Hyperlipidaemia is the term used to denote raised serum levels of one or more of total cholesterol (TChol), low-density lipoprotein cholesterol (LDL-C), triglycerides (TGs), or both TChol and TG (combined hyperlipidaemia).
Dyslipidaemia is a wider term that also includes low levels of high-density lipoprotein cholesterol (HDL-C).1,2 Many types of hyperlipidaemia carry an increased risk of cardiovascular disease (CVD). HDL-C confers protection. It is important as one of the three main modifiable risk factors for CVD (the others being smoking and (hypertension
Epidemiological evidence suggests a:5
1% increase in coronary heart disease (CHD) risk for each 1% increase in LDL-C.
2-3% reduction in CHD risk for each 1% increase in HDL-C.
See separate articles Primary Prevention of Cardiovascular Disease and Secondary Prevention of Cardiovascular Disease.
Fredrickson's Classification is now seldom used but listed five types of hyperlipidaemia (Fredrickson I to V).7
Risk factor screening (including the lipid profile) may be considered in:
Patients with hyperlipidaemia of any cause but no history of CHD, angina, stroke, transient ischaemic attack (TIA), peripheral vascular disease, diabetes or a monogenic lipid disorder should have a formal cardiovascular risk assessment.
Patients with hyperlipidaemia who have such a history do not require a formal risk assessment but every effort should be made to minimise their risk.
See separate articles Primary Prevention of Cardiovascular Disease and Secondary Prevention of Cardiovascular Disease (document links under 'Aetiology', above) and the separate article How to use the Coronary Risk Prediction Charts for Primary Prevention for more information.
The condition is often diagnosed during routine screening, as part of a risk assessment associated with comorbidities or other risk factors (e.g. obesity, smoking), or the patient may present as a relative of an index case with premature CVD. Rarely, there may be a genetic cause. Most familial dyslipidaemias go undiagnosed but, if identified, can enable more effective prevention and treatment in individuals and their families - where suspected, refer to secondary care.
Although the diagnosis is primarily biochemical, two physical signs may be evident in patients with familial hypercholesterolaemia (FH):
Suspect FH where:
The Simon Broom diagnostic criteria:10
DefiniteFH is diagnosed if an individual has:
A TChol level in an adult of >7.5 mmol/L (>6.7 mmol/L in a child) and an LDL-C of >4.9 mmol/L (>4.0 mmol/L in a child); PLUS
Tendon xanthomata or evidence of these signs in a first-degree or second-degree relative; OR
DNA evidence of an LDL receptor mutation, familial defective apo-B-100 or a PCSK9 mutation.
PossibleFH should be diagnosed if the cholesterol concentrations fit these criteria and the individual has at least one of the following:
A family history of myocardial infarction in a second-degree relative aged 50 years or younger, or in a first-degree relative aged 60 years or younger.
A family history of raised TChol greater than 7.5 mmol/L in adult first-degree or second-degree relatives or greater than 6.7 mmol/L in a child, brother or sister aged younger than 16 years.
This is the most common genetic dyslipidaemia, occurring in about 1 in 100 people but is usually polygenic in origin.
Lipid phenotypes in FCH vary considerably but suspect where:
Before considering pharmacological treatment of dyslipidaemias, always try to identify and correct/optimise any secondary or contributory causes.
If possible, blood sampling should be made after 12-hour fasting, but this is requested only for the evaluation of TG, needed for the calculation of LDL-C with the Friedewald formula.11
A lipid profile includes:
The aim of treating hyperlipidaemia is to prevent or reduce the risk and complications of CVD. Such risk reduction includes nondrug measures (such as addressing lifestyle factors) and drug treatment using lipid-lowering therapy.
It should be noted that cardiovascular risks exceeding the 5-10% level may be found in elderly gentlemen based on age (and gender) only, even when other CV risk factor levels are relatively low. This could lead to excessive usage of drugs in the elderly and should be evaluated carefully by the clinician.
See separate Primary Prevention of Cardiovascular Disease article, Secondary Prevention of Cardiovascular Disease article and the separate article Lipid-regulating Drugs, which includes using fibrates in primary care.
No authors listed; Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA. 2001 May 16;285(19):2486-97.
Lipid modification, NICE Clinical Guideline (May 2008); (Cardiovascular risk assessment and the modification of blood lipids for the primary and secondary prevention of cardiovascular disease.) amended May 2010
The Donald S. Fredrickson Papers, Profiles in Science, 2006
Cardiovascular disease - statins, NICE (January 2006); Statins for the prevention of cardiovascular events in patients at increased risk of developing cardiovascular disease or those with established cardiovascular disease
Friedewald WT, Levy RI, Fredrickson DS; Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem. 1972 Jun;18(6):499-502.
Frost PH, Havel RJ; Rationale for use of non-high-density lipoprotein cholesterol rather than low-density lipoprotein cholesterol as a tool for lipoprotein cholesterol screening and assessment of risk and therapy. Am J Cardiol. 1998 Feb 26;81(4A):26B-31B. [abstract]
Yusuf S, Hawken S, Ounpuu S, et al; Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004 Sep 11-17;364(9438):937-52. [abstract]