Upon entry into the circulation, chylomicrons (containing apo B-48) produced by the small intestine, and VLDL (containing apo B-100) produced by the liver undergo LPL–mediated lipolysis mainly in peripheral tissues, notably adipose tissue and muscle. Chapman M J et al. Eur Heart J 2011;32: Published on behalf of the European Society of Cardiology. All rights reserved. © The Author For permissions please
Metabolic pathways for HDL and triglyceride-rich lipoprotein remnants highlight their close interrelationship. Chapman M J et al. Eur Heart J 2011;32: Published on behalf of the European Society of Cardiology. All rights reserved. © The Author For permissions please
Lipoprotein cholesterol as a function of increasing levels of non-fasting triglycerides in the general population. Chapman M J et al. Eur Heart J 2011;32: Published on behalf of the European Society of Cardiology. All rights reserved. © The Author For permissions please
Chapman et al. EAS Consensus Panel. Eur Heart J 2011;32:
Hazard ratios for coronary heart disease and ischaemic stroke across quantiles of usual concentrations of triglycerides, HDL, and non-HDL cholesterol levels. Chapman M J et al. Eur Heart J 2011;32: Published on behalf of the European Society of Cardiology. All rights reserved. © The Author For permissions please
Relationship of non-fasting triglycerides (up to and >5 mmol/L or 440 mg/dL) and risk of myocardial infarction, ischaemic stroke, and total mortality. Chapman M J et al. Eur Heart J 2011;32: Published on behalf of the European Society of Cardiology. All rights reserved. © The Author For permissions please
Chapman et al. EAS Consensus Panel. Eur Heart J 2011;32:
Proposed algorithm for the management of high-risk individuals with elevated triglycerides and/or low HDL cholesterol at LDL cholesterol goal. aLDL-C at goal as recommended by the most recent European guidelines (2007);4 <2.5 mmol/L in high-risk patients, decreasing to <2.0 mmol/L in very high risk patients. Chapman M J et al. Eur Heart J 2011;32: Published on behalf of the European Society of Cardiology. All rights reserved. © The Author For permissions please
Disclosures This work including Consensus Panel meetings were supported by unrestricted educational grants to the European Atherosclerosis Society from Merck, Kowa, Roche, and AstraZeneca. This funding also supported the Open Access publication charges for this article. These companies were not present at the Consensus Panel meetings, had no role in the design or content of the Consensus Statement, and had no right to approve or disapprove of the final document. Chapman et al. EAS Consensus Panel. Eur Heart J 2011;32: