Clinical Practice Guideline Malaysia:

MANAGEMENT OF DYSLIPIDEMIA
2017
(A focus on updates and overview)

Name : Tan Yin Xin

Perceptor : Pn Nurul Adilah Abdul Mutalib
Rotation : PRIC (9th April – 4th May 2018)
Introduction
Introduction

According to the National Health and Morbidity Surveys (NHMS),

Prevalence increases with age

18-19 year old 55-59 year old

Dyslipidaemia refers to:

• Total cholesterol (TC) > 5.2 mmol/L
• HDL-Cholesterol (HDL-C) < 1.0 mmol/L (males) < 1.2 mmol/L
(females)
• Triglycerides (TG) > 1.7 mmol/L
• LDL-cholesterol (LDL-C) levels - depend on patient’s CV risk
Reference: CPG Malaysia on dyslipidaemia 2017
Measurement of Lipids and
Apolipoproteins
 the 2011

measured
2017 Measurement of lipids
Measurement of lipids and apolipoprotein

Photo sourced from Pharmacotherapy Handbook (2018)

Classification of Dyslipidaemia
Classification of Dyslipidaemia

Renal Hepatic

Drug Lifestyle
factor
Secondary
Primary

Metabolic/
endocrine
Classification

Reference: CPG Malaysia on dyslipidaemia 2017

Global Cardiovascular Risk
Assessment
use

2011

n Risk stratification
rst 2017
arent
Estimation of 10 Year CVD Points for MEN (Framingham Point Scores)
Estimation of 10 Year CVD Points for WOMEN (Framingham Point Scores)
Target Lipid Levels
 2011

Target Lipid Levels

2017
LDL-C Goals
Pathophysiology
 Atherogenesis

Photo sourced from Understanding pathophysiology (2008)

 Cholesterol transport in the tissue

Photo sourced from Rang and Dale’s pharmacology (2014)

Management of Dyslipidaemia
HMG CoA Reductase Inhibitors (Statins)

Photo sourced from Lippincott’s pharmacology (2012)

HMG CoA Reductase Inhibitors (Statins)

What to Monitor?

Initiation and Measure at 1 to 3

following a months
change in dose
Response to
therapy

Maintain same Repeat at 6 to 12

dose month intervals

Reference: CPG Malaysia on dyslipidaemia 2017

HMG CoA Reductase Inhibitors (Statins)

Safety/
Liver function
adverse effect

Hepatic transaminases
Measure on

Baseline 1 to 3 months a change

after starting in dose
treatment

When transaminase levels (especially ALT) are > 3 times the

upper limit of normal (ULN) on 2 occasions, stop the drug

Reference: CPG Malaysia on dyslipidaemia 2017

HMG CoA Reductase Inhibitors (Statins)

Suspected statin myopathy

Discontinue for 2-3 weeks

Unresolved Symptoms Resolved

• Unlikely to be statin • Lower dose/ decrease

related frequency to less than
• Continue on same daily.
dose of statin • Treat with the highest
tolerable dose of
statin + cholesterol
absorption inhibitor
Reference: CPG Malaysia on dyslipidaemia 2017
Cholesterol Absorption Inhibitors

How it works?
selectively blocks intestinal absorption of both dietary and
biliary cholesterols and other phytosterols -> ↓ delivery of
intestinal cholesterol to liver

Adverse effect?
Moderate elevations of liver enzymes and muscle pain.

Example?
Ezetimibe

Reference: CPG Malaysia on dyslipidaemia 2017

PCSK 9 inhibitor

How it works?
Inhibits binding of PCSK9 to the LDL-receptors -> ↓ degradation
of the LDL-receptors -> higher LDL-receptors density at the cell
surface -> ↑clearance + ↓ LDL-C levels

Side effects?
Injection-site swelling, flu-like symptoms, nausea, joint pains

Possible indications as add on therapy?

• high CV risk individuals who have persistently elevated LDL-C
despite optimum lipid-modifying therapy
• familial hypercholesterolemia

Example?
Evolocumab, alirocumab
Reference: CPG Malaysia on dyslipidaemia 2017
Fibric Acid Derivatives (fibrates)

Limitation?
treatment of patients with very
high TG levels who do not
respond to non-
pharmacological measures

Example?
Fenofibrate, gemfibrozil

Reference: CPG Malaysia on dyslipidaemia 2017

Photo sourced from Lippincott’s pharmacology

(2012)
Bile Acid Sequestrants (Anion exchange resins)

Adverse effect?
Gastrointestinal

Precaution?
Other medications should
be taken 1 hour before
and/or 4 hours after resins.

Reference: CPG Malaysia on dyslipidaemia 2017

Photo sourced from Lippincott’s pharmacology (2012)

Nicotinic acid (Niacin)

Indication?
Alternative therapy to
fibrates in individual with
elevated TG not responsive
to non-pharmacological
method

Reference: CPG Malaysia on dyslipidaemia 2017

Photo sourced from Lippincott’s pharmacology

(2012)
Prevention of Dyslipidaemia
Primary prevention

Healthy Lifestyle

1. All individuals > 30 years old

2. Individuals at high risk of
developing CVD > 18 years
old

Reference: CPG Malaysia on dyslipidaemia 2017

Secondary prevention

High intensity statin therapy

irrespective of baseline cholesterol levels

on admission in all prior to PCI and CABG and

individuals with ACS continued indefinitely

Lipid lowering therapy with statins should be considered in

all individuals with previous non cardioembolic ischaemic
stroke or transient ischaemic attack.

Reference: CPG Malaysia on dyslipidaemia 2017

Management in Specific Condition
Management in specific condition

Asymptomatic
Atherosclerotic Disease

Hypertension Initiate statin Heart Failure

Diabetes Mellitus Renal Disease

Reference: CPG Malaysia on dyslipidaemia 2017

Management in Specific Groups
Management in specific group

Goals of lipid lowering therapy

Women is similar in both gender and
elderly (depends on CV risk)

• Start at lower dose and

Elderly titrate cautiously
• Consider co-morbidities

Children and May have genetic dyslipidaemia

adolescent if lipid level ↑↑

Reference: CPG Malaysia on dyslipidaemia 2017

References
References

1. Clinical Practice Guideline Malaysia: management of

dyslipidaemia 5th Ed (2017)
2. Clinical Practice Guideline Malaysia: management of
dyslipidaemia 4th Ed (2011)
3. DiPiro C, Schwinghammer T, DiPiro J, Wells B. Pharmacotherapy
handbook. 10th ed. 2018.
4. Clark M, Finkel R, Rey J, Whalen K. Lippincott's illustrated
reviews. 5th ed. Wolters Kluwer; 2012.
5. Rang H, Dale M. Rang and Dale's pharmacology. 7th ed.
Edinburgh etc.: Elsevier/Churchill Livingstone; 2014.
6. Huether S, McCance K. Understanding pathophysiology. St.
Louis: Elsevier / Mosby; 2008.
Thank you