Dyslipidaemia

Introduction

There is ample evidence linking high blood cholesterol levels to Cardiovascular Disease (CVD) events, including myocardial infarction, strokes, and peripheral vascular disease.
On the other hand, there is also evidence for significant reduction in morbidity and mortality from CVDs by reducing blood cholesterol levels in those at risk (primary prevention) and those who have suffered a CVD event (secondary prevention).
The commonly assessed blood lipid parameters are total cholesterol, HDL cholesterol, LDL cholesterol and triglycerides.
However, the primary target for intervention is the LDL-cholesterol level.
As treatment may be for long periods or lifelong, periodic monitoring of liver and muscle enzymes (transaminases and creatine kinase) and blood glucose are advisable to forestall medication-related side effects.

Causes of dyslipidaemia

The following are some of the known causes of dyslipidaemia:

  1. High dietary intake of saturated fats (animal fat)
  2. Lack of physical activity
  3. Metabolic syndrome (a combination of several of the following; obesity, hypertension, type 2 diabetes, dyslipidaemia, gout etc.)
  4. Hereditary factors
  5. Excessive alcohol intake
  6. Hypothyroidism
  7. Nephrotic syndrome

Symptoms of dyslipidaemia

  • Usually none
  • Abdominal pain from pancreatitis related to hypertriglyceridaemia

Signs of dyslipidaemia

There is usually no sign of dyslipidaemia patients.
Occasionally, patients can present with the following signs:

  • Whitish ring around the cornea (corneal arcus)
  • Yellowish skin eruptions around the eyes (xanthelasmata)
  • Whitish blood sample (lipaemic blood)
  • Fasting blood lipid profile
  • Thyroid function test (if lipid levels very high)
  • Plasma protein (if lipid levels very high, to exclude nephrotic syndrome)
  • Urine protein (if lipid levels very high, to exclude nephrotic syndrome)

Treatment for dyslipidaemia

Treatment Objectives

The treatment objectives of dyslipidaemia include following:
1. To reduce the risk of clinical atherosclerotic cardiovascular events and related deaths in:

  • Healthy individuals at risk (primary prevention)
  • Individuals who have suffered a CVD event (secondary prevention)
  1. To reduce the LDL-C level to the following targets:
  • At least a 50 % LDL-C reduction for primary prevention (in the general population i.e. individuals > 21 years of age with an un treated LDL-C 24.9 mmol/L) 30-49 % LDL-C reduction for primary prevention (in individuals 40 to 75 years of age with diabetes with an untreated LDL-C 1.8-4.9 mmol/L)
  • LDL – C < 1.8 mmol/L for secondary prevention (in adults who have previously suffered a heart attack, stroke or peripheral vascular disease)

Non-pharmacological treatment

  • Dietary measures: a low calorie, low saturated fat (animal fat), high polyunsaturated fat (plant fat) diet is recommended under the supervision of a dietician
  • Weight reduction in patients who are overweight or obese
  • Reduction in alcohol consumption, where this is excessive
  • Regular physical activity or exercise tailored to the individual patient

Pharmacological treatment

A. Low CVD risk – primary prevention

1st Line Treatment
Evidence Rating: [A]
Simvastatin, oral,

  • Adults: 10-20 mg at night

B. Moderate CVD risk – Diabetes and CVD risk equivalents

Evidence Rating: [A]
Atorvastatin, oral,

  • Adults: 10-20 mg daily

Or

Rosuvastatin, oral,

  • Adults: 5-10 mg daily

Or

Simvastatin, oral,

  • Adults: 20-40 mg at night

C. High CVD risk – Secondary prevention

Atorvastatin, oral,

  • Adults: 40-80 mg daily

Or

Rosuvastatin, oral,

  • Adults: 20-40 mg daily

Referral Criteria

Refer all patients who remain outside the target values despite adequate dietary, exercise and medication therapy to a specialist