Dyslipidemia: Causes, Risk Assessment, Lifestyle Changes, Treatment

lesterol (TC) and low-density lipoprotein cholesterol (LDL-C) increase the risk of an individual developing cardiovascular disease (CVD). In contrast, high-density lipoprotein cholesterol (HDL-C) confers protection against CVD, with the risk reducing as HDL-C increases. It is, therefore, clear that the term hyperlipidaemia, which was formerly used to describe disorders of lipoprotein metabolism, is inappropriate.

It is more appropriate to use the term dyslipidemia, which encompasses both abnormally high levels of specific lipoproteins, for example, LDL-C, and abnormally low levels of other lipoproteins, for example, HDL-C, as well as disorders in the composition of the various lipoprotein particles.

Causes

Primary dyslipidemia

Up to 60% of the variability in cholesterol fasting lipids may be genetically determined, although expression is often influenced by interaction with environmental factors. The common familial (genetic) disorders can be classified as:

• the primary hypercholesterolaemia such as familial hypercholesterolaemia in which LDL-C is raised
• the primary mixed (combined) hyperlipidemias in which both LDL-C and triglycerides are raised
• the primary hypertriglyceridemia such as type III hyperlipoproteinemia, familial lipoprotein lipase deficiency and familial apoC-II deficiency

Secondary dyslipidemia

Dyslipidaemias that occur secondary to a number of disorders, dietary indiscretion or as a side effect of drug therapy account for up to 40% of all dyslipidaemias. Fortunately, the lipid abnormalities in secondary dyslipidemia can often be corrected if the underlying disorder is treated, effective dietary advice implemented or the offending drug withdrawn. On occasion, a disorder may be associated with dyslipidemia but not the cause of it. For example, hyperuricemia (gout) and hypertriglyceridemia co-exist in approximately 50% of men. In this particular example, neither is the cause of the other and treatment of one does not resolve the other. There are, however, two notable exceptions to the rule with this example: nicotinic acid and fenofibrate. Both drugs reduce triglyceride levels but nicotinic acid increases urate levels while fenofibrate reduces them by an independent uricosuric effect.

Drugs

• A number of drugs can adversely affect serum lipid and lipoprotein concentrations:
• Antihypertensive agents. , Oral contraceptives, Corticosteroids, Hepatic microsomal enzyme inducers, Cyclosporin
• Risk Assessment

Primary prevention

In patients with no evidence of CHD or other major atherosclerotic disease, there are a number of CVD risk prediction charts, including those produced by the Joint British Societies (JBS2) (British Hypertension Society, 2009) for males and females. JBS2 recommends that all adults from the age of 40 years, with no history of CVD or diabetes, and not receiving treatment for raised blood pressure or dyslipidemia, should receive opportunistic screening every 5 years in primary care. The cardiovascular risk calculated using the JBS2 charts is based on the number of cardiovascular events expected over the next 10 years in 100 women or men with the same risk factors as the individual being assessed.

Secondary prevention

Patients with CVD and levels of TC >4 mmol/L and LDL-C >2 mmol/L are the ones most likely to benefit from treatment with lipid-lowering agents. Typical of individuals who fall into this category are patients with a history of angina, myocardial infarction, acute coronary syndrome, coronary artery bypass grafting, coronary angioplasty or cardiac transplantation as well as patients with evidence of atherosclerotic disease in other vascular beds such as patients post-stroke or TIA, and those with peripheral arterial disease.

Lifestyle changes

When a decision is made to start treatment with a lipid lowering agent, other risk factors must also be tackled as appropriate, such as smoking, obesity, high alcohol intake and lack of exercise. Underlying disorders such as diabetes mellitus and hypertension should be treated as appropriate.

• Lifestyle target
• Do not smoke
• Maintain ideal body weight (BMI 20–25kg/m2 )
• Avoid central obesity
• Reduce total dietary intake of fat to ≤30% of total energy intake
• Reduce intake of saturated fats to ≤10% of total fat intake
• Reduce intake of dietary cholesterol to <300mg/day
• Replace saturated fats by an increased intake of monounsaturated fats
• Increase intake of fresh fruit and vegetables to at least five portions per day
• Regularly eat fish and other sources of omega-3 fatty acids (at least two portions of fish each week)
• Limit alcohol intake to <21 units/week for men and <14 units/ week for women
• Restrict intake of salt to <100 mmol day (<6g of sodium chloride or <2.4g sodium/day)
• Undertake regular aerobic exercise of at least 30 min/day, most days of the week
• Avoid excess intake of coffee or other caffeine-rich containing products

Treatment

Drugs

If an individual is found to be at risk of CVD (primary prevention) it may be appropriate to give a trial of dietary and lifestyle changes for 3–6 months. This rarely achieves the required effect on the lipid profile and drug therapy is required. This must not, however, negate a sustained effort by the individual to make appropriate dietary and lifestyle adjustments. In an individual requiring treatment for secondary prevention, a delay of several months in starting treatment is not appropriate and treatment will normally be commenced immediately with a lipid-lowering agent.

Treatment normally includes:

• a lipid-lowering agent such as simvastatin 40 mg/day (or alternative) but no treatment targets are set
• personalised information on modifiable risk factors including physical activity, diet, alcohol intake, weight and tight control of diabetes
• advice to stop smoking
• advice and treatment to achieve blood pressure below 140 mmHg systolic and 90 mmHg diastolic