MOH/P/PAK/277.

14 (GU)
Statement of Intent

This clinical practice guidelines (CPG) is meant to be a guide for clinical

practice, based on the best available evidence at the time of development.
Adherence to these guidelines may not necessarily guarantee the best
outcome in every case. Every health care provider is responsible for the
management of his/her patient based on the clinical picture presented by
the patient and the management options available locally.

Period of validity
This CPG was issued in 2014 and will be reviewed in 5 years or sooner if new
evidence becomes available.

CPG Secretariat
c/o Health Technology Assessment Unit
Medical Development Division
Ministry of Health Malaysia
4th Floor, Block E1, Parcel E
62590, Putrajaya.

Electronic version available on the following website:

http://www.moh.gov.my http://wwtttamed.org.my

This is an update to the Clinical Practice Guidelines on Heart Failure (published 2000
and 2007). This CPG supersedes the previous CPG’s on Heart Failure (2000,2007).

1
 Message From The Director
General Of Health

Heart Disease is an important cause of morbidity and mortality in Malaysia.

Most patients who survive a myocardial infarction or develop hypertension,
will eventually develop heart failure. With ageing of the population, the
prevalence of heart failure is expected to increase. Thus the publication
of this Clinical Practice Guidelines on Heart Failure by the National Heart
Association of Malaysia, Academy of Medicine and Ministry of Health is
important and timely.

This Guidelines updates all health care providers on the latest developments
in the field of Heart failure. This is the 3rd edition of the Clinical Practice
Guidelines. As in previous editions, it uses an evidence based approach
and grades each recommendation accordingly thus allowing the physician
in charge to apply the latest technology, knowledge and standard of care
in the management of his or her patient. It provides a choice of therapy
and thus allows the healthcare provider to adapt this to the local situation
wherever possible.

For this Clinical Practice Guidelines to be a success, it must be acceptable to

our local setting and must be used widely.

Lastly, I would like to commend the Expert Committee for their hard work
and effort in updating the guidelines for the benefit of all practicing
physicians.

Datuk Dr. Noor Hisham Abdullah

(Director General of Health Malaysia)

2
Members Of The Expert Panel

Chairperson:
Dr. Jeyamalar Rajadurai Consultant Cardiologist,
Subang Jaya Medical Center

Members
(in alphabetical order)
Dr. David Chew Consultant Cardiologist,
Institute Jantung Negara

Dr. Hasri Samion Consultant Paediatric Cardiologist,

Institute Jantung Negara

Dr. Kannan Pasamanickam Consultant Cardiologist,

Subang Jaya Medical Center

Dr. Mohd Rahal Yusof Specialist in Internal Medicine,

Hospital Kuala Lumpur

Dr. Nik Mazlina binti Mohammad Family Medicine Specialist,

Klinik Kesihatan Kajang

Dr. Robaayah Zambahari Senior Consultant Cardiologist,

Institute Jantung Negara

Dr. Sim Kui Hian Consultant Cardiologist,

Pusat Jantung Hospital Umum Sarawak

Dr. Sree Raman Senior Consultant Physician,

Tuanku Ja’afar Hospital Seremban

Dr. Wan Azman Wan Ahmad Consultant Cardiologist,

Pusat Perubatan Universiti Malaya

3
 List Of External Reviewers
(in alphabetical order)

Dr. Aris Chandran Senior Consultant Physician,

Hospital Raja Permaisuri Bainun Perak

Dr. Alan Fong Consultant Cardiologist,

Pusat Jantung Hospital Umum Sarawak

Dr. Nik Sherina Famliy Medicine Specialist,

Rawatan Utama Pusat Perubatan Universiti Malaya

Dr. Mimi Omar Family Medicine Specialist,

Klinik Kesihatan Kelana Jaya Kuala Lumpur

Dr. Wong Kai Fatt General Practitioner,

Klinik Tan Kuala Lumpur

Dr. Santha Kumari Senior Consultant Physician,

Hospital Tengku Ampuan Rahimah Selangor

Dr. Liew Houng Bang Consultant Cardiologist,

Hospital Queen Elizabeth II Sabah

Dr.Mohd Nizam Mat Bah Consultant Paediatric Cardiologist,

Hospital Sultanah Aminah Johor

Dr. Hung Liang Choo Consultant Paediatrician & Paediatric Cardiologist

Paediatric Institute Hospital Kuala Lumpur

4
Rationale and Process of Guidelines
Development

Cardiovascular disease is an important cause of morbidity and mortality in

Malaysia. Heart Failure (HF), the end stage of most diseases of the heart,
is a common medical problem encountered in general practice and is an
important cause of hospital admissions. With aging of the population the
prevalence of HF is expected to increase.

The 1st Clinical Practice Guidelines (CPG) in HF was published in 2000 with
the 2nd edition in 2007. This current document is an update of the last
edition. Since then, there have been many new developments in this field.
Thus the publication of this 3rd edition is timely.

This CPG was drawn up by a committee appointed by the National Heart

Association of Malaysia and Ministry of Health. It comprises cardiologists,
family and general physicians from the government, private sectors and
the public Universities.

Objectives:
The objectives of this CPG are to assist the health care provider in:
• the prevention of HF
• the diagnosis and treatment of HF
• reducing the morbidity associated with the condition and
improving the quality of life of these patients
• improving survival of patients with HF

Process:
The previous CPG published in 2007 was used as a base. In addition to the
previous clinical questions that needed to be updated, the Expert Panel
formulated new questions that needed to be addressed. These clinical
questions were then divided into sections and each member was assigned
one or more topics.

A review of current medical literature on HF from 2007 (the date of the

last CPG) till 30thSeptember 2013 was performed. Literature search
was carried out using the following electronic databases – PubMed and
Cochrane Database of Systemic Reviews.The following MeSH terms or free
text terms were used either singly or in combination:

“Heart Failure”, “Congestive cardiac failure”, “Acute Heart Failure,

“Chronic Heart Failure” “Right heart failure”, “left heart failure”, [MeSH],
“Heart Failure Reduced Left Ventricular Function” , Heart Failure Preserved
Left Ventricular Function”[MeSH]

5
 The search was filtered to clinical trials and reviews, involving humans and
published in the English language. The relevant articles were carefully
selected from this huge list. In addition, the reference lists of all relevant
articles retrieved were searched to identify further studies.Experts in the
field were also contacted to obtain further information. International
guidelines on HF-the American Heart Association/American College of
Cardiology and European Society of Cardiology - were also studied. All
literature retrieved were appraised by members of the Expert Panel and
all statements and recommendations made were collectively agreed by the
group. The grading of evidence and the level of recommendation used in
this CPG was adapted from the American College of Cardiology/ American
Heart Association and the European Society of Cardiology (pg 6).

After much discussion, the draft was then drawn up and submitted to the
Technical Advisory Committee for Clinical Practice Guidelines, Ministry of
Health Malaysia and key health personnel in the major hospitals of the
Ministry of Health and the private sector for review and feedback.

Clinical Questions Addressed:

• How do you make a diagnosis of HF?
• Who are individuals at high risk of developing HF and how do you
prevent them from developing HF?
• How do you treat acute and chronic HF effectively using current
knowledge and available resources?
• How do you prevent recurrent admissions for acute decompensated HF
• How do you treat the following special groups?
- the asymptomatic individual with reduced left ventricular (LV) function.
- the individual with HF due to preserved LV function
- the pregnant patient with HF
- infants and children with HF
- the individual with refractory and terminal HF

Target Group:
This CPG is directed at all healthcare providers treating patients with
HF - general practitioners, general and family physicians, both adult and
paediatric cardiologists and obstreticians.

Target Population:
It is developed to treat all adults, pregnant women and children with HF.

Dr. Jeyamalar Rajadurai

Chairperson

6
Levels of Evidence and Grades of
Recommendations

Grades Of Recommendation

A Data derived from multiple randomized clinical trials or meta

analyses

B Data derived from a single randomized clinical trial or large

non randomized studies

C Only consensus of opinions of experts, case studies or standard of care

Levels Of Evidence

I Conditions for which there is evidence and/or general agreement that

a given procedure/therapy is beneficial, useful and/or effective.

II Conditions for which there is conflicting evidence and/or divergence

of opinion about the usefulness/efficacy of a procedure/therapy.

II-a Weight of evidence/opinion is in favor of its usefulness/efficacy.

II-b Usefulness/efficacy is less well established by evidence/opinion.

III Conditions for which there is evidence and/or general agreement

that a procedure/ therapy is not useful/effective and in some cases
may be harmful.

Adapted from the American Heart Association and the European Society of Cardiology

(Available at: http://assets.cardiosource.com/Methodology_Manual_for_ACC_AHA_Writing-_Committees and at

http://www.escardio.org/guidelines-surveys/escguidelines/about/Pages/rules-writing.aspx).

7
 Summary
• Heart Failure (HF) is a clinical diagnosis. To satisfy the definition of HF,
symptoms, signs and/or objective evidence of cardiac dysfunction must
be present. (see Fig 1, pg 9)
• HF may occur in the presence of reduced left ventricular (LV) function,
the left ventricular ejection fraction (LVEF) ≤ 40% (HFrEF) or with normal
LV function, the LVEF ≥ 50% (HFpEF). If the LVEF is 41% - 49% it is called
HFpEF, borderline.
• It may be classified as Acute HF or chronic HF depending on the acuteness
of the clinical presentation.
• It is important to determine and treat the underlying etiology. Common
causes are coronary artery disease and hypertension.
• Prevention and early intervention wherever appropriate, should be the
primary objective of management.
• For the management of Acute HF and Chronic HF and grades of
recommendations, see Flow Chart I, pg 10 and Table 1, pg 11 and Flow
chart II, pg 12 and Table 2, pg 13 respectively
• Non pharmacological measures involves counseling the patient and
family about the disease, diet and fluid intake, regular exercise and
appropriate lifestyle changes such as smoking cessation and abstinence
from alcohol.
• Performance measures should be instituted to assess quality of care.

8
Figure 1 : Algorithm for the diagnosis of Heart Failure
or LV dysfunction

Suspected Heart
Failure because of
symptoms/sign

ECG
Chest Radiograph
Natriuretic Peptides
(where available)

Test normal but Test normal but

Tests abnormal clinical suspicion high clinical suspicion low

Echocardiography

Tests abnormal Tests normal

Determine : Additional diagnostic Heart Failure or LV

• Underlying cause tests where approprate dysfunction unlikely.
• Severity (eg: Coronary Consider other
• Precipitating Factors Angiography, Nuclear diagnosis such as:
• Type of LV Imaging & CMR) • coronary artery
Dysfunction disease (angina
(systolic +/- diastolic) equivalent)
• pulmonary disease
• obesity

Treat accordingly

9
Flowchart I : Management of Acute HF
Acute Heart Failure (HF)

• Oxygen
• IV Diuretics

Blood Pressure*

SBP ≥ 100mmHg Arrhythmia Present SBP < 100mmHg

• Nitrates Treat accordingly • Noradrenaline

(in the absence of (first line)
valvular stenosis) • Dopamine (next)
• Morphine

Improved No Improvement SBP ≥ 100mmHg SBP > 100mmHg

**Oral • Diuretics, continous infusions

Medications + Combination with thiazides
• Nitrates
• low dose dopamine
• dobutamine

Improved No Improvement

**Oral • Correct hypoxia and acidosis

Medications • Consider invasive ventilation
• refer to tertiary centres
NOTE:
* It is important to look for tissue hypoperfusion - cool peripheries, sweating, low volume pulse,
decreasing urine output
** Flow Chart II

From onset, evaluate to identify correctable/reversible lesions

Special situations: Myocardial ischaemia / infarction: Treat accordingly
Hypertension: Control BP quickly
Valvular heart disease: Corrective surgery/balloon valvuloplasty
Refer :
• section 7.1 for drug details and table V for dosages
• section 8.2 for guidelines for referral to tertiary cardiac centres

10
Table I : Grading of Recommendations in the Management of Acute HF

Intervention Grades of Level Of Comments

Recommendation Evidence

Initial Management Consists Of :

Maintain the oxygen
Oxygen I C saturation above 95%

Indicated for fluid

Diuretics I B retention

Contraindicated if SBP
<100mmHg. Use with
Nitrates I B caution in valvular
stenosis.

