HYPERCHOLESTEROL

EMIA
MANAGEMENT
BASED ON MALAYSIAN CPG
MANAGEMENT OF DYSLIPIDEMIA 2011
4TH EDITION

SECONDARY DYSLIPIDAEMIA
METABOLIC/ENDOCRINE

Hypothyroidism
Type 2 Diabetes Mellitus
Metabolic Syndrome
Cushings Syndrome

RENAL
End stage renal disease
Nephrotic syndrome

HEPATIC
Obstructive liver disease
Primary biliary cirrhosis

DRUGS
Alcohol
Thiazide diuretics
Beta blockers

FRAMINGHAM CARDIOVASCULAR RISK

SCORE

DYSLIPIDAEMIA RISK FACTOR

FOR CVD
Elevated LDL-C
Low HDL-C
Elevated TG
Elevated non-HDL-C
Atherogenic Dyslipidaemia

MAJOR RISK FACTORS FOR CVD

Positive risk factors
Male 45 years of age
Female 55 years of age or premature menopause without
hormonal replacement therapy
Hypertension
Current cigarette smoking
Family history of myocardial infarction or sudden death prior to
age 55 in a male parent or male first degree relative and prior to
age 65 in a female parent or other
female first degree relative
HDL-C < 1.0 mmol/L
Negative Risk Factors
HDL > 1.6 mmol/L

LDL LEVEL AND DRUG THERAPY

Global Risk

LDL levels to
initiate drug
therapy

Target LDL levels

0 -1 risk factor

4.9

<4.1

2 or more risk
factors

3.4

3.4

CVD and CVD risk

equivalents

2.0 to 2.6

< 2.0

CHOLESTEROL SYNTHESIS

LIPID-LOWERING AGENTS

STATINS
inhibitors of HMG CoA reductase , the rate limiting enzyme in
hepatic cholesterol synthesis
suitable first-line agents in familial hypercholesterolemia, for
primary prevention of CVD, secondary prevention of CVD and CHD
equivalents
Serum lipids and alanine aminotransferase should be measured at
6-8 weeks after starting treatment and thereafter as necessary
especially
doses
are increased
Lipid
EffectswhenSide
Effects
Contraindicati Initial dosage
ons
LDL 18-55%
HDL 5-15%
TG 7-30%

Myopathy
Increased
liver
enzymes

Absolute:
Active or
chronic liver
disease
Pregnancy
and lactation
Relative:
Concomitant
use of certain
drugs eg
cyclosporin,

Lovastatin
20mg ON
Simvastatin
20mg ON
Atorvastatin
10mg ON

FIBRATES
Peroxisome Proliferator Activated Receptor (PPAR) agonist
which in turn stimulates synthesis of fatty acid oxidation
particularly useful in individuals with combined (mixed)
dyslipidaemia and hypertriglyceridaemia. Alternative treatment in
individuals with mild to moderate hypercholesterolemia who are
statin intolerant
Serum alanine aminotransferase should be monitored when
starting
therapySide
or when
doses are
increased.
Lipid
Effects
Effects
Contraindicati
Initial dosage
ons
LDL 5-20%
HDL 10-35%
TG 20-50%

Dyspepsia
Gallstones
Myopathy

Absolute:
Severe
hepatic
disease
Severe renal
disease
Pregnancy
and lactation
Relative:
Concomitant
use of certain

Bezafibrate
200mg OD
Fenofibrate
300mg OD
Gemfibrozil
300mg BD
Ciprofibrate
100mg OD

RESINS
bind to bile acids to promote their secretion into the intestines
Monotherapy has a modest effect on CHD in primary prevention
Combination with a statin may be necessary in severe
hypercholesterolaemia.

Lipid Effects

Side Effects

Contraindicati
ons

Initial dosage

LDL 15-30%
HDL 3-5%
TG /

GIT distress
Constipation
Decreased
absorption of
certain drugs
eg PCM,
NSAIDs, TCA

Absolute:
Dysbetalipop
roteinemia
TG > 4.5
mmol/l
Relative:
TG > 2.3
mmol/l

Not available in
Malaysian
market

NICOTINIC ACID
decrease mobilization of free fatty acids from adipose tissues
the first to show mortality reduction in individuals with CHD

Lipid Effects

Side Effects

Contraindicati
ons

Initial dosage

LDL 5-25%
HDL 15-35%
TG 20-50%

Flushing
Hyperglycemi
a
Hyperuricemi
a (or gout)
Upper-GIT
distress
Hepatotoxicit
y

