Apolipoproteins versus lipids as indices of coronary risk and as targets for statin treatment

Ad, Sniderman; Furberg, C.D.; Keech, A; Lennep, Jeanine E. Roeters van; Fröhlich, Jiří; Jungner, Ingmar; Walldius, G; Wagner, Anne

doi:10.1016/s0214-9168(04)78954-8

Cited by 99 publications

(166 citation statements)

References 12 publications

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“…In the general population, high levels of apoB lead to an increased risk of IHD (Walldius et al 2001), and in patients on statin therapy, apoB levels have recently been proposed as a more accurate therapy guidant than LDL-C (Miremadi et al 2002;Sniderman et al 2003) The findings of the present study suggest that these relationships may not have a simple molecular basis in the APOB gene.…”

Section: Discussionmentioning

confidence: 65%

“…Apolipoprotein B (apoB) is the sole protein component of this particle, and plasma levels of apoB are also associated with cardiovascular disease. Indeed, evidence is accumulating that apoB may be a better risk indicator for cardiovascular events than LDL-C (Sniderman et al 2003). In a large survey of 175,553 subjects, the apoB concentration was associated with the risk of fatal myocardial infarction, even after adjustment for total cholesterol (Walldius et al 2001).…”

Section: Introductionmentioning

confidence: 99%

“…LDL-C levels are less predictive of cardiovascular events in patients treated with statin therapy. Hence, apoB-guidance of statin treatment may more accurately predict the effect on cardiovascular risk (Miremadi et al 2002;Sniderman et al 2003) Several mechanisms may explain the role of apoB in atherogenesis. ApoB serves as the ligand for LDL-receptor mediated clearance of LDL.…”

Section: Introductionmentioning

confidence: 99%

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Molecular variation at the apolipoprotein�B gene locus in relation to lipids and cardiovascular disease: a systematic meta-analysis

et al. 2003

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Apolipoprotein B (apoB) is the sole protein component of low-density lipoprotein (LDL) and is thought to play an important role in atherogenesis. We performed a meta-analysis of the associations between the three most frequently investigated polymorphisms (XbaI, signal peptide insertion/deletion, EcoRI) in the apolipoprotein B (APOB) gene, lipid parameters, and the risk of ischemic heart disease (IHD). We restricted our analysis to Caucasians. Homozygotes for the XbaI X+ allele had significantly elevated levels of LDL cholesterol (LDL-C) and apoB, but a decreased risk (OR=0.80; 95%CI: 0.66-0.96) of IHD. Homozygosity for the signal peptide deletion allele was associated with similarly increased levels of LDL-C and apoB, and with an increased risk of IHD (OR=1.30; 95%CI: 1.08-1.58). Subjects homozygous for the rare EcoRI allele had significantly decreased levels of total and LDL cholesterol, but unaltered risk of IHD. We conclude that all three polymorphic apoB sites are associated with altered lipid levels, but not necessarily with a consistently altered risk of IHD. These data suggest that the relationship between apoB levels, hypercholesterolemia and IHD risk cannot have a simple molecular basis in the apoB gene.

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Section: Discussionmentioning

confidence: 65%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Molecular variation at the apolipoprotein�B gene locus in relation to lipids and cardiovascular disease: a systematic meta-analysis

et al. 2003

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“…ApoB is a marker of all atherogenic particles present because all potentially atherogenic particles contain one copy of apoB-100 associated with various levels of cholesterol and triglycerides. Therefore apoB is a better predictor of the risk of coronary artery disease and other clinical manifestations of atherosclerosis than values of total cholesterol (TC), LDL cholesterol (LDL-C) and non-HDL cholesterol (non-HDL-C), as proved repeatedly by numerous prospective epidemiological studies dealing with lipids and apolipoprotein B [2][3][4][5][6]. The use of TG value in this algorithm is justified as well.…”