Indicated in pts
Morphine IIb B who are dyspnoeic
and restless

Not Responsive To Initial Treatment And Sbp≥100mmHg

Continuous infusion;
combination with
Diuretics IIa B nitrates, dopamine,
dobutamine or
thiazide

Dopamine IIa B To improve renal

(<2-3μg/kg/min) perfusion and
promote diuresis

Indicated for
peripheral
Dobutamine IIa B hypoperfusion +/-
pulmonary congestion

Not Responsive To Initial Treatment And Sbp<100mmHg

Noradrenaline IIa B Indicated to increase
the BP
Dopamine IIb B Indicated to increase
(>5μg/kg/min) the BP
Indicated as a bridge
IABP I B till myocardial
recovery or heart
transplant
Indicated as a bridge
Ventricular Assist IIa B till myocardial
Device (VAD) recovery or heart
transplant

11
 Flowchart II: Optimizing Drug Therapy in Chronic HF
Signs & Symptoms Of
Volume Overload

No Yes

• ACE-I(or ARB if ACE-I • ACE-I(or ARB if ACE-I

intolerant) intolerant)
• β-blockers • Diuretics

Clinical Improvement

No Yes

Add: Continue with:

• MRA • Diuretics: low maintenance dose
• Consider β-blocker • ACE-I/ARB: titrate to max tolerated dose
If no pulmonary congestion • + β-blocker

Clinical Improvement

No Yes

Add: Continue with:

• Digoxin • Diuretics
• And/or ivabradine (if sinus • ACE-I / ARB
rhythm & HR > 70bpm • MRA
(if not already on)
• + β-blocker

Clinical Improvement

No Yes

See flowchart I (pg10) Continue with:

(Consider referral to tertiary cardiac centres) • Diuretics
• Loop diuretics + thiazides • ACE-I / ARB
• Short term parenteral positive inotropes • MRA
• Consider if suitable:
• Digoxin
> CRT
> IABP • and/or ivabradine
> VAD • + β-blocker
> Cardiac transplant
Refer :
• section 7.2.2 for drug details and table S VI-IX for dosages
• section 8.2 for guidelines for referral to tertiary cardiac centres
12
 Table II: Grading of Recommendations in the Management of
Chronic HF
Intervention Grades of Levels of Comments
Recommendation Evidence

Indicated For Fluid Retention In NYHA II - IV

Not shown to improve
Diuretics I B survival.

Indicated In All Patients

Improves survival and delays
ACE-I I A progression in all classes
of HF

ARB I A In ACE-I intolerant patients

Improves survival and delays

β-blockers I A progression in all classes
of HF

In Addition To The Above , The Following Are

Indicated In Selected Patients
In pts post MI and
ARB I B LVEF<40%,Valsartan
shown to be comparable to
captopril
Mineralocorticoid Improves survival and
receptor reduces hospitalizations in
antagonists I B moderate to severe HF and
(Spironolactone, in post MI pts with mild HF
Eplerenone)

I B In pts with HF and AF

No effect on survival.
Digoxin Reduces hospitalizations
IIa B when added to optimal
medical therapy
Reduces hospitalizations
when added to optimal
Ivabradine IIa B medical therapy in patients
in sinus rhythm and heart
rate > 70bpm

Improves survival in pts with

I A resuscitated cardiac arrest,
VF or sustained VT
ICD (implantable Improves survival in pts > 40
cardioverter I A days post MI, LVEF ≤30%, on
optimal medical treatment,
defibrillator) and in NYHA II or III

Improves survival in pts (no

IIa B prior MI), LVEF ≤ 35%, on
optimal medical treatment,
and in NYHA II or III

Improves survival in pts on

CRT (cardiac optimal medical treatment,
resynchronization I A in NYHA III, in sinus rhythm
and who have cardiac
therapy) dyssynchrony.

13
Table Of Contents
Statement of intent 1
Message from the Director General of Health 2
Members of the Expert Panel 3
List of External Reviewers 4
Rationale and process of guideline development 5-7
Summary 8
Algorithm and Flow Charts 9 - 11
Grades of recommendations & levels of evidence 12 - 13
Table of content 14
1. INTRODUCTION 15
2. DEFINITION 15
3. PATHOPHYSIOLOGY 15 - 16
4. AETIOLOGY 17
5. DIAGNOSIS 18 - 20
6. PREVENTION 20 - 22
7. MANAGEMENT
7.1 Acute Heart Failure 23 - 30
7.2 Chronic Heart Failure
7.2.1 Non Pharmacological Measures 30 - 32
7.2.2 Pharmacological Management 32 - 38
7.2.3 Device Therapy In Heart Failure 39 - 40
7.2.4 Surgery for Heart Failure 40 - 41
7.2.5 Heart Transplantation 41
7.3 Special Groups
7.3.1 Asymptomatic Left Ventricular Dysfunction 42 - 43
7.3.2 Heart Failure With Preserved Left 43 - 45
Ventricular Systolic Function
7.3.3 Heart Failure in Pregnancy 45 - 48
7.3.4 Heart Failure in Infants and Children 48 - 53
7.3.5 Refractory Heart Failure 53
7.3.6 End of Life Care 54
7.3.7 Terminal Heart Failure 54
8. ORGANIZATION OF CARE
8.1 Monitoring and Follow Up 54 - 55
8.2 Cardiology Referral 55
8.3 Heart Failure Clinics 56
9. FUTURE DEVELOPMENT 56
10. PERFORMANCE MEASURES 56 - 57
11. IMPLEMENTING THE GUIDELINES AND RESOURCE IMPLICATIONS 57
APPENDIX 58 - 60
REFERENCES 61 - 71
ACKNOWLEDGEMENTS 72
DISCLOSURE STATEMENT 72
SOURCES OF FUNDING 72
1. Introduction
Heart failure (HF) is a clinical syndrome and represents the end stage
of most heart diseases. The prevalence of HF varies between 3-20
per 1000 population, although in persons over the age of 65 years, it
could be as high as 100 per 1000 population1.

Coronary Artery Disease (CAD) and Hypertension (HTN) are the main
causes of HF among adults in Malaysia accounting for almost 70%
of all cases.2 This is similar to that noted in Western countries.3 The
prognosis for HF remains poor. The one year mortality rate varies
between 5% to 52% depending on the severity and the presence
of co-morbidity.4,5 In a large community based study, about 40% of
individuals with HF died within a year of initial diagnosis.6 HF is an
important cause of hospitalization accounting for about 6% - 10%
of all acute medical admissions in Malaysia.2,7 It is also an important
cause of hospital re-admissions. About 25% of patients with HF are
readmitted within 30 days for acute decompensation.8,9 Therefore HF
poses a major health and economic burden.

This guidelines provides evidence based recommendations to help

health care providers in the management of their patients with HF.
Patient care should however be individualized and sound clinical
judgement plays an important role in decision making.

2. Definition
HF is an abnormality of cardiac structure or function leading to an
impairment of ventricular filling or ejection of blood. It is a clinical
syndrome in which patients have typical symptoms (e.g. breathlessness,
ankle swelling and fatigue) and signs (e.g. elevated jugular venous
pressure, ankle edema, pulmonary crackles, and displaced apex beat).
Occasionally some patients may present without signs or symptoms of
volume overload.

3. Pathophysiology
HF may be the result of any disorder of the endocardium,
myocardium, pericardium or great vessels although commonly, it
is due to myocardial dysfunction. Myocardial contractility is often
reduced resulting in heart failure with reduced ejection function
(HFrEF). Occasionally, myocardial contractility may be preserved and
left ventricular ejection fraction (LVEF) is normal, the symptoms being
due to diastolic dysfunction ie heart failure with preserved ejection
fraction (HFpEF).Often patients with a reduced LVEF have features of
diastolic dysfunction as well. (Table III,pg 16)

15
 3.1 HFrEF
In HFrEF, cardiac output is reduced due to depressed myocardial
contractility. This initiates a complex pathophysiological process which
includes haemodynamic alterations and structural changes within the
myocardium and vasculature. Activation of the neurohumoral systems
such as the sympathetic nervous system and the renin-angiotensin-
aldosterone system, play a pivotal role in this process.

3.2 HFpEF
Up to 50% of patients presenting with HF have normal systolic
function (LVEF≥50%) with predominantly diastolic dysfunction.10,11.12
Diastolic dysfunction leads to impaired left ventricular (LV) filling
due to decreased relaxation (during early diastole) and/or reduced
compliance (early to late diastole) leading to elevated filling pressures.
These haemodynamic changes lead to clinical symptoms and signs
similar to those of HFrEF.

Many different classifications of HF have been used to emphasize

some aspect of the condition. For practical purposes, it may be
sufficient to classify HF into:
• Acute heart failure (Acute HF)
• Chronic heart failure (Chronic HF)

Acute HF is defined as the rapid onset of symptoms and signs of HF

due to an acute deterioration of cardiac function. Chronic HF is the
chronic state when patients have stable symptoms. In these patients
an acute precipitating or aggravating factor(s) may cause acute
cardiac decompensation.

Older terms such as congestive cardiac failure may be used if patients

present with both right and left ventricular fluid overload.

Table III : Pathophysiological Classification of Heart Failure (HF)

Classification LVEF(%)
I. Heart Failure with Reduced Ejection Fraction (HFrEF) ≤40%
II. Heart Failure with Preserved Ejection Fraction 41-49%
(HFpEF),borderline
III Heart Failure with Preserved Ejection ≥50%
Fraction (HFpEF)

16
4. Aetiology
Heart failure is not a complete diagnosis. It is important to identify the
underlying disease and the precipitating cause(s), if present. Although
systolic and diastolic dysfunction are separate pathophysiological
entities, they often share common aetiologies.

The most common underlying causes of HF in adults are:

• Coronary artery disease
• Hypertension

Slightly less common causes include:

• Dilated cardiomyopathy-idiopathic, familial
• Valvular heart disease
• Diabetic cardiomyopathy

Other causes of HF include:

• Congenital heart disease
• Cor pulmonale
• Pericardial disease: constrictive pericarditis, cardiac tamponade
• Hypertrophic cardiomyopathy
• Viral myocarditis
• Acute rheumatic fever
• Toxic: Alcohol, adriamycin, cyclophosphamide
• Endocrine and metabolic disorders: thyroid disease, acromegaly,
phaechromocytoma
• Collagen vascular disease: systemic lupus erythematosis,
polymyositis, polyarteritis nodosa
• Tachycardia induced cardiomyopathy
• Miscellaneous
- severe anemia
- peripartum cardiomyopathy
- large A-V shunts
- stress (Takotsubo) cardiomyopathy

Patients with Chronic HF may occasionally develop acute

decompensation. Factors that can contribute to this Acute HF are
listed in Table IV,pg 23. The more important causes are:
• Acute myocardial infarction/myocardial ischemia
• Arrhythmias (e.g. atrial fibrillation)
• Uncontrolled Blood Pressure
• Infections (e.g. pneumonia)
• Non-compliance to medications
• Excessive fluid and salt intake
• Anemia
• Development of renal failure
• Adverse effects of drug therapy (e.g. Non Steroidal Anti
Inflammatory Drugs)

17
 5. Diagnosis (See Figure 1, pg 9)
There is no single diagnostic test for HF because it is a clinical diagnosis
based on a careful history and physical examination.

