.7 years, and 48% were men. The median TG/HDL-C ratio was 2.2. Across increasing TG/HDL-C ratios, we found steadily increasing levels of RLP-C, non-HDL-C and LDL density. Among the lipid parameters studied, RLP-C and LDL density had the highest relative increase when comparing individuals with elevated TG/HDL-C levels to those with lower TG/HDL-C levels using established cut-off points. Approximately 47% of TG/HDL-C ratio variance was attributable to RLP-C. In the present analysis, a higher TG/HDL-C ratio was associated with an increasingly atherogenic lipid phenotype, characterized by higher RLP-C along with higher non-HDL-C and LDL density.

The effects of atorvastatin treatment on the mean platelet volume and red cell distribution width in patients with dyslipoproteinemia and comparison with plasma atherogenicity indicators—A pilot study

ObjectivesThe mean platelet volume (MPV) and red cell distribution width (RDW) have recently arisen interest because of their association with an increased cardiovascular risk. The aim of our study was, therefore, to determine whether an association exists between MPV, RDW and lipoprotein sub-fractions, and to show the impact of statin therapy on these new possible biomarkers of atherosclerotic risk. Design and methodsA cohort of 40 patients with hypercholesterolaemia (29 females, mean age 62.9±9years), without previous hypolipidaemic treatment were enrolled. The patients were treated with atorvastatin 40mg/day for 12weeks. Total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density cholesterol (HDL-C), triglycerides (TG), LDL-C sub-fractions [large LDL-C 1–2 and small dense (sd)-LDL-C 3–7], apolipoproteins (apoA1, apoB), apoB/apoA1 ratio, atherogenic index of plasma (AIP), haematological parameters (including MPV, RDW) and safety parameters (renal, hepatic) were measured before and after 12weeks of atorvastatin treatment. ResultsAt baseline, a strong correlation between HDL-C, TG, sd-LDL-C, apoB, apoB/apoA1, and AIP with MPV (r=−0.55, p<0.001; r=0.57, p<0.001; r=0.73, p<0.001; r=0.41, p<0.05; r=0.52, p<0.001; r=0.61, p<0.001, respectively) and RDW (r=−0.49, p<0.001; r=0.62, p<0.001; r=0.67, p<0.001; r=0.41, p<0.05; r=0.43, p<0.05; r=0.65, p<0.001, respectively) was found. After 12weeks of treatment with atorvastatin, MPV and RDW values underwent significant modification only in those patients displaying the strongest lipid-lowering effect. ConclusionsValues of MPV and RDW seem to reflect a pro-atherogenic lipoprotein profile mainly represented by the presence of sd-LDL-C.

Letter by Kuller and Mackey Regarding Article, “Lipids and Lipoproteins and Risk of Different Vascular Events in the MRC/BHF Heart Protection Study”

To the Editor: The results of the Heart Protection Study (HPS) comparing detailed lipoproteins versus low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C),1 and a subsequent editorial by Ockene,2 raise an important question about the value of measuring lipoprotein subfractions to predict risk of coronary heart disease (CHD) and therapeutic decisions. In the past, many believed that measuring the LDL-C subfraction was unnecessary because it was highly correlated with total cholesterol, a robust predictor of CHD events in the population. LDL-C replaced total cholesterol because total cholesterol was less closely associated with risk (1) for women with high HDL-C levels but not elevated LDL-C and (2) for individuals …

Association of CETP and LIPC Gene Polymorphisms with HDL and LDL Sub-fraction Levels in a Group of Indian Subjects: A Cross-Sectional Study

