Presentation Dyslipidaemia 1

Dyslipidaemia
(Hyperlipidaemia)
Narayan Ghimire
M.Sc. MB
Dyslipidemia
(Hyperlipidemia)
• Dyslipidemia is elevation of plasma cholesterol, triglycerides (TGs), or

both, or a low high-density lipoprotein cholesterol level that contributes
to the development of atherosclerosis.
• Causes may be primary (genetic) or secondary.
• Diagnosis is by measuring plasma levels of total cholesterol, TGs, and

individual lipoproteins.
• Treatment involves dietary changes, exercise, and lipid-lowering drugs.

Classification of Dyslipidemia
Dyslipidemias were traditionally classified by patterns of elevation in lipids

and lipoproteins (Fredrickson phenotype), A more practical system
categorizes dyslipidemias as primary or secondary and characterizes them by
• Increases in cholesterol only (pure or isolated hypercholesterolemia)
• Increases in TGs only (pure or isolated hypertriglyceridemia),
• Increases in both cholesterol and TGs (mixed or combined

hyperlipidemias)
Etiology of Dyslipidemia
Dyslipidemias may be
• Primary: Genetic
• Secondary: Caused by lifestyle and other factors

Primary causes
• Primary causes are single or multiple gene mutations that result in either
overproduction or defective clearance of triglycerides and LDL, or in
underproduction or excessive clearance of HDL.
Secondary causes
• The most important secondary cause of dyslipidemia is
A sedentary lifestyle with excessive dietary intake of total calories, saturated
fat, cholesterol, and trans fats.
• Trans fats are polyunsaturated or monounsaturated fatty acids to which

hydrogen atoms have been added; they are used in some processed foods
and are as atherogenic as saturated fat.
• Other common secondary causes of dyslipidemia include

• Diabetes mellitus
• Chronic kidney disease
• Alcohol overuse
• Hypothyroidism
• Primary biliary cirrhosis and other cholestatic liver diseases
Secondary causes
• Drugs, such as thiazides, beta-blockers, retinoids, highly active antiretroviral
agents, cyclosporine, tacrolimus, estrogen and progestins, and glucocorticoids
•
• Secondary causes of low levels of HDL cholesterol include cigarette smoking, anabolic
steroids, HIV infection , and nephrotic syndrome .
•
Secondary causes
• Diabetes is an especially significant secondary cause because patients tend to
have an atherogenic combination of high TGs; high small, dense LDL fractions;
and low HDL (diabetic dyslipidemia, hypertriglyceridemic hyperapo B).
• Patients with type 2 diabetes are especially at risk. The combination may be a
consequence of obesity, poor control of diabetes, or both, which may increase
circulating free fatty acids (FFAs), leading to increased hepatic very-low-density
lipoprotein (VLDL) production. TG-rich VLDL then transfers TG and cholesterol to
LDL and HDL, promoting formation of TG-rich, small, dense LDL and clearance of
TG-rich HDL.
• Diabetic dyslipidemia is often exacerbated by the increased caloric intake and

physical inactivity that characterize the lifestyles of some patients with type 2
diabetes.
• Women with diabetes may be at special risk of cardiac disease as a result of this
form of dyslipidemia.
Symptoms and Signs of Dyslipidemia
• coronary artery disease (CAD)

• stroke
• peripheral arterial disease .
• acute pancreatitis
• hepatosplenomegaly
• paresthesias
• dyspnea
• confusion
• xanthomas
• dysbetalipoproteinemia
• Severe hypertriglyceridemia
Diagnosis of Dyslipidemia
• Serum lipid profile (measured total cholesterol, TG, and HDL cholesterol and
calculated LDL cholesterol and VLDL cholesterol)
• Dyslipidemia is suspected in patients with characteristic physical findings or

complications of dyslipidemia (eg, atherosclerotic disease).
Primary lipid disorders are suspected when patients have
• Physical signs of dyslipidemia such as tendon xanthomas, which are

pathognomonic for familial hypercholesterolemia
• Onset of premature atherosclerotic disease (men < 55 years, women < 60 years)
• A family history of premature atherosclerotic disease or severe hyperlipidemia
• Serum cholesterol > 190 mg/dL (> 4.9 mmol/L)

Lipid profile measurement
• Total cholesterol, triglycerides, and HDL cholesterol are measured directly.
• TC and TG values reflect cholesterol and TGs in all circulating lipoproteins, including
chylomicrons, VLDL, intermediate-density lipoprotein (IDL), LDL, and HDL.
• TC values can vary by 10% and TGs by up to 25% day-to-day even in the absence of a
disorder.
• TC and HDL cholesterol can be measured in the nonfasting state, but most patients
should have all lipids measured while fasting (usually for 12 hours) for maximum
accuracy and consistency.
• Testing should be postponed until after resolution of acute illness because TG and
lipoprotein(a) levels increase and cholesterol levels decrease in inflammatory states.
Lipid profiles can vary for about 30 days after an acute myocardial infarction (MI);
however, results obtained within 24 hours after MI are usually reliable enough to
guide initial lipid-lowering therapy.
• LDL cholesterol values are most often calculated as the amount of cholesterol not
contained in HDL and VLDL. VLDL is estimated by TG ÷ 5 because the cholesterol
concentration in VLDL particles is usually one fifth of the total lipid in the particle. Thus,
• This calculation is valid only when TGs are < 400 mg/dL (< 4.5 mmol/L) and patients are
fasting because eating increases TGs. The calculated LDL cholesterol value incorporates
measures of all non-HDL, nonchylomicron cholesterol, including that in IDL and
lipoprotein.
• LDL can also be measured directly using plasma ultracentrifugation, which
separates chylomicrons and VLDL fractions from HDL and LDL, and by an
immunoassay method.
• Direct measurement may be useful in some patients with elevated TGs,