The clinical suspicion of HF should be supported by objective evidence

of cardiac dysfunction. Breathlessness with orthopnoea, paroxysmal
nocturnal dyspnoea (PND), reduced exercise tolerance and ankle
swelling are the characteristic symptoms of HF.

Signs which are more specific for HF are an elevated jugular venous
pulse (JVP), third heart sound, laterally displaced apical impulse in
the presence of a cardiac murmur. Other supportive signs include
peripheral edema, tachycardia, narrow pulse pressure, pulmonary
crepitations, hepatomegaly and ascites. The presence of jugular
venous distension and a third heart sound are associated with
adverse outcomes.13 A fourth heart sound is more frequent in
patients with HFpEF.

These symptoms and signs are sometimes difficult to interpret in

the elderly, the obese and in patients with chronic lung disease.
The clinical signs may resolve completely following medical therapy,
making the findings at presentation essential for the diagnosis.14
Occasionally symptoms and signs of volume overload may be absent
and the patient may present with fatigue only.

Exercise capacity is assessed by the New York Heart Association

(NYHA) functional classification. (Appendix I,pg 57)

Once the diagnosis of HF has been made, it is important to establish

the aetiology of the syndrome (see section 4,pg 17)

The diagnosis of HFrEF requires these conditions to be satisfied:

• Symptoms and signs typical of HF
• Objective evidence of reduced LVEF

In the diagnosis of HFpEF the requirements are:15,16

• Symptoms and signs typical of HF
• Objective evidence of a normal, non-dilated LV and/or evidence of
diastolic dysfunction
• Relevant structural heart disease (LV hypertrophy/LA enlargement)

18
Investigations
Basic investigations include:
• 12 lead ECG - to identify heart rate, heart rhythm, QRS morphology,
QRS duration, QRS voltage, evidence of ischaemia, LV hypertrophy
and arrhythmias
• Chest radiograph - to identify pulmonary congestion, cardiac size
and shape, and presence of other underlying lung pathology.
Patients with HFpEF may have a normal cardiac size.
• Blood tests - FBC, renal function, liver function, serum glucose,
lipid profile
• Urinalysis - evidence of proteinuria, glycosuria
Other important investigations include:
• Echocardiography : This will allow assessment of :
- LV chamber size, volumes and systolic function
- LV wall thickness, evidence of scarring and wall motion abnormality
- Diastolic function of the heart
- Valvular structure and function
- Congenital cardiac defects
- LV mechanical dyssynchrony
• Natriuretic peptides (Brain natriuretic peptide (BNP) or N-terminal
pro BNP (NTproBNP)
BNP or NTproBNP are a family of hormones secreted by the ventricles
in response to wall stress. They are useful in 2 situations :
- In the emergency setting, it is a useful “rule out” test for patients
presenting with acute dyspnea. A level of <100pg/ml for BNP
and <300pg/ml for NTproBNP makes the diagnosis of acute HF
unlikely.17,18,19 Levels of natriuretic peptides increase with age,
but is reduced in obesity.
- A high level supports the diagnosis of acute HF and very high
levels correlate with the severity of HF and adverse outcomes.
Additional investigations when indicated;
• Blood tests:
- serum cardiac biomarkers (troponins, creatine kinase (CK), creatine
kinase-myoglobin band (CKMB) - to look for myocardial necrosis)
- thyroid function tests
- C-reactive protein (to look for inflammation)
• Tests for myocardial ischemia and/or viability:
- treadmill exercise test
- stress echocardiography (exercise or pharmacological)
- radionuclide studies
- cardiac magnetic resonance imaging (CMR)
• Invasive tests:
– coronary angiography
– cardiac catheterization
– endomyocardial biopsy

19
 • Others:
- Holter electrocardiography, loop recorders and long-time ECG
Recording
- pulmonary function tests

Key Message:
• To satisfy the definition of HF, symptoms, signs and/or
objective evidence of cardiac dysfunction must be present.

6. Prevention
Prevention of HF should always be the primary objective of
management. It is directed at individuals:
• at high risk of developing cardiac disease
• with cardiac disease but who still have normal myocardial function
• who have impaired myocardial function but who do not as yet
have signs or symptoms of HF

6.1 Individuals who are at high risk of developing HF/CAD but who
do not as yet have structural heart disease. These include individuals
with:
• multiple risk factors for developing CAD or who already have
evidence of atherosclerotic disease in other vascular beds
(e.g. cerebral, peripheral vascular disease)
• hypertension
• diabetes
• the metabolic syndrome
• severe hyperlipidemia
• a family history of cardiomyopathy
• thyroid disorders
• renal disease
• cardiotoxins – excessive alcohol consumption, chemotherapeutic agents
• sleep-disordered breathing especially obstructive sleep apnoea
130/80 in high risk hypertensive patients. 140/90 in most hypertensive patients
In these individuals the following measures should be taken:
I, A • Treating hypertension to target levels-This has been shown to
reduce the incidence of HF by as much as 50%.20 The elderly have
an absolute risk reduction of 1.5-2.5% in the incidence of HF over
a period of 2-4 years and in those over the age of 80 years, there is
a 64 % reduction in new onset HF.21-24
I, B • Smoking cessation-Current smokers have a higher risk of HF
compared to non-smokers and ex-smokers.25 Quitting smoking
appears to have a substantial and early effect (within two years) on
decreasing morbidity and mortality in patients with left ventricular
dysfunction, which is at least as large as proven drug treatments
recommended in patients with left ventricular dysfunction.26

20
• Treating lipids to goal in all individuals to prevent cardiovascular I, A
disease. Even low risk individuals benefit from statin therapy
although the use of pharmacotherapy for primary prevention should
be individualized.27,28 (See 4th Ed. Malaysian CPG on Dyslipidemia,
2011)
• Optimizing the control of diabetes- Diabetes, especially in the I, B
presence of poor glycemic control, has been shown to increase the
risk of HF independent of co-existing hypertension and/or CAD.29-31
However there has been no evidence that intensive diabetic control
will prevent HF.
• Managing the metabolic syndrome appropriately with treatment of I, C
risk factors to target goals.
• Detecting and treating thyroid disease early to prevent thyroid heart I, C
disease.
• Stressing the importance of a healthy life style and avoiding behavior I, C
that could increase the risk of HF such as excessive alcohol intake.
• Regular physical exercise and maintenance of ideal body weight. I, B
• Reducing salt intake to<5gm/day32 I, B
• Studies on the prevention of HF by n-3 fatty acids have been IIa, B
mixed.33,34 A recent study in patients with multiple cardiovascular risk
factors or atherosclerotic vascular disease who had no previous MI,
showed that n-3 fatty acids did not reduce cardiovascular mortality
and morbidity.35
• When administering potentially cardiotoxic chemotherapy, monitor IIa, C
regularly for deteriorating LV function.
Small studies with β-blockers and angiotensin converting enzyme IIb, B
inhibitors (ACE-I) or angiotensin receptor blockers (ARB) have been
shown to prevent cardiotoxic cardiomyopathy.36,37 Treatment
currently has to be individualized.
• Obstructive sleep apnoea has been associated with HF although IIb, B
the use of Continuous Positive Airway Pressure (CPAP) has not been
shown to reduce the incidence of HF.38,39

6.2 Individuals with cardiac disease but who do not as yet have
evidence of myocardial dysfunction. In addition to that mentioned in
section 6.1, other strategies include:
• Early triage and appropriate treatment of patients with acute I, A
coronary syndrome.40-42
• Patients with CAD should be treated appropriately with antiplatelet I, A
agents,43-47 β-blockers,48,49 ACE-I50 and statins.51,52 These patients should
undergo coronary revascularization as indicated.
• Patients with hypertension and left ventricular hypertrophy (LVH) I, B
should have their blood pressure control optimized. Regression of
LVH has been shown to be associated with a lower incidence of new
onset HF.53

21
 I, B • Patients with haemodynamically significant valve disease should
undergo early intervention as indicated.54
I, C • Arrhythmias should be treated early and appropriately.55
I, C • Patients with congenital cardiac lesions should have these corrected
early whenever indicated.
These individuals should be regularly monitored for signs of HF, assessing
LV function and progression of the underlying structural cardiac disease
by clinical examination and appropriate investigations.
In addition to the measures stated above, the following have been
shown to help prevent HF:
I, A • ACE-I - have been shown to reduce the incidence of HF by 23%
in individuals with CAD and normal LV systolic function.20 These
medications also reduce new onset HF in patients with atherosclerotic
vascular disease 56,57, diabetes and hypertension with associated
cardiovascular risk factors.58
Ila, A • ARB - in patients with atherosclerotic vascular disease, diabetes
and hypertension with associated cardiovascular risk factors ARBs
have been shown to reduce cardiac events.59-62 These agents are
non-inferior to ACE-I and should be considered in ACE-I intolerant
patients.63
I, A • β-blockers - in patients post myocardial infarction (MI)64,65
I, A • Statins in patients with CAD27,51,66

6.3 Individuals with myocardial dysfunction but who do not as yet

have signs and symptoms of HF. (Asymptomatic Left Ventricular
Dysfunction) Measures include:
I, C • Treat the underlying cause wherever possible.
• Prevent progression to HF by modulating cardiac remodeling. See
section on the management of Asymptomatic Left Ventricular
Dysfunction (Section 7.3.1)

Key Message:
• Prevention and early intervention wherever appropriate,
should be the primary objective of management.

22
7.1 Acute Heart Failure
Acute heart failure (Acute HF) is described as the rapid onset, or rapid
worsening of the symptoms and signs of HF. The “rapidness” of the
deterioration in symptoms can be within hours to several days depending
on the cause of the Acute HF. It may present de novo (first presentation)
or more commonly, as a result of deterioration of a previously diagnosed
stable patient with HF.
The spectrum of clinical findings may range from worsening of peripheral
oedema to life threatening pulmonary oedema or cardiogenic shock.
Myocardial Infarction/Ischaemia is an important and common cause of
Acute HF. The other causes and factors contributing to decompensation
in patients with stable HF are as listed in Table IV.
Most patients with Acute HF would require hospitalization. The more I, C
ill patients should be managed in the Coronary Care Unit or High
Dependency Unit with continuous hemodynamic monitoring.

Table IV : Factors Contributing to Decompensation in a

Patient with Stable HF

Patient factors
• Non compliance to medications
• Dietary indiscretion especially salt and fluid intake
• Inappropriate medications e.g. NSAIDS and COX-2 inhibitors
• Alcohol consumption
Cardiac Causes
• Superimposed myocardial ischaemia or infarction (often
asymptomatic)
• Uncontrolled hypertension
• Arrhythmias
• Pulmonary embolism
• Secondary mitral or tricuspid regurgitation
Systemic Conditions
• Superimposed infections
• Anemia
• Thyroid disease
• Electrolyte disturbances
• Worsening renal disease

23
 Essential Investigations in Acute HF include:
• ECG
• Chest Radiograph
• Blood Investigations: hemoglobin, serum electrolytes, urea,
creatinine, cardiac biomarkers (troponin, CKMB, Natriuretic Peptides)
• Blood gases may be considered
• Echocardiography
Assessment and management must be made promptly and
simultaneously.
The principles of management are:
• Rapid recognition of the condition
• Identification and stabilization of life threatening hemodynamics
• Identification and treatment of the underlying cause and
precipitating/ aggravating factors
• Relief of clinical symptoms and signs
After initial clinical assessment of vital signs, treatment of Acute HF
should be instituted as outlined in Flowchart I,pg 10. For grading of
recommendations and levels of evidence, see Table I,pg 11.
Therapy (for dosages see Table V,pg 25)
The initial management includes a combination of the following
first line therapy:
l, C • Oxygen - Aim to achieve oxygen saturation of more than 95% in
order to maximize tissue oxygenation and to prevent end organ
dysfunction or multi organ failure.
Elective ventilation using non invasive positive pressure ventilation
(CPAP or Bi-level Positive Airway Pressure [BiPAP]) should be
considered early if necessary.67-70
lla, C Should the oxygen saturation be inadequate or the patient
develops respiratory muscle fatigue, then endotracheal intubation
and mechanical ventilation is necessary.
l, B • Frusemide – Intravenous (i.v.) frusemide 40 - 100mg. The dose
should be individualized depending on the severity of the clinical
condition.71
lla, B Administration of a loading dose followed by a continuous
infusion has been shown to be more effective than repeated
bolus injections alone in producing greater diuresis and weight
reduction.72-75 The dose should be titrated according to clinical
response and renal function. There is a lack of data on short term
mortality at present.75
l, B • Nitrates - If the BP is adequate (SBP > 100 mmHg), nitrates should
be considered.76-78 It should be administered intravenously. Patients
should be closely monitored for hypotension. This commonly
occurs with concomitant diuretic therapy.

24
 Studies have shown that the combination of i.v. nitrate and I, B
low dose frusemide is more efficacious than high dose diuretic
treatment alone.78
Extreme caution should be exercised in patients with aortic and mitral
stenosis. Nitrates are contraindicated in severe valvular stenosis.
• Morphine sulphate - i.v. 1- 3 mg bolus (repeated if necessary, up Ilb, B
to a maximum of 10mg). It reduces pulmonary venous congestion
although its effect on venodilation has actually been shown to be
minimal.79 It reduces anxiety and is most useful in patients who are
dyspnoeic and restless. Intravenous anti-emetics (metoclopramide
10mg or prochlorperazine 12.5mg) should be administered
concomitantly.
Morphine should be used with caution as some recent data seem
to indicate that it may actually do more harm.80,81 Care must be
exercised in patients with chronic respiratory disease.
An attempt should be made to identify the underlying cause and
precipitating factors e.g. acute myocardial infarction/myocardial
ischemia, valvular heart disease and hypertension. This would
enable the appropriate treatment to be instituted early.
Table V: Drugs Commonly Used in Acute HF
Route of Admin Dosages
Diuretics
Frusemide
IV 40mg-100mg
Infusion 5-20mg/hour (better than
intermittent very high
bolus doses)
Vasodilators
Nitroglycerin Infusion 5 – 200mcg/min
Isosorbide dinitrate Infusion 1 – 10mg/hr
Nitroprusside Infusion 0.1 – 5mcg/kg/min
Sympathomimetics
Dobutamine Infusion 2 – 20mcg/kg/min
Dopamine Infusion <2 – 3mcg/kg/min
- renal arterial vasodilation
2 – 5mcg/kg/min -
inotropic doses
5 – 15mcg/kg/min
- peripheral vasoconstriction
Noradrenaline Infusion 0.02 – 1mcg/kg/min till
desired blood pressure is
attained

25
 Response to drug therapy should be assessed continuously. Parameters
to assess during treatment include:
• symptoms and signs
• Vital signs
- oxygen saturation
- heart rate
- blood pressure
- respiratory rate
- urine output
- body weight
• Investigations
- renal function tests
- Serum potassium, sodium and magnesium
- Invasive haemodynamic monitoring (if necessary)
- pulmonary capillary wedge pressure, cardiac index
An adequate response would be reflected by an improvement in the
patient’s clinical condition, decrease in his heart rate, an improvement
in his oxygen saturation and urine output. Generally, a SBP ≥ 90mmHg
would be considered adequate if the patient feels well and has good
tissue perfusion as shown by the absence of giddiness, warm skin and
stable renal function with good urine flow.
In most cases of mild to moderate Acute HF the following measures
would suffice. If the patient fails to respond to the above therapy,
further management would depend upon the blood pressure and
tissue perfusion.

A) In the presence of an adequate blood pressure :-

l, B • Frusemide: i.v. frusemide infusion 5-20mg/hour. Combination of
a loop diuretic at low doses with nitrates is superior to high dose
diuretic therapy alone.78
lla, B Combination with:
lla, C - dopamine82
- dobutamine
are also more effective than increasing the dose of diuretic alone.
lla, B Alternatively one could consider adding an oral thiazide diuretic72,83,84
An attenuated diuretic response has been shown to be associated
with poor prognosis and increased risk of death.85
• Inotropes:
lla, B - Dopamine : Low dose at <2-3mcg/kg/min to improve renal flow
and promote diuresis86
llb, B - Dobutamine infusion : Started at 2 – 5mcg/kg/minute and titrated
by 1- 2mcg/kg/minute increments at 30 minute intervals until the
desired clinical and haemodynamic response is attained.
Dobutamine improved cardiac output but did not reduce pulmonary
capillary wedge pressure or hospital stay. It was associated with
significant ventricular tachyarrhythmias.87,88,89

26
• Vasodilators:
- Sodium Nitroprusside would be useful in patients not responsive lla, B
to nitrates.90 This drug is particularly useful in cases of
uncontrolled hypertension, acute mitral or aortic regurgitation
Continuous intra-arterial monitoring is necessary as acute changes in
blood pressure with hypotension can occur. Infusion should not be
continued beyond 3 days because of the danger of cyanide poisoning.
Infusion should be for shorter periods in patients with hepatic and
renal impairment.

B) If the blood pressure is low at initial presentation (SBP <100mmHg)

or drops during treatment :-
• Noradrenaline infusion. The use of noradrenaline was associated lla, B
with less adverse events compared to dopamine in the treatment
of shock.91 A small study showed that the combination of
noradrenaline and dobutamine was a more reliable and safer
strategy that using an adrenaline infusion.92
• Dopamine infusion91 llb, B
• Avoid vasodilators (nitrates, nitroprusside) and morphine until l, C
the blood pressure has stabilized
• Over diuresis or hypovolaemia - correct accordingly. l, C
In Right Ventricular (RV) Infarction, the hypotension may respond to
volume loading.

Other Measures
• Intubation and mechanical ventilation - Should the oxygen lla, C
saturation be inadequate or the patient develops respiratory
muscle fatigue, then endotracheal intubation and mechanical
ventilation is necessary.
• Correction of acidosis l,C
• Invasive haemodynamic monitoring - where available, would
be useful in patients not responsive to medical therapy and are
llb, B
hypotensive. This can include arterial pressure line, central venous
pressure line and pulmonary artery catheter. This would allow a
more accurate assessment of the fluid status of the patient and
allow better titration of medications.93-95
• Intra-aortic balloon counterpulsation (IABP) - would be useful in patients
who are not responding optimally to medical therapy as a bridge to lla, B
definitive treatment. IABP would be particularly useful in patients with
intractable myocardial ischaemia or acute mitral regurgitation.96,97
In acute MI complicated by cardiogenic shock, IABP has been found
to be effective in patients undergoing reperfusion by fibrinolytic
therapy. In those undergoing primary PCI, IABP has not been shown
to reduce mortality.98,99
IABP is contraindicated in patients with aortic regurgitation or aortic
dissection.

27
lla, B
• Ventricular Assist Devices (VAD) - would be useful as a bridge
in patients for whom recovery from Acute HF is expected or for
whom heart transplantation is an option.100-102
Following adequate response to intravenous therapy, the patient
should be converted to optimal oral medications. (see Flow Chart II,
pg 12) The initial dose of oral diuretics required is generally higher
than the intravenous dose.
There are other agents such as tolvapton, levosimendan and nesiritide
have shown symptomatic improvement in Acute HF but have been
associated with either neutral or an increase in adverse events.103-106

Special Situations
• Myocardial Ischaemia / Infarction: Reversible myocardial ischaemia
causing Acute HF, needs early recognition, rapid stabilization and
referral for urgent coronary angiography. In acute MI, reperfusion
therapy by fibrinolytic or primary Percutaneous Coronary
Intervention (PCI) may significantly improve or prevent Acute
HF. Long term management strategy should include adequate
coronary revascularization, anti platelet therapy, ACE-I and/or
ARB, β-blockers and statins.
• Hypertension: Typically presenting as “flash pulmonary edema”
with hypertensive crisis. Systolic LV function tends to be normal.
The blood pressure needs to be reduced relatively quickly. It is
generally suggested that the SBP be reduced by 25% over 3 to
12hours. This is best achieved with parenteral drugs such as
intravenous nitrates or nitroprusside. No attempt should be made
to restore “normal” values of BP as this may cause deterioration of
organ perfusion. Look for secondary causes of hypertension such
as renal artery stenosis and phaeochromocytoma.
• Valvular Heart Disease: Acute HF can be caused by valvular
conditions such as acute mitral or aortic valve incompetence or
stenosis, bacterial endocarditis, aortic dissection and prosthetic
valve thrombosis. Vasodilator therapy would be beneficial in
acute valvular regurgitation, but is contraindicated in severe
valvular stenosis. Early access to echocardiography is crucial for
the diagnosis and management. Percutaneous intervention such
as mitral valve commissurotomy can be life saving in patients with
severe mitral stenosis.

• Arrhythmias: Tachyarrhythmias particularly atrial fibrillation / atrial

flutter with fast ventricular rates need to be identified and treated
appropriately e.g. electrical or pharmacological cardioversion.

28
• Renal Failure: Acute HF and renal failure can co-exist and either
may give rise to the other. Renal failure influences the response to
drug therapy.107 In these patients with refractory fluid retention,
continuous ultrafiltration may be considered.108

Cardiogenic Shock
Cardiogenic shock carries a very high mortality rate. Features include:
• SBP<90mmHg not improved with fluid administration
• Signs of hypoperfusion-cold extremities, altered mental
status, restlessness
• Reduced urine output (<20cc/hour)
• Cardiac index of < 1.8 L/min/m2 without support or 2.2 L/min/m2
with support
It is important to establish the aetiology and institute appropriate
resuscitative therapy immediately. An ECG should be obtained and
continuous monitoring begun. Venous access should be secured,
preferably via central venous cannulation (subclavian or internal jugular)
Important considerations are:-
• Ventricular Function: Echocardiography would allow rapid
determination of LV function and mechanical causes (e.g. acute
valve regurgitation, acute septal rupture, cardiac tamponade)
of cardiogenic shock. In the presence of preserved LV systolic
function, other causes of shock such as sepsis and intravascular
volume depletion should be considered.
• Intra Vascular Volume Status: An absolute or relative reduction in
LV filling pressures may be present. This may be due to excessive
diuretic or vasodilator therapy, concomitant gastro-intestinal
bleed or RV infarction. In the absence of signs of LV failure,
fluid challenge with normal saline should be administered (usual
recommended volume : 200 - 500mls). Invasive haemodynamic
monitoring would be useful to guide fluid therapy.
• Arrhythmias: Should be identified and appropriate treatment such
as cardioversion or pacing instituted. Resistant arrhythmias would
require additional anti-arrhythymic drug therapy.

In the presence of cardiogenic shock or near shock (hypoperfusion with

adequate blood pressure) treatment would include the following :-
• Inotropic support: Noradrenaline and/or dopamine. If blood
pressure is adequate in the setting of near shock, dobutamine may
be used.
• Mechanical device support : Intra-aortic balloon pump or LV
assist device

29
 Identifying correctable causes:
This includes myocardial ischaemia/infarction. Cardiogenic shock in
this setting could be due to:
- pump failure- These patients should be identified early and
treated aggressively with prompt revascularization by PCI. Often
they would require ventilatory support and IABP.
- mechanical complications such as ventricular septal rupture and
acute mitral regurgitation. Echocardiography will be useful in the
diagnosis. Urgent surgery is beneficial but carries a high mortality.

7.2 CHRONIC HEART FAILURE

7.2.1 NON PHARMACOLOGICAL MEASURES

These include the following :-
a) Education
b) Diet & Nutrition
c) Lifestyle
d) Exercise
e) Sleep Disorders
f) Social Support

A) Education
l, B • The patient and family should receive both education and counseling
about the HF syndrome, its prognosis and drug treatments.109-112
• Counseling on the warning signs and symptoms of worsening HF
particularly with emphasis on sudden weight gain - more than 2 kg
in 3 days.
• Provide prognostic information to enable patients to make realistic
decisions and plans. This is important in patients with severe HF.
Chronic HF is a highly lethal disease, as lethal as several common
malignancies (Appendix I,pg 58)
• Educate patients on their drug regime, emphasizing the need
for compliance. Patients should be made aware of the expected
benefits and the potential common side effects of these drugs.
• Patients should be warned about self-medication and potential
drug interactions. (Appendix II,pg 58)

B) Diet & Nutrition

l, B It is important to maintain good nutrition.113 Obese patients should
be encouraged to reduce weight. Excessive weight loss and leanness
however, are important predictors of poor prognosis in Chronic HF.114
lla, B Patients should be advised on salt restriction particularly in severe
HF.115-119 A good rule of thumb is to avoid adding salt and soya sauce
while cooking or at the table. Refer to Appendix III,pg 58 on salt
content of common Malaysian food.
l, C Fluid intake should be restricted to 1-1.5 liter/day if HF symptoms are
still not well controlled with medications.116,117

30
C) Lifestyle
• Patients with alcoholic cardiomyopathy must abstain from alcohol.
Similar abstinence is strongly encouraged in all other patients with
HF.120
• Smoking should be stopped.121 l, B
• Patients with severe HF (NYHA Class III-IV) should be advised lla, C
against pregnancy because of high maternal mortality.122,123
• Recommended contraceptive methods include low-dose
oestrogen and third generation progesterone. Intra-uterine
contraceptive devices (IUCDs) may be used except in patients
with valvular heart disease.122
In severe HF, sexual dysfunction is common and sexual practices
may need to be modified to accommodate patients with impaired
effort tolerance. Presently, phosphodiesterase-5-inhibitors
(sildenafil, tadanafil and vardenafil) are not recommended in
advanced HF. Nitrates should not be given within 24 – 48 hours of
phosphodiesterase-5-inhibitor use and vice versa. Patients in NYHA
class II are at intermediate risk and patients in class III – IV are at high
risk of cardiac decompensation triggered by sexual activity.124

D) Exercise
Recent studies have shown that patients with compensated HF can
l, A
exercise safely.125-127 Regular dynamic exercise :
• improves psychological and physical well-being
• reduces harmful neuro-hormones
• improves muscle blood flow and function
• increases the electrical stability of the heart
• reduces hospitalization
Activities such as walking, cycling, swimming, golfing and bowling
should be encouraged with gradual build-up to target activity levels.
Specific recommendations include dynamic aerobic exercise (walking) 3
to 5 times a week for 20 to 30 min, or cycling for 20 min at 70-80% of
peak heart rate 5 times a week. If the patient can physically manage to
work without undue symptoms, this too can be continued.
220 - peak heart rate

E) Sleep Disorders
Causes of sleep disturbances in HF include pulmonary congestion,
nocturnal diuresis due to diuretics and anxiety.
Up to 53% of adults with HF have been shown to have either central or
obstructive sleep apnea.128-130 Adverse effects of obstructive sleep apnoea
include hypoxemia, hypercapnia and increased afterload. Treatment
will include weight loss and CPAP. In patients with sleep apnea and HF, lla, B
CPAP can increase LVEF and improve quality of life. To date, there is no
conclusive evidence that CPAP improves prognosis in HF patients.130-134

31
 F) Social support
This reduces stress and helps in maintaining a healthy lifestyle
and compliance to treatment. Absence of social support has been
associated with higher hospitalization rates.135-137

7.2.2 PHARMACOLOGICAL MANAGEMENT

Drug therapy is the mainstay of management of Chronic HF as
outlined in Flowchart II,pg 12. For grading of recommendations and
levels of evidence, see Table II,pg 13.

A) Diuretics
Diuretics are indicated in all patients with HF in whom there are signs
l, C
and symptoms of fluid retention.138
The dose of diuretic used is variable and dependent on individual
requirements. In the presence of severe congestive HF, oral diuretic
therapy may be ineffective. Intravenous therapy may be preferred.
Adequate doses of diuretic should be used. However, these patients
should be monitored closely as overdiuresis can cause intravascular
volume depletion leading to hypotension and deterioration of renal
function. Hypokalaemia is a common problem with diuretic use and
oral potassium supplementation is usually necessary.
Thiazide diuretics may be preferred in patients with hypertensive HF
and mild fluid retention. For most patients however, a loop diuretic
is often required. Responsiveness to loop diuretics diminishes as
HF progresses. In this situation, combination of thiazides and loop
diuretics are useful as these drugs work synergistically to improve
diuresis.83 In patients with a glomerular filtration rate below 30ml/
min, thiazides are not effective alone but may be used synergistically
with loop diuretics. (Table VI for dosages)
Patients should be advised to record their daily weight and if there
is a consistent increase in weight of more than 2kg in 3 days, they
may be advised to increase their diuretic dose until “dry weight”
is regained. If the weight gain and symptoms worsen, the patient
should seek medical help.

32
 Table VI: Diuretics Used In Heart Failure
Route of
Usual Daily Dose
Administration
LOOP DIURETICS
• Frusemide IV / Oral 20 - 80mg
• Bumetanide IV / Oral 0.5 - 2mg
(up to 10 mg max)
THIAZIDES
• Hydrochlorothiazide Oral 25 - 50mg
• Chlorothiazide Oral 250 - 500mg

MINERALOCORTICOID
ANTAGONISTS
• Spironolactone Oral 12.5mg – 50mg
• Eplerenone Oral 25mg - 50mg

B) Angiotensin Converting Enzyme Inhibitors (ACE-I)

ACE-I improve survival and quality of life in all classes of HF.139-141 ACE-I l, A
are the first-line drugs for the treatment of HF and should be given
to all patients in whom there is evidence of LV systolic dysfunction as
reflected by an LVEF of <40%.
The available data suggest that there are no differences among
available ACE-I in their effects on symptoms or survival.141
In the initiation of ACE-I, the following steps are recommended:-
• Care should be exercised in the following patients for whom
referral to a specialist may be considered.
- SBP <100mmHg
- Creatinine > 250 µmol/L
• Avoid excessive diuresis before treatment. If patients are on large doses
of diuretics, the blood pressure and renal function should be monitored.
• Start with a low dose. Patients should not remain on the initial low
dose indefinitely. The dose should be increased gradually to the
target dose (Table VII) or the maximum tolerated dose.
• Monitor blood urea, creatinine and serum potassium at 7-14 days,
especially in patients with impaired renal function. If the rise in
serum creatinine level is >20% compared to baseline, then ACE-I
therapy may need to be stopped temporarily.
• Avoid non steroidal anti-inflammatory drugs
A number of different ACE-I are available. The dose should be titrated
up to the target level as shown in Table VII.

33
 Table VII: Recommended doses of ACE-I used in HF
ACEI Initiating Dose Target Dose
Captopril 6.25 mg tid 50 mg tid
Enalapril 2.5 mg bid 10 mg bid
Lisinopril 2.5 mg daily 20 mg daily
Quinapril 2.5-5 mg daily 20 mg bid
Perindopril 2 mg daily 8 mg daily
Ramipril 1.25-2.5 mg daily 5 mg daily
Fosinopril 10 mg daily 20 mg daily

Major adverse effects of ACE-I are :-

• cough
• hypotension
• renal insufficiency
• hyperkalaemia
• Angioedema

C) β-Blockers
l, A Large clinical trials have shown that β-blockers reduce morbidity and
mortality in patients with NYHA II-IV HF, of both ischaemic and non-
ischaemic aetiology, on top of standard therapy.142-150
β-blockers should be initiated when pulmonary congestion is absent and the
patient is clinically stable. All stable patients with current or prior symptoms
of HF and reduced LVEF should be given β-blockers unless contraindicated.
lla, B Initiating therapy with a β-blocker first is non-inferior to the standard
approach of starting with an ACE-I.145
The benefits seen with both these drugs are additive.
In initiating β-blocker therapy the following should be considered :-
• The initial dose should be small. (Table VIII)
• The dose should be slowly titrated upwards till target dose or
maximum tolerated dose is achieved.
• Contraindications include the following :
- bronchial asthma or severe chronic obstructive airway disease
- symptomatic bradycardia or hypotension
- second or third degree heart block without a pacemaker
- a requirement for beta agonist therapy or positive
inotropic support
Patients who decompensate and are admitted in Acute HF should be
maintained on the same dose of β-blockers unless the clinical condition
(hypotension or significant bradycardia) warrants a temporary reduction
in the dose. After the patient has been stabilized and is no longer in overt
HF, an attempt should be made to up-titrate to the target or maximum
tolerated dose of β-blockers.

34
 Table VIII: Recommended doses of β-Blockers used in HF*
β-Blockers Initiating Dose Target Dose
Carvedilol 3.125 mg daily 25 mg bid
Bisoprolol 1.25 mg daily 10 mg daily
Metoprolol succinate CR** 12.5 – 25 mg daily 200 mg daily
Nevibolol*** 1.25 mg 10 mg daily
* Only the above mentioned β-blockers have been shown to improve CV outcomes.
** Currently only metoprolol tartrate is available in Malaysia
*** one study showed reduction in composite endpoint of death or CV

D) Mineralocorticoid Receptor Antagonists (MRA)

The addition of spironolactone to ACE-I, loop diuretics and digoxin l, B
in patients with severe HF reduces mortality and rehospitalization.151 l, B
Similarly, eplerenone, another MRA, when added to β-blockers and
ACE-I in patients post MI with impaired LV function and mild HF, has
been shown to be beneficial.152,153 (Table VI,pg 33)
Care should be exercised in patients with renal impairment. Serum
potassium should be monitored regularly. Potassium supplements
may need to be reduced or stopped. If hyperkalemia persists, then
the dose of MRA should be reduced or stopped.
Spironolactone can cause breast enlargement and discomfort in men
; this is infrequent with eplerenone.

E) Angiotensin II Receptor Blockers (ARB)

In patients intolerant to ACE-I, ARB should be considered.154-158 l, A

In patients post MI with impaired LV function the ARB, Valsartan, was l, B

found to be as effective as captopril.159 (Table IX)
In patients who are still symptomatic despite being on ACE-I and llb, B
β-blockers and in whom a MRA is not tolerated, the addition of an
ARB may be considered to reduce hospitalization due to HF.154,160,161

Table IX: Recommended doses of ARB in HF

ARB Initiating Dose Target Dose
Losartan 25 mg daily 150 mg daily
Valsartan 40 mg daily 160 mg bid
Candesartan 4 mg daily 32 mg daily

35
 F) Ivabradine
Ivabradine slows the heart rate in sinus rhythm but has no effect on
lla, B
the ventricular rate in atrial fibrillation. In patients on optimal medical
therapy with diuretics, ACE-I and β-blockers and a resting heart rate
of >70/min, the addition of Ivabradine resulted in a reduction in
hospitalization, improvement in LV function and quality of life without
an effect on mortality.162,163 It would be useful in patients who have
contraindications to β-blockers.
Ivabradine can cause symptomatic bradycardia and visual disturbances.
G) Digoxin
In the past digoxin was used as first line therapy in patients with HF
and atrial fibrillation.164,165 However at present, β-blockers are an
integral component of HF management. Digoxin may be considered
lla, C in patients with HF and AF in the following situations:
• rate control is inadequate on β-blockers alone.
lla, C
• β-blockers are contra indicated.
lla, C • rapid control of the ventricular rate with parenteral drugs is required
lla, B Combination of digoxin and β-blockers is superior to either agent
alone in patients with atrial fibrillation.166,167
llb, B In patients with HF and normal sinus rhythm, digoxin may be
added if symptoms persist despite diuretics, ACE-I, β-blockers and
low dose MRA. Digoxin has no effect on mortality but reduces
hospitalization.168-170
No loading dose is required for Chronic HF. The usual maintenance dose
of digoxin is 0.125mg to 0.25mg daily. Lower doses should be used in
the elderly and in patients with impaired renal function. Current data
indicates that lower doses of digoxin and lower levels of serum digoxin
(0.5- 0.8 ng/ml) are efficacious and appear adequate in most patients
with compensated HF.171,172
H) Anti-Coagulation Therapy
Patients with the following risk factors for thromboembolism should
be anti-coagulated with warfarin unless there are contraindications:
l, A - atrial fibrillation 173,174
Atrial fibrillation is a common problem among patients with HF.
All patients with atrial fibrillation should be anti-coagulated with
warfarin unless contraindicated.175
lla, B New anticoagulant drugs – oral direct thrombin inhibitors
(dabigatran) or factor Xa inhibitors (rivaroxaban, apixaban) may be
used in place of warfarin. Care has to be exercised with these agents
in renal impairment. Disadvantages include absence of antidotes in
the event of bleeding and significantly increased costs compared to
warfarin. 176,177,178
lla, C - intracardiac thrombus (except for organized mural thrombus)
lla, C - past history of thromboembolic episode(s)

36
I) Other Concurrent Therapies
Calcium channel blockers are not recommended for the treatment of lll, A
HF due to systolic dysfunction.179-181
Second generation dihydropyridine calcium channel blockers such lla, B
as amlodipine or felodipine may be considered for the treatment of
concurrent hypertension and angina.182,183
Nitrates have many theoretical benefits when used in HF.These effects llb.C
are however short lived due to the development of tolerance and
pseudotolerance. Almost all the large clinical trials have been with
the hydralazine- nitrate combination which seem to be most benefial
in black patients.184

J) Anti – Arrhythmic Drug Therapy

Arrhythmias are common in HF. The more common ones are:
• atrial fibrillation
• ventricular tachyarrhythmias
• bradyarrhythmias

J.1) Atrial Fibrillation

These patients can be managed by either rate control or rhythm control.
• Rate control.
This can be achieved by using either:
- β-blockers165,166,174,185 and/ or l, A
- digoxin174 llb, B

β-blockers are preferred over digoxin as it provides rate control

during exercise and improves morbidity and mortality in patients with
HF. Rate control is better when digoxin and β-blockers are used in
combination rather than with each drug individually.166,167
• Rhythm control
This is indicated in patients intolerant of AF even after rate control. It can llb, B
be achieved either by pharmacological cardioversion with amiodarone or
by elective electrical cardioversion after a period of anticoagulation.174
Sinus rhythm can be maintained by using amiodarone.174 lla, B

J.2 Ventricular Arrhythmias

Studies show that 40-50% of deaths in HF are sudden, the risk increasing
with the severity of HF.186,187 This is most often due to either sustained
ventricular tachycardia (VT) or ventricular fibrillation (VF) although
sometimes it may be due to a bradyarrhythmia or electromechanical
dissociation.188,189 Occasionally rapid supraventricular tachycardias may
give rise to malignant ventricular tachyarrhythmias.190

37
 The following medications have been shown to reduce the incidence
of sudden cardiac death (SCD) :
l, A - β-blockers:- These agents were shown to reduce SCD in the clinical
trials done on patients post MI as well as in the HF trials190-193
l, B - Mineralocortocoid antagonist have been shown to reduce the
incidence of SCD193,194,195
l, A - ACE-I: Analysis of trials done following myocardial infarction
showed that ACE-I reduced SCD.193,196-198
llb, B - Statins:- have a modest beneficial effect on SCD199
In addition to the above, in patients with ventricular tachyarrhythmias,
the following are important:
l, C • Identify contributing factors such as electrolyte disturbances,
ischemia and drugs.
• Implantable cardioverter defibrillator (ICD) (section 7.2.3) These
have been found to improve survival in both
l, A - secondary prevention 200,201,202
lIa,A - primary prevention203,204 in selected patients.
lla, B • Anti-arrhythymic drug therapy with amiodarone can be considered
as adjunctive therapy in patients with ICD to reduce the number of
shocks and in patients who are not candidates for ICD.205

l, A Patients with significant bradyarrhythmias, trifascicular blocks and high-

degree AV blocks should be considered for pace-maker therapy.206
Prior to implanting a conventional pacemaker, the need for an ICD or
Cardiac Resynchronisation Therapy (CRT) device should be considered.

38
7.2.3 DEVICE THERAPY IN HEART FAILURE

A) Cardiac Resynchronization Therapy (CRT)

Patients who remain persistently symptomatic (NYHA class II - III) despite
optimal medical therapy should be considered for CRT with a bi-ventricular
pacemaker if there is evidence of left ventricular dyssynchrony.
Selection criteria for CRT include all of the following:
• sinus rhythm
• LVEF <35%
• a widened QRS interval (>120 ms) on the resting ECG
CRT has been shown to improve symptoms, hospitalizations and l, A
mortality, though up to 30% of patients may be non-responders.207-211
Patients with milder symptoms and in NYHA class II are more likely to
benefit if their QRS>150ms and they have a left bundle branch block
(LBBB) pattern in their resting ECG.212-215
Patients with permanent atrial fibrillation are less likely to respond
unless they have atrio-ventricular block, which would allow continuous
ventricular pacing.216,217
Regular monitoring is recommended after device implantation to
adjust medical therapies and reprogram the device as necessary.

B) Implantable Cardioverter Defibrillator (ICD)

SCD due to sustained ventricular fibrillation or ventricular tachycardia
can be decreased by the use of an ICD. An ICD can be implanted as
secondary prevention in patients with previous sudden cardiac arrest
or documented sustained ventricular arrhythmias.200,201,202
It may also be used as primary prevention to reduce the risk of SCD in
patients with HF who are at risk.203,204, 218-220 An ICD should be considered
in patients who fulfill the eligibility criteria and who otherwise have
good clinical function and prognosis to improve their survival.
Secondary prevention:
The following should be considered for implantation of ICD:
• Patients resuscitated from SCD due to ventricular fibrillation or
hemodynamically unstable sustained ventricular tachycardia
(provided that it is not associated with acute MI or ischemia).200,201,202 l, A
These cardiac arrest survivors have a high risk of recurrent events and
implantation of an ICD has been shown to reduce mortality.
• Patients with chronic HF and a low EF who experience syncope of llb, C
unclear origin have a high rate of subsequent SCD and should also
be considered for placement of an ICD.

39
 Primary prevention (prophylactic ICD implantation):
Prophylactic ICD implantation to reduce the risk of SCD may be
reasonable in patients with:
lla, A • prior MI and LVEF<30% at least one month after an MI and 3 months
after revascularization by PCI or CABG, when appropriate.203,218,219

lla, B • LVEF <35% and mild to moderate HF symptoms (NYHA II–III).204,220

The decision regarding the balance of potential risks and benefits
of ICD implantation for an individual patient remains complex.

C) Combined Biventricular Pacing with ICD Capabilities

lla, B This should be considered in patients who have malignant ventricular
arrhythmias and also fulfill the criteria for biventricular pacing implant
(symptomatic heart failure with LVEF <35% and ventricular dysynchrony
with QRS duration >120ms) to reduce mortality and morbidity.221,222

7.2.4 SURGERY FOR HEART FAILURE

Patients with HF should undergo surgery if the pathology causing the
HF is amenable to surgical treatment. However the decision to subject
a patient to surgery should take into account the functional status,
prognosis and comorbid conditions of the patient.
Surgical procedures include the following:
A) Revascularization Procedures
Patients with CAD and HF may benefit from revascularization by either
l, C PCI or coronary artery bypass surgery (CABG), particularly if they have
angina and anatomy that is suitable for revascularization (left main
stem or triple vessel disease).The benefit of revascularization is likely
to be more in patients with mild left ventricular dysfunction, severe
CAD with angina, viable myocardium and reversible ischemia.
The STICH trial found no difference in total mortality between CABG
or medical therapy in patients with severe heart failure (LVEF < 35%)
lla, B
and significant CAD, but patients who underwent CABG had reduced
combined risk of cardiovascular (CV) death and CV hospitalizations.223
Coronary revascularization (by either CABG or PCI) should be considered
in patients with HF and suitable coronary anatomy if they have:
lla, C • refractory angina or acute coronary syndrome, for relief of symptoms.

lla, C • significant inducible ischemia and/or large areas of hibernating

myocardium.
Myocardial ischemia and viability should be demonstrated by tests
such as dobutamine stress echocardiography, radionuclide myocardial
perfusion scan or cardiac magnetic resonance imaging.

40
B) Valve Surgery
Patients with HF and severe mitral regurgitation, non ischemic llb, C
in origin, may have symptomatic improvement after mitral valve
surgery. If the LVEF <30%, mitral valve repair is preferred as mitral
valve replacement is associated with poorer outcomes.224
Patients with LV systolic dysfunction undergoing surgical coronary lla, B
revascularization who also have moderate to severe mitral regurgitation
secondary to ventricular dilatation may be considered for concomitant
mitral valve repair or replacement.225,226 A recent small studied observed no
significant difference in left ventricular reverse remodeling or survival at 12
months between patients who underwent mitral-valve repair and those
who underwent mitral-valve replacement for ischemic mitral reguritation.227
C) LV Reduction Surgery
LV aneurysmectomy is indicated in patients with a large discrete LV
aneurysm who develop HF, angina pectoris, thromboembolism, and l, C
tachyarrhythmias due to the aneurysm.228
Patients with HF undergoing surgical coronary revascularization,
who have areas of LV dyskinesia or akinesia do not benefit from llb, B
concomitant LV reduction surgery.229
D) LV Assist Devices
Left ventricular assist devices have been used to bridge patients with HF to
heart transplantation, to support patients with acute severe myocarditis lla, B
with a view to recovery, and is increasingly being used for long term
haemodynamic support in eligible patients (destination therapy).230-232
Patients awaiting heart transplantation who have become refractory
to medical therapy and require inotropic support should be considered
for a mechanical support device as a bridge to transplant.

