High-risk groups 1–4

  • Those overweight, obese or with diets high in saturated fat
  • Aboriginal and Torres Strait Islander people > 18 years of age
  • Those with a history of CHD, diabetes, CKD or familial dyslipidaemia
  • Those with SBP ≥ 180 mmHg or DBP ≥ 110 mmHg
  • Sedentary lifestyle
  • Smokers and those who consume alcohol above recommended limits
  • Women with Polycystic Ovarian Syndrome (PCOS)

Considerations in pregnancy 2

  • Encourage lifestyle modification for pregnant women
  • Discuss medicine use with women contemplating pregnancy already on statins
  • Pharmacotherapy should be avoided outside of specialist care

Referral 

  • Refer patients with comorbidities and resistant high cholesterol levels (triglyceride level > 8 mmol/L or total cholesterol > 9 mmol/L) despite treatment to:
    • a specialist related to their comorbidity and
    • a dietitian

1. What is dyslipidaemia? 3

  • Abnormalities of lipids (fats) or lipoproteins in the blood
  • Ingested fats are processed by the liver and returned to the bloodstream as cholesterol
  • Cholesterol is produced for many metabolic processes including:
    • building cell membranes
    • making hormones e.g. oestrogen and testosterone
    • the production of vitamin D and bile acids
  • High blood cholesterol can build up fatty deposits in blood vessel walls
  • Arteries can narrow and block completely, leading to heart disease or stroke
  • Lipoproteins carry the following cholesterols in the blood:
    • high density lipoprotein cholesterol (HDL-C) is considered beneficial
    • low density lipoprotein cholesterol (LDL-C) is considered harmful
    • very low density lipoprotein cholesterol (VLDL-C) carry triglycerides (TG) in the bloodstream
  1. Primary dyslipidaemia
    • Genetic or hereditary high cholesterol i.e. familial dyslipidaemia
  2. Secondary dyslipidaemia
  • Caused by lifestyle factors, chronic conditions or medicines. See Table 1.

Table 1. Common causes of secondary dyslipidaemia 2

Cause

Effect on lipid profile

Hypothyroidism, nephrotic syndrome, cholestasis, anorexia nervosa

  • ↑ LDL-C

Type 2 diabetes, obesity, renal impairment, smoking, drug therapy

  • ↑ TG
  • ↓ HDL-C

Diet high in saturated fat

  • ↑ LDL-C

Alcohol misuse, oestrogen use

  • ↑ TG

Sedentary lifestyle

  • ↑ LDL-C
  • ↓ HDL-C

ß-blockers

  • ↑ TC
  • ↓ HDL-C

Diuretics

  • ↑ TC
  • ↓ TG

2. Diagnosis of dyslipidaemia 2–6

  • Dyslipidaemia is identified by a venous lipid result outside of target values. See Table 2.

3. Management of dyslipidaemia

  • Management goals are to reduce or eliminate the risk of Coronary heart disease or stroke by:
    • Lifestyle modifications
    • addressing the cause. See Table 1.
    • meeting target goals. See Table 2.
    • identifying and addressing comorbidities in relation to estimate CVD risk using the Australian cardiovascular disease risk calculator:
      • Heart failure
      • Chronic kidney disease,
      • Coronary heart disease
      • Diabetes
      • Hypertension
      • Overweight and obesity (adult)
      • Overweight and obesity (child)
      • Stroke and transient ischaemic attack

Table 2. Target goals to manage dyslipidaemia 1,2,4,7

Test

Target

TC

  • < 4.0 mmol/L*

TG

  • < 2.0 mmol/L*

HDL-C

  • ≥ 1.0 mmol/L*

LDL-C

  • < 2.0 mmol/L for primary prevention*
  • < 1.8 mmol/L for secondary prevention with coronary stent* and post stroke/TIA

Non-HDL-cholesterol (N-HDL-C)

  • < 2.5 mmol/L

TC:HDL-C

  • ≤ 4.5 mmol/L

Blood pressure (BP)

  • < 130/80

Alcohol intake

  • Zero or ≤ 2 standard drinks per day

Physical activity

  • At least 30 minutes of moderate physical activity on most/all days of the week (total ≥ 150 minutes/week)

Body mass index (kg/m²)

Waist circumference (cm)

Women

Men

  • Normal weight 18.5–24.9

< 80

< 90

  • Overweight 25–29.9

< 90

< 100

  • Obese 30–34.9

< 105

< 110

  • Morbidly obese ≥ 35

< 115

< 125

* For patients on lipid lowering therapy

Each 1.0 mmol/L reduction in LDL-C is associated to a 22% reduction in cardiovascular disease mortality and morbidity

  1. Support patient self-management 3,4,6
    • Discuss:
      • the positive effects of Lifestyle modifications on lipid levels with particular regard to Diet and nutrition. See Table 3–4.
      • dyslipidaemia and its association with heart disease, stroke and pancreatitis
    • Provide dyslipidaemia resources. See Resources 1.
    • Encourage the patient to identify barriers to adequate lifestyle modification and medical adherence and create goals to overcome those barriers. See Engaging our patients
  2. Social-emotional support
    • See Social-emotional wellbeing

Table 3. Lifestyle modification effect on lipid levels1–3

Lifestyle intervention

To reduce TC and LDL-C levels

To reduce
TG levels

To increase HDL-C levels

Reduce excessive body weight

♥ ♥ ♥

♥ ♥

Increase physical activity

♥ ♥

♥ ♥ ♥

Reduce dietary trans fat

♥ ♥ ♥

 

♥ ♥ ♥

Reduce intake of sugar products

 

♥ ♥ ♥

Reduce dietary saturated fat

♥ ♥ ♥

  

Consume foods high in phytosterol

♥ ♥ ♥

  

Alcohol in moderation only

 

♥ ♥ ♥

♥ ♥

Reduce total amount of dietary carbohydrates

 

♥ ♥

 

Consume polyunsaturated fat

 

♥ ♥

 

Increase dietary fibre

♥ ♥

  

Reduce dietary cholesterol

♥ ♥

  

Reduce dietary carbohydrates and replace with unsaturated fat

  

♥ ♥

Smoking cessation

  

Consume soy protein products

  

Replace saturated fat with mono- or polyunsaturated fat

 

 

♥♥♥ Great effect
♥♥ Good effect
♥Adequate effect

  1. Diet and nutrition 1–4,6
    • Overweight and obesity (adult) contributes to dyslipidaemia by lowering HDL
    • Provide the patient with nutrition and diet related resources. See Resource 3.
    • Frequent consumption of:
      • saturated fats raise LDL-C levels e.g. takeaway and processed foods
      • food and drinks with added sugar including alcohol raises TG levels
      • polyunsaturated fats reduce LDL-C levels and cardiovascular risk e.g. oily fish, unsalted nuts, polyunsaturated margarines and oils
      • vegetable oils found in legumes, avocados, plain nuts, fruit, vegetables, whole grains and cereals, reduces blood cholesterol levels
    • To lower lipid levels commence diet modification:
      • for 6 weeks for low-risk groups
      • if lipid levels remain high, commence medicines
      • start medicine concurrently for high-risk groups
    • See Tables 3 and 4.
    • See Diet and nutrition
  2. Physical activity
  • Encourage any form of Physical activity and sleep that encourages the benefits of exercise and interaction e.g. walking groups, ball sports, mens shed

Table 4. Dietary options to lower TC and LDL-C 2–4

Types

Examples

Cereals

  • Whole grains, oats

Vegetables

  • Raw, cooked, frozen or tinned

Legumes

  • Beans, lentils, including soy and soy protein

Fruit

  • Fresh, frozen or tinned

Eggs, meat and fish

  • Lean meat, oily fish, skinless chicken and egg white

Dairy foods

  • Skimmed milk and yoghurt

Cooking methods

  • Grilling, boiling, steaming, oven bake and microwave

4. Medicines for dyslipidaemia 1,3,6

  • Commence and regularly review lipid lowering therapy according to estimated risk using the Australian cardiovascular disease risk calculator to meet target lipid levels (Table 2.). If estimated 5 year CVD risk is:
    • high > 10 % then start immediately
    • intermediate 5–10 % and 3–6 months of inadequate lifestyle modification then start therapy
    • Low < 5 % then therapy usually not required
  1. General lipid lowering therapy 3,6
    • Before commencing drug therapy:
      • address lifestyle behaviour causes of raised blood lipids
      • consider risks and benefits in treating those > 74 years with comorbidities
      • be alert to medicine interactions:
        • ß-blockers increase TC and decreases HDL
        • diuretics increase TC and TG
        • caution: only cease these medicines if they are not indicated e.g. ß-blockers for hypertension alone
    • Use statins as first line therapy
      • if LDL-C levels not reduced with maximum tolerated dose or intolerant of statins, add ezetimibe
  2. For raised triglycerides 3,5
    • Consider treatment with one of the following:
      • fenofibrate (especially if HDL is below target)
      • fish oil