but these direct measurements are not routinely necessary.
• The role of apo B testing is under study because values reflect all non-HDL
cholesterol (in VLDL, IDL, and LDL) and may be more predictive of CAD risk
than LDL cholesterol.
• Non-HDL cholesterol (TC − HDL cholesterol) may also be more predictive

of CAD risk than LDL cholesterol, especially in patients with
hypertriglyceridemia.
Other tests
• Patients with premature atherosclerotic cardiovascular disease, cardiovascular disease
with normal or near-normal lipid levels, or high LDL levels refractory to drug therapy
should have Lp(a) levels measured.
• Lp(a) levels may also be directly measured in patients with borderline high LDL
cholesterol levels to determine whether drug therapy is warranted.
• C-reactive protein may be measured in the same populations.
• Measurements of LDL particle number or apoprotein B-100 (apo B) may be useful in

patients with elevated TGs and the metabolic syndrome.
• Apo B provides similar information to LDL particle number because there is one apo B
molecule for each LDL particle.
• Apo B measurement includes all atherogenic particles, including remnants and Lp(a).
Tests for secondary causes of dyslipidemia
Tests for secondary causes of dyslipidemia should be done in most patients

with newly diagnosed dyslipidemia and when a component of the lipid profile
has inexplicably changed for the worse. Such tests include measurements of
• Creatinine
• Fasting glucose
• Liver enzymes
• Thyroid-stimulating hormone (TSH)
• Urinary protein
Screening
• Screening is done using a fasting lipid profile (TC, TGs, HDL cholesterol,
and calculated LDL cholesterol). Different medical societies have different
recommendations on when to begin screening.
• Lipid measurement should be accompanied by assessment for other

cardiovascular risk factors, including
o Cigarette use
o Diabetes mellitus
o Family history of CAD in a male 1st-degree relative before age 55 or a
female 1st-degree relative before age 65
o Hypertension
Screening in children
• Most physicians recommend screening per the2012 National Heart Lung

and Blood Institute
Guidelines for Cardiovascular Health and Risk Reduction in Children and A
dolescents
as follows
o Children with risk factors (eg, diabetes , hypertension, family history of

severe hyperlipidemia or premature CAD): Fasting lipid profile once at age
of 2 to 8 years.
o Children with no risk factors: Non-fasting or fasting lipid profile once

before puberty (usually age 9 to 11) and once more at age of 17 to 21
years.
Screening in adults
• Adults are screened at age 20 years and every 5 years thereafter.
• A definite age after which patients no longer require screening has not
been established, but evidence supports screening of patients into their
80s, especially in the presence of atherosclerotic cardiovascular disease.
• Patients with an extensive family history of heart disease should also be

screened by measuring Lp(a) levels.
Treatment of Dyslipidemia
• Risk assessment by explicit criteria
• Lifestyle changes (eg, exercise, dietary modification)
• For high LDL cholesterol, statins, bile acid sequestrants, ezetimibe,

bempedoic acid, and PCSK9 (proprotein convertase subtilisin/kexin type 9)
inhibitors.
• For high TG, fibrates, omega-3 fatty acids.

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Dyslipidaemia

• Dyslipidemia is elevation of plasma cholesterol, triglycerides (TGs), or

• Causes may be primary (genetic) or secondary.

• Diagnosis is by measuring plasma levels of total cholesterol, TGs, and

• Treatment involves dietary changes, exercise, and lipid-lowering drugs.

Dyslipidemias were traditionally classified by patterns of elevation in lipids

• Increases in cholesterol only (pure or isolated hypercholesterolemia)

• Increases in TGs only (pure or isolated hypertriglyceridemia),

• Increases in both cholesterol and TGs (mixed or combined

• Secondary: Caused by lifestyle and other factors

• Trans fats are polyunsaturated or monounsaturated fatty acids to which

• Other common secondary causes of dyslipidemia include

• Diabetic dyslipidemia is often exacerbated by the increased caloric intake and

• coronary artery disease (CAD)

• Dyslipidemia is suspected in patients with characteristic physical findings or

Primary lipid disorders are suspected when patients have

• Physical signs of dyslipidemia such as tendon xanthomas, which are

• A family history of premature atherosclerotic disease or severe hyperlipidemia

• Serum cholesterol > 190 mg/dL (> 4.9 mmol/L)

• Direct measurement may be useful in some patients with elevated TGs,

• Non-HDL cholesterol (TC − HDL cholesterol) may also be more predictive

• C-reactive protein may be measured in the same populations.

• Measurements of LDL particle number or apoprotein B-100 (apo B) may be useful in

Tests for secondary causes of dyslipidemia should be done in most patients

• Lipid measurement should be accompanied by assessment for other

• Most physicians recommend screening per the2012 National Heart Lung

o Children with risk factors (eg, diabetes , hypertension, family history of

o Children with no risk factors: Non-fasting or fasting lipid profile once

• Adults are screened at age 20 years and every 5 years thereafter.

• Patients with an extensive family history of heart disease should also be

• Risk assessment by explicit criteria

• Lifestyle changes (eg, exercise, dietary modification)

• For high LDL cholesterol, statins, bile acid sequestrants, ezetimibe,

• For high TG, fibrates, omega-3 fatty acids.

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