7.2.5 HEART TRANSPLANTATION lla, C

Heart transplantation is an established treatment of refractory end
stage HF but it is limited by the lack of donor organs.233,234
Patients with severe HF despite optimal medical therapy, and
who meet the eligibility criteria, should be considered for heart
transplantation and referred for further evaluation.
Indicators of severe HF and consideration for heart transplantation include:
• Poor LVEF (<25%)
• Recurrent admissions or major limitation of the patient’s daily activities
• Poor effort tolerance i.e. peak VO2 less than 10 ml per kg per min
• iv inotropic dependence
Contraindications to cardiac transplantation include any malignancy within
5 years, diabetes mellitus with widespread microvascular complications,
chronic kidney, liver or lung disease, pulmonary hypertension, or other
medical or psychosocial issues that would impact survival.

41
 7.3.1 ASYMPTOMATIC LEFT VENTRICULAR DYSFUNCTION
The prevalence of Asymptomatic LV Systolic Dysfunction (ASLVSD)
varies with the diagnostic LVEF criteria that is used as a cutoff as well
as the population studied. About 0.9-2.1% in the general population
have asymptomatic LVEF<40%.235,236
Patients with ASLVD (LVEF <40%) carry substantially higher risk for
subsequent morbidity and mortality than the general population. The
rate of progression to symptomatic HF was estimated to be 9.7% per year
and the risk of death or HF hospitalization was 8%.237,238 Outcomes are
worse if effective therapy is initiated after patients develop overt HF.239
Asymptomatic moderate to severe LV diastolic dysfunction is also
common (5.6%) and associated with an adverse prognosis.236
Screening may be done by: 240
• Resting ECG - not very specific or sensitive
• Echocardiography - this is the most specific test
• BNP levels - may be used to identify individuals who may need an
echocardiogram.
These screening tests are more cost effective and of greater value when
used to screen high risk individuals.240-242 These include patients with:
• coronary artery disease
• hypertension
• diabetes mellitus
• peripheral arterial or cerebrovascular disease
• excessive alcohol intake
• family history of cardiomyopathy
• abnormal resting ECG
• cardiomegaly on the CXR
The goals of treatment in these patients are to:
• slow down the progression of the disease
• prevent the development of symptoms of HF
• improve survival
l, C Wherever possible, the underlying disease should be treated
appropriately to prevent the development of HF.
Drug therapy. This includes:
l, A • ACE-I: Long term treatment with an ACE-I has been shown to delay
the onset of symptoms of HF and decrease the combined risk of
death and hospitalization.237,238,243,244
• ARB: There has been no study of the use of ARB in patients with
asymptomatic left ventricular dysfunction. The ARB, Valsartan, may be
an alternative in post MI patients who cannot tolerate an ACE-I.I59
l, A • β-blockers: In post MI patients and in those with CAD, β-blockers
are recommended. They may be considered in all patients with
LVEF<40%.245,246

42
• Diuretics and digoxin: There is no role for these agents in this group lll, C
of asymptomatic patients.
• Calcium channel Blockers: The use of calcium channel blockers with lll, C
negative inotropic effects is not recommended in asymptomatic post
MI patients with LVEF <40%.247

Key Message:
• Identify patients who are at high risk of developing LV
dysfunction and treat the underlying disease appropriately.
• ACE-I and β-blockers ( post MI ) have been shown to slow down
the onset of symptoms and reduce cardiac morbidity.

7.3.2 HEART FAILURE WITH PRESERVED LEFT

VENTRICULAR FUNCTION
The prevalence of HF with preserved LV systolic function (HFpEF)
varies between 40-71% depending on the LVEF criteria used as cut off.
248,249
HFpEF constitutes more than half of HF in older adults and the
prevalence is increasing over time. 247,248 Commonly, these patients are
older women who have hypertension. Significant co morbid conditions
such as diabetes mellitus, CAD, obesity and / or atrial fibrillation are
also often present.248- 250 The presence of diabetes, a lower systolic BP,
hemoglobin and estimated Glomerular Filtration Rate (eGFR) were
associated with a poorer outcome.250
HFpEF is a clinical diagnosis and largely one of excluding mitral valve
disease, fluid overload, cor pulmonale and other potential non cardiac
causes of dyspnea.
Criteria that have been proposed to diagnose HFpEF include:15,16
• clinical signs or symptoms of HF such as exertional dyspnea,
orthopnea, atrial gallop sounds, and pulmonary rales combined
with a suggestive chest X-ray and a favorable response to diuretics,
• evidence of preserved or normal LVEF (>50% or more within 72 hours
of the event) and LV end diastolic volume index (LVEDVI)< 97mL/m2
• evidence of abnormal LV diastolic dysfunction that can be determined
by Doppler echocardiography or cardiac catheterization. Invasive
hemodynamic measurements complemented, where necessary, by
additional exercise testing with assessment of LV volumes and pressures to
detect exercise-induced elevation of filling pressures is the gold standard
for diagnosing diastolic dysfunction. However, echocardiography with
tissue doppler is obtained more easily and several criteria have been
proposed to diagnose diastolic dysfunction.15

43
 Hypertension remains the most important cause of HFpEF, with a
prevalence of 60% to 89% from large controlled trials, epidemiological
studies, and HF registries.251 Diastolic dysfunction may be due to
myocardial or pericardial disease. (see Table X,pg 45)
The management of these patients remains empiric, since trial data
are limited. It includes:
l, C • Identifying and treating the underlying cause(s) appropriately.
l, A - Hypertension should be treated to target goals.252.253 Improved BP
control has been shown to reduce hospitalization for HF.252
l, C - CAD is common in patients with HFpEF and this should be treated
appropriately.
l, C • Tachyarrhythmias should be treated and sinus rhythm restored
whenever possible. If the patient remains in persistent atrial
fibrillation, β-blockers or calcium channel blockers alone or in
combination are the usual first line agents used for rate control.
l, A Patients with paroxysmal or persistent atrial fibrillation should be
anticoagulated.173,174
• Pharmacological treatment
Treatment options include:
- Diuretics: These are necessary to control pulmonary congestion
l, C and peripheral edema but should be used cautiously so as not to
lower preload excessively and thereby reduce stroke volume and
cardiac output.
- β-blockers: This could be given to lower heart rate and increase
lla, C the diastolic filling period. At present, however, there is no good
demonstration that β-blockers is beneficial in the treatment of
HFpEF.150,254
lla, C - Calcium Channel Blockers (Verapamil and diltiazem): These may be
used to lower the heart rate and has been shown to be beneficial.255
lla, B - Verapamil has been shown to improve functional capacity in
patients with hypertrophic cardiomyopathy.256
llb, B - ARB trials have shown mixed results. One large trial showed a reduction
in hospitalization while another large trial was neutral.257,258
llb, B - ACE-I may improve relaxation and cardiac distensibility directly and
may have long term activity via their antihypertensive action and
regression of hypertrophy and fibrosis. One small study showed an
almost significant trend toward reduction in the primary end point
of combined all-cause mortality and unexpected hospitalization for
HF while another trial was neutral.259,260
- MRA: Recent studies showed that spironolactone improved
llb, B
diastolic function and reduced hospitalization but did not result
in improvement in symptoms, exercise capacity or quality of
life.261-263 Hyperkalemia was more common in those on MRA.
• Exercise training: This is safe and improves exercise capacity and quality of
life.264 It should consist of dynamic isotonic and not static exercise.

44
Key Message:
• HFpEF is a common cause of HF in the elderly.
• Hypertension is an important cause and should be treated
according to guidelines.
• Management remains empiric since trial data are limited.

Table X: Causes of Diastolic Dysfunction

Myocardial disorders
Myocardial diseases
Infiltrative Amyloidosis
Sarcoidosis
Fatty infiltration
Noninfiltrative Ischemic cardiomyopathy
Idiopathic cardiomyopathy
Diabetic cardiomyopathy
Hypertrophic cardiomyopathy
Endomyocardial diseases Endomyocardial fibrosis
Hypereosinophilic syndrome
Storage disease Hemochromatosis
Glycogen storage disease
Pericardial disorders
Pericardial constriction Constrictive pericarditis
Effusive constrictive pericarditis
Pericardial effusions Pericardial effusion with cardiac compression
Glycogen storage disease
Adapted from: van Kraaij DJ, van Pol PE, Ruiters AW, de Swart JB, Lips DJ, Lencer N, et al.
Diagnosing diastolic heart failure. Eur J Heart Failure 2002;4:419-430.

7.3.3 HEART FAILURE IN PREGNANCY

About 0.5 – 4% of pregnant women have cardiac disease.265 Common causes of
HF in pregnancy are hypertension, eclampsia, undetected valvular heart disease
especially mitral stenosis, congenital heart disease, and occasionally peripartum
cardiomyopathy. The prevalence of peripartum cardiomyopathy (PPCM) in
Malaysia is estimated at 34 per 100,000 life birth.266 The prevalence of PPCM in
other parts of the world varies from 0.88 per 100,000 live births in USA to 250 per
100,000 live birth in Haiti.267
Normal haemodynamic changes that occur in pregnancy are:
• Cardiac output increases by 30 – 50% during normal pregnancy.
• Cardiac output increases to 80% above baseline during labour and delivery.
• Haemodynamic changes return to baseline 2 – 4 weeks after vaginal
delivery and up to 6 weeks after caesarian delivery.

45
 In women with heart disease, these changes may have a deleterious
effect on their cardiovascular system and precipitate HF. The periods
of greatest risk for cardiac events during pregnancy are early third
trimester, at delivery and in the immediate post-partum period.
Most forms of cardiac disease can be detected by physical examination,
ECG and echocardiography.
Predictors of maternal risk for cardiac complication include.122,267
• History of HF before pregnancy
• Prior arrhythmia (symptomatic sustained tachyarrhythmia or
bradyarrhythmia requiring treatment)
• NYHA class > 2
• Valvular stenosis (aortic or mitral valve area < 1.5 cm2) and LV
outflow tract obstruction (peak gradient > 30mmHg)
• Myocardial dysfunction (LVEF < 40%)
• Pulmonary hypertension
Pregnancy is contra-indicated in:122,267
• severe pulmonary hypertension (pulmonary artery pressure > ¾
systemic pressure)
• Eisenmengers’ syndrome
• Cardiomyopathy with class III or IV HF
• Severe obstructive lesions (aortic stenosis [valve area <0.7cm2], mitral
stenosis [valve area < 1.0cm2], coarctation [systolic gradient > 20mmHg],
hypertrophic obstructive cardiomyopathy [outflow tract gradients of
more than 30-50mmHg at rest and 75-100mmHg after provocation)
• Marfan’s syndrome with aortic root ≥40mm
• Severe maternal cyanosis(oxygen saturation<85%)
• Past history of peripartum cardiomyopathy with persistent LV
dysfunction and/or HF
In the management of HF in Pregnancy, the following issues need
to be considered:
• gestational age at presentation
• clinical presentation, either as Acute HF or Chronic HF
• response to medical therapy
• potential maternal and foetal risks
• timing and mode of delivery
Pregnant women with HF should be managed by a multidisciplinary
team consisting of physicians, obstetricians and paediatricians.
Management during pregnancy involves:
• Non pharmacological measures
The management of patients with mild symptoms consists mainly of
non- pharmacological measures such as:
– limiting strenuous exercise
– adequate rest
– maintaining a low salt diet
– treating anemia and infections early
– frequent antenatal examinations