Table 5. Recommended medicines and combinations for dyslipidaemia 3,6

Statin

  • Rosuvastatin 5–40 mg daily (40 mg cautiously). Caution in renal impairment
  • Atorvastatin 10–80 mg daily
  • Simvastatin 10–40 mg daily
  • Pravastatin 20–80 mg daily (80 mg cautiously)
  • First line treatment
  • Reduces LDL-C up to 60%
  • Increases HDL-C by 5–10%
  • In order of decreasing potency
  • Adjust dose if renally impaired

Ezetimibe

  • When statin intolerant or lipid targets not reached with statin alone
  • Ezetimibe 10 mg daily
  • Second line treatment
  • Reduces LDL-C by 15–22%
  • When intolerant of statin or as add-on when target not reached
  • Reduces LDL-C by a further 20–25% when used with statin

Bile acid binding resins

  • Colestyramine 4–8 g daily initially increasing to a max. 24 g in divided doses
  • Third line treatment
  • Reduces LDL-C by 18–25%
  • GI adverse effects may limit maximum dose

Statin + bile acid binding resins

  • As above
  • Reduces LDL-C by a further 10–20%

Fibrates (with statin)

  • When statin intolerant or lipid targets not reached with statin alone
  • Fenofibrate 145 mg daily
    • eGFR 20–60 mL/min 48 mg daily (to a max. 96 mg daily)
    • eGFR < 20 mL/min avoid
  • Reduce dose in patients with renal impairment
  • Reduces TG levels
  • Modest HDL-C raising effects
  • Reduces LDL by > 25%
  • Preferred agent when used in combination
  • Gemfibrozil 600 mg bd
  • Contraindicated with simvastatin
  • Reduces TG levels
  • Modest HDL-C raising effects

PCSK9 inhibitor

  • May be considered after specialist consultation in patients at very-high risk not achieving target lipd levels on maximum tolerated dose of statin and ezetimibe

5. Cycle of care

Cycle of care summary for dyslipidaemia

Action

Dx

Frequency

BMI

12 mthly

Weight

6 mthly

Waist circumference

6 mthly

Pulse rate

6 mthly

Blood pressure

6 mthly

UEC and LFTs

12 mthly. If LFTs increase and remain > 3 x ULN with optimal lifestyle modification then cease lipid therapy

Lipid profile

  • 8 weeks after starting or adjusting treatment
  • Annually once target levels reached. Inform patient

ALT

  • Before statin therapy
  • Routine control of ALT thereafter is not recommended unless on fibrate or evolving liver disease symptoms
  • If < 3 x ULN continue therapy and recheck in 4–6 wks
  • If ≥ 3 x ULN stop or reduce statin and recheck in 4–6 wks

Creatinine kinase (CK)

  • Before statin therapy. If > 4 x ULN do not start therapy
  • Routine monitoring not required
  • Check immediately if patient develops:
    • myalgia. Be alert to myopathy in high-risk patients i.e. the elderly, polypharmacy, liver or renal disease or athletes
    • muscle pain and weakness:
      • If > 10 x ULN; cease treatment; check ACR, eGFR; monitor every 2 wks
    • If < 10 x ULN and:
      • no symptoms; continue therapy; monitor every 2 wks
      • with symptoms; cease treatment; monitor and consider rechallenge with a lower statin dose
    • If < 4 x ULN and:
      • no symptoms; continue therapy
      • with symptoms; monitor symptoms and CK regularly
      • symptoms persist; cease treatment; check in 6 wks; re-evaluate indication for treatment

HbA1c

  • If at high-risk of developing Diabetes and on high-dose statin treatment

Pt self-management

Each visit

Lifestyle behaviours

Each visit

Diet and nutrition

Once a week for 6 wks

Social-emotional wellbeing

Each visit

Influenza, pneumococcal and COVID-19 vaccines

Recommended. See the Australian Immunisation Handbookfor schedule

Medicine review

Each visit

Dentist

12 mthly

HW/RN review

6 mthly

MO/NP review

6 mthly

Dietitian review

12 mthly

Specialist review

 

If resistant high cholesterol levels persist despite treatment

6. References

7. Resources

  1. Heart Foundation Dietary Fat and Heart Healthy Eating information
  2. Queensland Health nutrition and diet related resources
  3. The Australian Dietary Guidelines