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Managing dyslipidaemia for the primary prevention of cardiovascular disease

BMJ 2018; 360 doi: (Published 23 March 2018) Cite this as: BMJ 2018;360:k946
  1. Aidan Ryan, academic clinical fellow1,
  2. Simon Heath, partner2,
  3. Paul Cook, consultant in chemical pathology and metabolic medicine1
  1. 1Metabolic Medicine, Department of laboratory medicine, University Hospital Southampton, Southampton, UK
  2. 2General Practice, Hazelwood Group Practice, Warwickshire, UK
  1. Correspondence to A Ryan aidan.ryan{at}

What you need to know

  • Assess lipid status as part of an overall cardiovascular risk assessment using a risk calculator

  • Routinely record a family history of premature cardiovascular disease, and consider an underlying familial dyslipidaemia

  • Explain to patients their cardiovascular risk and the benefits and harms of treatment

Sources and selection criteria

We carried out an electronic search through PubMed and Cochrane database of systematic reviews using the following search terms: “primary prevention,” “dyslipidaemia,” “cardiovascular disease,” “statins,” “statin intolerance,” “ezetimibe,” “PCSK9,” “hypercholesterolaemia diagnosis and treatment.” We also interrogated relevant dyslipidaemia guidelines and personal archives for supporting evidence as discussed and as referenced.

Cardiovascular disease (CVD) is the most common underlying cause of death worldwide, accounting for 17.3 million of 54 million total deaths per year. Of these, 8.2 million were caused by ischaemic heart disease and 6.5 million by stroke.1 Mean total cholesterol, calculated low density lipoprotein (LDLc), and triglyceride concentrations have declined over the last 20 years. However, some observational cohort evidence suggests that long term exposure to even modestly elevated cholesterol concentrations is associated with CVD in later life.12

Cholesterol made in the liver and from the diet is transported to peripheral cells by apoB-containing lipoproteins in the blood (fig 1). In a fasting sample, the LDL particles constitute most of the circulating apoB lipoproteins. However, in clinical practice LDL is not measured directly but is calculated (LDLc) (box 1). LDLc has become a metric for treatment success and for diagnosis.

Fig 1

Apolipoprotein B, non-HDL lipid transport, and atherosclerosis. Lipoproteins involved in cholesterol are transported from gut and liver to the peripheral tissues, providing fuel, membrane structure, and hormones. Lipoproteins carrying apolipoprotein B (apart from chylomicrons) have the potential to be atherogenic. APOE: apoliprotein ε receptor; Chol: cholesterol; FA: fatty acids; IDL: intermediate density lipoprotein; TG: triglyceride; C: chylomicron; CR: chylomicron remnant; LDL: low density …

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