Absolute:
Chronic liver
disease
Severe Gout
Relative:
Diabetes
(high doses
only)
Hyperuricemi
a
Peptic-Ulcer

Niacin 150mg
BD

CHOLESTEROL ABSORPTION
INHIBITORS
selectively block intestinal absorption of both dietary and biliary

cholesterols and other phytosterols

leads to a reduction in hepatic cholesterol delivery
usually used in combination with statins to further lower LDL
monotherapy for primary hypercholesterolemia in patients who
cannot tolerate statin or fibrate
Lipid Effects

Side Effects

LDL 18-25%
HDL 3-5%
TG 8-14%

Headache
Abdominal
pain
Diarrhea

Contraindicati
ons

Initial dosage
Ezetimibe 10mg
OD

LIPID LOWERING DIET

Decrease dietary cholesterol
Reduce intake of organ meat eg liver heart brains kidney to
fortnightly

Decrease total fat/oil

Grill/steam/boil/bake/microwave to reduce use of oils and fats

Reduce use of saturated fat

Eg butter, full cream milk, santan

Increase use of polyunsaturated oils

Eg olive/sunflower/corm/palm/soybean/peanut oils

Increase intake of complex carbohydrates and fiber

Eg rice, bread, pasta, fruits, vegetables

Choose food high in protein and low in saturated fat

Eg fish, tofu, egg whites, peas and beans, dhal

ELEVATED TG
Once LDL-C achieved, next target is TG <1.7mmol/L
Borderline high TG (1.7 2.3 mmol/L)
Lifestyle changes

High TG (2.3 - 5.7mmol/L)

Lifestyle changes
+ intensify statin therapy if LDL-C target not achieved or add
fibrate as combination therapy

Very high TG (>5.7mmol/L)

If >10mmol/L: treatment goal is to prevent acute pancreatitis

Start fibrate or nicotinic acid
Statins are not useful as a first line therapy
Levels of TG<2.3 mmol/L are acceptable for these individuals

COMORBID:
DIABETES MELLITUS
PRIMARY TARGET:
LDL-C <2.6mmol/L (<1.8mmol/L if established CVD)

SECONDARY TARGET
Non-HDL-C <3.4mmol/L (if TG >2.3mmol/L)
HDL-C >1.0mmol/L (male) and >1.2mmol/L (female)
TG <1.7mmol/L

Improvement of glycaemic control alone will not fully

correct atherogenic dyslipidaemia

Statins should be initiated in all individuals above the age of

40 years with T2DM regardless of baseline LDL-C

COMORBID:
CORONARY HEART DISEASE
Fasting lipid profile within 24 hours of hospitalization
Initiate statin regardless of baseline LDL-C and diet
modifications and continue indefinitely
Re-test lipids 2-3 months after the start of statin therapy
LDL-C target <2.0mmol/L
All cardiac patients post-revascularization should be on long
term statin therapy, the dose adjusted to achieve target lipid
levels
Irrespective of baseline LDL-C level, statin therapy reduces risk
of major cardiovascular events by 24%

COMORBID:
HYPERTENSION
Hypertensive individuals without established CVD but
with moderate to high CV risk (>10% risk of events in 10
years) should be considered for statin therapy
irrespective of baseline LDL-C levels
Effects of antihypertensive agents on lipid levels (eg high
dose thiazide increase TC, LDL-C and TG) are modest and
should not affect selection of antihypertensive agents

COMORBID:
STROKE
Association has been found between raised serum lipids
and risk of ischaemic stroke. Statins have been shown to
prevent ischaemic stroke in high risk individuals
In-hospital lipid testing should be performed in
individuals with ischaemic stroke and TIA
Lipid lowering therapy with statins should be considered
in all individuals with previous ischaemic stroke or
transient ischaemic attack

COMORBID:
CKD
Dyslipidaemia occurs in all stages of CKD, on dialysis, after renal
transplantation and in individuals with nephrotic syndrome
Risk of death from CVD is higher than risk of requiring renal
replacement therapy
Individuals with CKD and those on dialysis: elevated TG, low HDL-C
In nephrotic syndrome: elevated TC and LDL-C
If TG >5.7mmol/L: initiate low dose fibrates cautiously to prevent
pancreatitis
Omega 3 fish oils 4g/d may also be used
Statins are safe in CKD whereas fibrates have a higher risk of
causing rhabdomyolysis