There is an increasing interest to understand the molecular basis of high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) subfractions and their association with coronary artery disease (CAD). The formation of these subfractions is greatly influenced by hepatic lipase (HL) and cholesteryl ester transfer protein (CETP) enzymes. To identify genetic markers influencing LDL and HDL subfractions and their role in CAD we performed a case-control genetic association study on 117 healthy controls and 119 angiographically verified CAD patients. Biochemical analysis was performed using standard assays. HDL-C and LDL-C subfractions were estimated using precipitation methods. Genotyping of C-514T (rs1800588) in the LIPC gene for HL and I405V (rs5882) in the CETP gene was done using PCR-based restriction enzyme analysis and sequencing. Both the polymorphisms were not associated with CAD. The C-514T was associated with increased HDL3-C levels in controls (P=0.049). The I405V polymorphism was found to be associated with low levels of small dense, LDL (P=0.038). A multiple regression analysis showed that the effects were dependent on gender and triglyceride levels. We conclude that these polymorphisms are not associated with CAD but are important determinants of HDL-C and small dense LDL particles in our population.

Effect of Ezetimibe/Atorvastatin Combination on Oxidized Low Density Lipoprotein Cholesterol in Patients With Coronary Artery Disease or Coronary Artery Disease Equivalent

Ezetimibe is effective in providing additional low-density lipoprotein (LDL) cholesterol lowering when coadministered with statins, but its effect beyond LDL cholesterol lowering is unknown. Oxidized LDL (ox-LDL) is a better predictor of adverse cardiovascular events than standard lipid parameters. The objective of this study was to investigate the effect of ezetimibe on ox-LDL. A total of 100 patients with coronary artery disease or coronary artery disease equivalent were randomized to atorvastatin 40 mg/day and ezetimibe 10 mg/day or to atorvastatin 40 mg/day and placebo. LDL cholesterol, LDL cholesterol subfractions, and ox-LDL were measured at baseline and after 8 weeks of therapy. The ezetimibe group had a larger reduction in total LDL cholesterol compared to placebo. This was due mainly to a larger reduction in large buoyant LDL (24% vs 10%, p = 0.008). Ox-LDL level did not change in the placebo group (50 +/- 13 vs 51 +/- 13 U/L), while it decreased in the ezetimibe group, from 51 +/- 13 to 46 +/- 10 U/L (p = 0.01 vs baseline and p = 0.02 vs final level in placebo). The change in ox-LDL correlated significantly with those in total LDL and in large buoyant LDL (r = 0.6 and r = 0.5, respectively, p <0.01 for both), but not with that of small dense LDL, high-density lipoprotein, or very low density lipoprotein. In conclusion, this study demonstrates that ezetimibe decreases ox-LDL cholesterol through reductions in total LDL cholesterol and in large buoyant LDL cholesterol.

Lipoprotein Subfraction Changes after Continuous or Intermittent Exercise Training

This study compared total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) and their respective subfractions after completing 4 wk of either intermittent (INT-EX) or continuous (CON-EX) aerobic exercise training (TRAIN). Untrained males (N = 7) and females (N = 11) completed 4 wk of TRAIN of supervised treadmill jogging occurring 5 d.wk(-1) for 30 min per session at 60% VO2max (75% HRmax). CON-EX was a single 30-min bout. INT-EX consisted of three 10-min bouts separated by 20 min of seated rest. Pre- and post-TRAIN fasting plasma samples were collected after subjects had followed 48 h of activity restriction and a 24-h repeated diet including a 12-h dietary fast. Postprandial lipemia was measured for 8 h following a standardized high-fat meal. Fasting triglycerides and very LDL-C were not affected by TRAIN, and TRAIN did not change postprandial area under the curve or peak in either group. With groups combined, TRAIN significantly decreased TC, total LDL-C, and the TC:HDL ratio, and increased HDL-C subfraction 2 and LDL mean particle size. Total intermediate-density lipoprotein cholesterol remained unchanged at post-TRAIN, and was not different between groups. To prevent dyslipidemia, our findings suggest that persons who are normolipidemic can improve the lipoprotein profile equally with CON-EX and INT-EX by lowered TC through the sum of changes in LDL-C subfractions, increased mean LDL particle size, and increased HDL-C subfraction 2 concentration.

