Dyslipidemia
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Introduction
Dyslipidemia is a major risk factor for atherosclerosis. Most evidence specifically implicates cholesterol - in particular low density lipoprotein (LDL), the delivery mechanism of cholesterol to the tissues. Elevated cholesterol levels are sufficient to induce plaque development, even if other risk factors are absent. High density lipoprotein (HDL), in contrast, is believed to mobilize cholesterol from developing and existing atheromas and transport it to the liver for excretion in the bile.
The Case of...
a simple case introducing clincial presentation and calling for a differential diagnosis to get students thinking.
Causes and Risk Factors
Pathophysiology
Signs and Symptoms
- history
- physical exam
History
Physical Exam
Signs of hyperlipidemia can be seen on physical exam, and include:
- xanthoma - plaques or nodules in skin, especially eyelids: composed of lipid-laden histiocytes
- tendinous xanthoma - lipid deposits in tendon: especially Achilles
- corneal arcus (arcus senilus) - lipid deposit in cornea
Investigations
- lab investigations
- diagnostic imaging
Lab Investigations
Lipid profiles include fasting total cholesterol, LDL, HDL, and triglycerides. Lipid levels should be measured every 5 years in healthy adults. More frequent screening/follow-up should be done in people with established risk factors.
Diagnostic Imaging
Differential Diagnosis
Management of Dyslipidemia
- target levels
- lifestyle modification
- medications
- isolated hypertriglyceridema
Target Levels
Target lipid values, and treatment plans, depend upon risk category (McPherson et al, 2006).
risk category |
LDL (mmol/L) |
ratio total/HDL |
high (10 yr risk >20%, or Hx of DM or CAD) |
<2.0 (<100) |
<4 |
medium (10 yr risk 11-19%) |
<3.5 (<130) |
<5 |
low (10 yr risk <10%) |
<5.0 (<130 with 2 or more risk factors, <160 with 0-1 risk factors) |
<6
|
If dyslipidemia is found, screen for secondary causes, including hypothyroidism, chronic kidney disease, diabetes mellitus, nephrotic syndrome, and liver disease.
Lifestyle Modification
Lifestyle approaches should be taken for at least 3 months before considering drug therapy.
High dietary intake of cholesterol and animal fats raises plasma cholesterol levels, while a low ratio of staurated-to-unsaturated fats lowers them.
- less than 7% of calories should be from saturated fat
- omega-3 fatty acids seem particularly beneficial.
- increase dietary fibre
Stop smoking.
Medications
Statins are the first line treatment. They decrease cholesterol production and increase LDL uptake. Myopathy and hepatotoxicity are rare but must be considered.
After initiating drug therapy, lipids should be measured at 6 weeks and 3 months.
Monitor ALT, AST, CK at baseline and every 6 weeks.
Other medications include:
- niacin - a vitamin which lowers VLDL synthesis in the liver
- ezetimibe - inhibits cholesterol absorption in the gut
- bile acid resins
Fibrates are excellent at lowering triglycerides and good at raising HDL levels.
- modest, at best, effects on decreasing CAD
- increase peripheral lipolysis and decrease hepatic TAG production.
Isolated Hypertriglyceridemia
An elevated TG but normal LDL and ratio should be principally managed with lifestyle modifications: weight loss, exercise, avoidance of smoking and alcohol, blood glucose control, and increase omega-3 fatty acid intake.
Consequences and Course
Resources and References
McPherson R et al. 2006. Canadian Cardiovascular Society position statement--recommendations for the diagnosis and treatment of dyslipidemia and prevention of cardiovascular disease. Canadian Journal of Cardiology. 22(11):913-27.
Topic Development
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