Section: Introductionmentioning

confidence: 97%

Prothrombotic markers in asymptomatic dyslipidemic subjects

Karásek

Vaverková

Halenka

et al. 2010

J Thromb Thrombolysis

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The aim of this study was to evaluate the plasma levels of prothrombotic markers--von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (t-PA)--in asymptomatic subjects with dyslipidemia. Asymptomatic subjects with dyslipidemia and their relatives (n = 234) were assessed for lipids and prothrombotic markers. Individuals were divided into four dyslipidemic phenotypes (DLP) according to apolipoprotein B (apoB) and triglycerides (TG): DLP1 (n = 58, apoB < 1.2 g/l and TG < 1.5 mmol/l), DLP2 (n = 47, apoB < 1.2 g/l and TG ≥ 1.5 mmol/l), DLP3 (n = 31, apoB ≥ 1.2 g/l and TG < 1.5 mmol/l) and DLP4 (n = 98, apoB ≥ 1.2 g/l and TG ≥ 1.5 mmol/l). Associations between prothrombotic markers and risk factors for atherosclerosis, markers of insulin resistance, and the intima-media thickness of the common carotid artery (IMT) were assessed too. Significant differences in PAI-1 between normolipidemic phenotype--DLP1 (62.5 (35.9-82.9) ng/ml) and hypertriglyceridemic phenotypes--DLP2 (82.2 (61.1-122.1) ng/ml, p < 0.01) and DLP4 (91.4 (63.5-111.8) ng/ml, p < 0.001) after adjustment for age, sex and body mass index, were found. Levels of t-PA were different only between DLP1 and DLP4 (1.9 (0.9-3.3) ng/ml vs. 5.3 (2.5-8.6) ng/ml, p < 0.05). There were no significant differences of vWF between DLPs. PAI-1 and t-PA correlated with lipid parameters, markers of insulin resistance, blood pressure and obesity. VWF was independently associated with IMT, which was increased in DLP4. Individuals with hypertriglyceridemic phenotypes showed increased levels of PAI-1 in comparison with normolipidemic subjects. The elevation of t-PA was presented only in patients with simultaneously elevated TG and apoB. The significant increase of IMT confirmed in the patients with DLP4 reveals individuals with the highest risk for atherosclerosis manifestation.

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“…In prospective epidemiologic trials, substantial variability in CHD risk is present across a wide range of cholesterol values [6,7]. Additionally, on-trial LDLC values often are weak predictors of CHD risk in intervention studies [7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Low-density lipoprotein and apolipoprotein B: Clinical use in patients with coronary heart disease

Cromwell

Barringer²

2009

Curr Cardiol Rep

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Managing low-density lipoprotein (LDL) is an integral part of clinical practice. What remains controversial is whether we are using the best measure of LDL quantity for this purpose. Historically, the cholesterol content of LDL particles (LDLC) has been used to express LDL quantity. However, because of variability in the cholesterol carried in LDL particles, frequent disagreement occurs between LDLC and particle measures of LDL quantity, including apolipoprotein B-100 (apo B) or nuclear magnetic resonance (NMR) LDL particle number (LDL-P). Studies consistently demonstrate apo B and LDL-P are superior predictors of coronary heart disease (CHD) risk and superior indicators of low CHD risk on lipid-lowering therapy. Recent recommendations advocate that, in addition to LDLC and non-high-density lipoprotein cholesterol, apo B (or NMR LDL-P) be used as a target of therapy. This article reviews the rationale supporting these recommendations and provides a model for integrating LDL particle measures in clinical practice.

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Apolipoproteins versus lipids as indices of coronary risk and as targets for statin treatment

Cited by 99 publications

References 12 publications

Molecular variation at the apolipoprotein�B gene locus in relation to lipids and cardiovascular disease: a systematic meta-analysis

Molecular variation at the apolipoprotein�B gene locus in relation to lipids and cardiovascular disease: a systematic meta-analysis

Prothrombotic markers in asymptomatic dyslipidemic subjects

Low-density lipoprotein and apolipoprotein B: Clinical use in patients with coronary heart disease

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