Effects of omega-3 fatty acid supplementation and exercise on low-density lipoprotein and high-density lipoprotein subfractions*1

<h2>Abstract</h2> The purpose of this study was to examine the effect of combining exercise with omega-3 fatty acids (n-3fa) supplementation on lipoprotein subfractions and associated enzymes. Subjects were 10 recreationally active males, aged 25 ± 1.5 years (mean ± SE), who supplemented n-3fa (60% eicosapentaenoic acid [EPA] and 40% docosahexaenoic [DHA]) at 4 g/d for 4 weeks. Before and after supplementation, subjects completed a 60-minute session of treadmill exercise at 60% Vo₂max. Following a 24-hour diet and activity control period, blood was collected immediately before and after the exercise session to assess lipid variables: high-density lipoprotein cholesterol (HDL-C) and subfractions, low-density lipoprotein cholesterol (LDL-C) and subfractions and particle size, lecithin:cholesterol acyltransferase (LCAT) activity, and cholesterol ester transfer protein (CETP) activity. Supplementation with n-3fa alone increased total HDL-C and HDL₂-C, while exercise alone increased total HDL-C, HDL₃-C, and total LDL-C. LDL subfractions, particle size, and LCAT and CETP activities were not affected by supplementation. Combination treatment resulted in an additive effect for HDL₃-C only and also increased LDL₁-C versus baseline. LCAT and CETP activities were not affected by treatments. These results suggest that n-3fa supplementation or an exercise session each affect total HDL-C and subfractions but not LDL-C or subfractions. In addition, the combination of n-3fa and exercise may have additional effects on total HDL-C and LDL-C subfractions as compared to either treatment alone in active young men.

Effects of omega-3 fatty acid supplementation and exercise on low-density lipoprotein and high-density lipoprotein subfractions

The purpose of this study was to examine the effect of combining exercise with omega-3 fatty acids (n-3fa) supplementation on lipoprotein subfractions and associated enzymes. Subjects were 10 recreationally active males, aged 25 ± 1.5 years (mean ± SE), who supplemented n-3fa (60% eicosapentaenoic acid [EPA] and 40% docosahexaenoic [DHA]) at 4 g/d for 4 weeks. Before and after supplementation, subjects completed a 60-minute session of treadmill exercise at 60% V o 2max. Following a 24-hour diet and activity control period, blood was collected immediately before and after the exercise session to assess lipid variables: high-density lipoprotein cholesterol (HDL-C) and subfractions, low-density lipoprotein cholesterol (LDL-C) and subfractions and particle size, lecithin:cholesterol acyltransferase (LCAT) activity, and cholesterol ester transfer protein (CETP) activity. Supplementation with n-3fa alone increased total HDL-C and HDL 2-C, while exercise alone increased total HDL-C, HDL 3-C, and total LDL-C. LDL subfractions, particle size, and LCAT and CETP activities were not affected by supplementation. Combination treatment resulted in an additive effect for HDL 3-C only and also increased LDL 1-C versus baseline. LCAT and CETP activities were not affected by treatments. These results suggest that n-3fa supplementation or an exercise session each affect total HDL-C and subfractions but not LDL-C or subfractions. In addition, the combination of n-3fa and exercise may have additional effects on total HDL-C and LDL-C subfractions as compared to either treatment alone in active young men.

Dyslipidemia in Type 2 Diabetes and the Effects of Thiazolidinediones

Type 2 diabetes is frequently accompanied by multiple metabolic abnormalities, including dyslipidemia. The dyslipidemia characteristic of type 2 diabetes involves increased plasma triglyceride levels, decreased high-density lipoprotein cholesterol concentrations and pro-atherogenic changes in low-density lipoprotein cholesterol subfractions. The association between type 2 diabetes and dyslipidemia represents 1 feature of the insulin resistance syndrome in which impaired insulin sensitivity underlies a clustering of cardiovascular risk factors, including vascular inflammation, endothelial dysfunction and hypertension, as well as dyslipidemia. Effective management of type 2 diabetes requires treatment not only to reduce blood glucose levels, but also to normalize the full range of metabolic abnormalities within the insulin resistance syndrome. Thus, the selection of appropriate antidiabetic therapy should be based not only on glucose-lowering activity, but also on effects across the range of cardiovascular risk factors in type 2 diabetes. The thiazolidinediones are the only antidiabetic agents to target insulin resistance directly and have beneficial effects on many components of the insulin resistance syndrome, including dyslipidemia and hypertension. Consequently, they can have benefits in reducing the burden of cardiovascular morbidity and mortality in patients with type 2 diabetes.

Treatment of Dyslipidaemias in Patients with Established Vascular Disease: A Revival of the Fibrates

SummaryThe key ‘statin trials’ focussed on the beneficial effect of lowering the circulating concentrations of low-density lipoprotein cholesterol (LDL). However, epidemiological surveys, mainly based on healthy populations, indicate that other lipid-related variables, such as high-density cholesterol (HDL), triglycerides (TG), dense LDL subfraction distribution, and possibly lipoprotein (a) (Lp(a)), are also predictors of vascular events. Furthermore, TG and HDL levels influenced outcome within some of the statin trials. Plasma fibrinogen levels have also been shown to be powerful predictors of vascular risk in healthy subjects and patients with established ischaemic heart disease. The fibrates exert beneficial effects on all these variables that predict vascular events.The results from recent trials, the Bezafibrate Infarction Prevention (BIP) study and the Veterans Administration HDL Intervention Trial (VA-HIT) have revived our interest in fibrates. These trials involved bezafibrate and gemfibrozil that have a relatively poor LDL-lowering capacity. Therefore, the benefits reported in BIP and VA-HIT must be attributed to actions on variables other than a reduction in LDL quantity.Ciprofibrate and fenofibrate have significantly greater LDL-lowering capacity than bezafibrate or gemfibrozil. This advantage may render them more effective, especially since they retain the additional beneficial actions associated with this class of lipidlowering drugs.

An audit of lipid screening and management in patients undergoing diagnostic cardiac catheterization. Brompton House Officer Audit Group.

The aim of this study was to audit the management of hyperlipidaemia in a cohort of 206 consecutive patients, with known or suspected coronary artery disease, referred for diagnostic coronary angiography. The association of lipid subfraction values with the presence and extent of coronary artery disease was explored to identify the indices of greatest potential value to the hospital cardiologist, in the management of secondary prevention. Patients were questioned about previous lipid tests performed, advice received and treatment prescribed. Referral letters and hospital notes were reviewed to identify documentation of lipid results and treatment strategies. De novo fasting lipid estimations were obtained on 205 subjects at the time of catheterization. In only 46/206 (22%) cases was some form of lipid result recorded in the existing hospital notes or referral documentation. No patient was aware of the levels of the high or low density lipoprotein cholesterol subfractions (HDL, LDL) nor were these specifically recorded, or the subject of clinical comment, in any of the referral documentation. Patients who knew their total cholesterol (in mmol.1-1) result either as a value or as a "high' or "normal' categorization proved accurate witnesses. In keeping with other angiographic studies, we found that low values of HDL and high TC/HDL ratios were significantly associated with both disease presence and extent. Total cholesterol, calculated LDL and triglyceride levels had no such association. In the group as a whole and despite current therapy, 169/206 (82%) patients had a total cholesterol > 5.2 and 163/206 (79%) a TC/HDL ratio > 5. Only 22 (11%) patients were on drug therapy with a further 43 (21%) practising dietary modification. In the vast majority of subjects receiving some form of lipid intervention, target lipid levels had not been achieved. This study identifies the need for more intensive management of hyperlipidaemia in patients with coronary artery disease. Knowledge of HDL levels may be of value in guiding lipid secondary prevention management in the patient population evaluated at an angiographic centre.