46
• Pharmacological Measures
The following drugs may be used in the pregnant patient with HF:
– Nitroglycerine can be used in pregnancy for after load reduction. IIa, C
– Digoxin is safe in pregnancy and during breast feeding. IIa, C
– Diuretics may be used for preload reduction. No teratogenic IIa, C
effects of diuretics have been described. However diuretics
impair uterine blood flow particularly placental perfusion. Thus
diuretics must be used with caution.
– β-blockers may result in intrauterine growth retardation, IIb, C
apnea at birth, fatal fetal bradycardia, hypoglycaemia and
hyperbilirubinemia. Selective β-blockers such as atenolol or
metoprolol are generally preferred.
- ACE-I and ARB are contraindicated in pregnancy. III, C
ACE-I can be used in the post partum period but not in breast-
feeding mothers.
• Other treatment considerations in the pregnant patient:
- Patients with atrial fibrillation who are hemodynamically
unstable should be promptly electrically cardioverted. This is
safe in pregnancy.
- Anticoagulation is indicated in the presence of atrial fibrillation,
dilated Left atrium or mechanical prosthetic heart valve
- Patients with valvular lesions who remain symptomatic despite
optimal medical treatment may be considered for percutaneous
valve Intervention or surgery
- Commonly recommended antihyperthensive drugs include
methyldopa, labetalol,calcium channel blockers and
hydralazine268,269,270
Management during delivery involves: 122,267
• Vaginal delivery with epidural anaesthesia is the preferred mode
of delivery in most cases. Caesarian section is indicated:
- for obstetric reasons
- in patients on warfarin
- in patients with severe pulmonary hypertension
• It is beneficial to shorten the second stage of labour by forceps or
vacuum assisted delivery
• Left lateral decubitus position is preferred to attenuate the
hemodynamic effects in the supine position
• Oxytoxic drugs are best avoided unless blood loss become excessive
• Routine antibiotic prophylaxis is not recommended in patients
with valvular heart disease undergoing uncomplicated vaginal
delivery or caesarian section.

47
 Post partum care and follow up:
• After delivery, careful monitoring of hemodynamics is important for
at least 24 hour or longer in high risk patients
• Patients with severe cardiac lesions should remain hospitalized for a
longer period because the hemodynamics may remain abnormal for
up to 10 days after delivery
• After the postpartum period, a full cardiac assessment should be
performed and appropriate contraception should be advised

7.3.4. HEART FAILURE IN INFANTS AND CHILDREN

HF in infants and children is an important clinical condition and has diverse
etiologies and clinical presentations. The common causes are;271
• congenital heart disease,
• acquired diseases such as rheumatic carditis, endocarditis and viral
myocarditis,
• cardiomyopathy,
• tachyarrhythmia,
• post cardiac surgery.
Regardless of the etiology, timely diagnosis and effective treatment are
important in preventing short-term and long-term sequelae.
The largest HF burden comes from infants and children born with
congenital heart disease.271 Among cardiac malformations, left to right
systolic shunts are the most common causes of HF as shown in table XI,
pg 49. In this situation, a volume overload on the left side of the heart
causes preload stress and ineffective pulmonary re-circulation.
Valvular regurgitation lesions, either acquired or congenital, also cause
volume overload to the heart. The most common are mitral and aortic
regurgitation due to rheumatic valve disease. Severe prolapse of the
aortic valve cusp in the setting of neglected doubly-committed sub-
aortic ventricular defect may also cause aortic regurgitation.
Right sided volume overload presenting with HF rarely occurs in large
atrial septal defect and anomalous pulmonary venous drainage. The
latter will present in the neonatal period when there is an associated
obstructive lesion. Generally, the highly compliant right ventricle can
cope with volume overload and only fails after many years.
Severe obstructive lesions (critical aortic stenosis, critical pulmonary
stenosis or neonatal coarctation) often present with HF in the early
neonatal period, when the ductus arteriosus closes.
HF in an anatomically normal heart is less common in infants and
children. It is either due to a primarily cardiac pathology or part of a
systemic illness as illustrated in table XII,pg 50.

48
 Table XI: Structural Heart Diseases That May Cause
HF in Infants And Children
Shunt Lesions
• Ventricular septal defect
• Patent ductusarteriosus
• Aortopulmonary window
• Atrioventricularseptal defect
• Single ventricle without pulmonary stenosis
• Atrial septal defect (rare)
Valvular Regurgitation
• Mitral regurgitation
• Aortic regurgitation
Inflow Obstruction
• Cortriatriatum
• Pulmonary vein stenosis
• Mitral stenosis
Outflow Obstruction
• Aortic stenosis (valve/sub-valve/supravalvular)
• Pulmonary stenosis
• Aortic coarctation
Total/Partial Anomalous Pulmonary Venous Connection

Cardiomyopathy is a genetically related disease that occur approximately

1.13 in 100,000 children.273 In these cases, HF symptoms are due to an
enlarged ventricle with poor ventricular systolic function. They may also
present with cardiac arrhythmias.

Clinical Presentation
Clinical presentation varies from mild to severe HF requiring ventilator
support. The most common congenital causes of HF can be easily classified
based on age of presentation as in Table XIII,pg 51. Clinical symptoms of HF
include poor feeding, tachypnea, poor weight gain and failure to thrive.
Older children may complain of shortness of breath on exertion. Signs of
HF include respiratory distress, tachycardia, weak and thready pulse, gallop
rhythm, lung crepitations and hepatomegaly.274

Clinical Investigations
- Pulse oximetry - is helpful in identifying infants with HF with
underlying congenital cyanotic heart disease.
- ECG - is useful to determine the type of structural cardiac lesion
but not helpful in deciding whether HF is present or not. ECG is
essential in looking for arrhythmias.

49
 - Chest X-ray - May be pathognomonic for certain cardiac lesions.
It has a high specificity but low sensitivity for detecting cardiac
enlargement. The absence of cardiomegaly almost rules out HF.275
- Echocardiography - Not useful for the diagnosis of HF but it is essential
to determine the structural cause of HF and to assess cardiac function.
- Cardiac biomarkers - These have been used extensively in
assessing the severity and also predicting the course of the
disease in adults. Its clinical use in infants and children is however
limited.276

Table XII : Etiology of HF in infants and Children with

Structurally Normal Heart
Primary Cardiac Pathology
• Cardiomyopathy
• Myocarditis
• Myocardial infarction
• Acquired valve disorders
• Hypertension
• Kawasaki syndrome
• Arrhythmia (bradycardia or tachycardia)
Non-cardiac Pathology
• Anemia
• Sepsis
• Hypoglycemia
• Diabetic ketoacidosis
• Hypothyroidism
• Other endocrinopathies
• Arteriovenous fistula
• Renal failure
• Muscular dystrophies

Management
In treating HF in infants and children it is important to determine the
underlying etiology. Prompt diagnosis as well as timely referral for
treatment either by surgical correction or an interventional procedure
can prevent or ameliorate HF.
The principle of managing HF in infants and children includes
supportive measures, anti-failure medications and definitive structural
relief/correction as outlined below:271

50
Principles of managing heart failure
a) General measures:
These include:
- Oxygen therapy
- Correcting acidosis, hypoglycemia, hypocalcaemia and anaemia
- Treating respiratory infections aggressively
- Nasogastric tube feeding to reduce feeding effort and prevent
aspiration in neonates
- Treating gastroesophageal reflux aggressively

Table XIII :Common Causes of HF Based on Age

of Presentation
1. First week of life
• Transposition of the great arteries with ventricular septal defect
• Obstructed total anomalous pulmonary venous drainage (TAPVD)
• Hypoplastic left heart syndrome
• Large systemic A-V fistulas
• PDA in premature infants
• Critical aortic stenosis
• Neonatal coarctation
2. First one month
• Transposition of the great arteries with ventricular septal defect
• Coarctation of the aorta with associated lesions
• Critical aortic stenosis
• Large left to right shunt in premature infants (VSD,PDA)
• TAPVD, systemic A-V fistula, transposition of the great arteries
3. First 6 months
• Large left to right shunts
– Ventricular septal defect
– Patent ductus arteriosus
– Atrioventricular septal defect
– Truncus arteriosus
• Anomalous left coronary artery from the pulmonary artery
(ALCAPA)

51
 b) Anti-failure medication: Generally, this is guided by information
derived from studies in adults. Given the many causes of HF in this group,
it is likely that they will respond differently to these medications.
• Loop diuretics - are the mainstay of treatment in patients with
volume overload conditions such as left to right shunts and/or
pulmonary congestion. Diuretics should be used with caution if HF
is not due to vascular congestion.277
• Digoxin - It is mainly used in patients with impaired ventricular
function. Its role in the management of HF due to left to right
shunts is unclear.278
• Afterload–reducing agents - Captopril and enalapril improve
haemodynamics and HF symptoms. Use with caution in neonates,
starting with a low dose.279,280
- Captopril 0.1 mcg/kg/dose (1 - 3 times per day)
- Enalapril 0.1-0.5 mcg/kg/dose (daily dose)
- Milrinone–This has vasodilatory effects in the systemic and
pulmonary vascular beds, making it ideal for the management
of HF in the post-operative period. It does not interact with
β-blockers and thus does not cause tachycardia, increase
myocardial oxygen consumption or increase after load.
• Inotropic agents - Norepinephrine, dopamine and dobutamine are
used as inotropes in the setting of acute decompensated HF. These
drugs are less effective in neonates compared to infants and children
because neonates have a higher level of sympathetic activity.

c) Definitive transcatheter/surgical intervention

• Transposition of the great arteries with ventricular septal defect
Elective arterial switch surgery within the first 3 months of age
• Patent ductus arteriosus
- Ventilator dependent: Surgical ligation regardless of age and
body weight
- Non-ventilator dependent: Optimize anti-failure medication
and elective surgical ligation or transcatheter occlusion
• Total anomalous pulmonary venous drainage
- Obstructed: Urgent surgical correction
- Unobstructed: Early surgical correction
• Obstructive lesions (Aortic stenosis, pulmonary stenosis)
- critical stenosis: Urgent relief of obstruction after stabilization
- severe stenosis: Early relief o fthe obstructive lesion
• Coarctation of the aorta
- Infants less than 3 months: Surgical correction
- Infants more than 3 months: Balloon dilatation
• Large septal defects
- Ventilatordependent: Surgical intervention
- Non-ventilator dependent: Optimize anti-failure therapy and
elective surgical closure

52
• Truncus arteriosus
- Surgery within the first 3 months of life
• Anomalous left coronary artery from the pulmonary artery (ALCAPA)
- Surgery at diagnosis
The ultimate therapy for HF that is unresponsive to treatment is
cardiac transplantation. The decision is institutional preference and
generally based on the availability of specialized clinical support unit,
anticipated quality of life and donor availability.

Prognosis
The outcome of infants and children with HF depends largely on its
etiology. When non-anatomical disorders are the cause, the success is
related to the treatment of the underlying cause.
For many structural congenital defects (volume load conditions), surgery
and interventional treatment can be curative. In some patients, it may
only be palliative with improvement in clinical symptoms.

7.3.5. REFRACTORY HEART FAILURE

These are patients with severe symptoms despite maximal medical
therapy. When patients become refractory to therapy, hospital
admission is usually indicated. Meticulous control of fluid balance is
important. Aggravating causes of HF as listed in Table IV,pg 23 should
be identified and treated.
These patients may need specialized treatment such as continuous
inotrope infusion, ventricular assist devices and consideration for
cardiac transplantation.
The following may be required :-
• Frusemide infusions. These patients may require combination Ilb, C
loop diuretics and thiazides.
• Ultrafiltration in patients who are fluid overloaded.108 In most IIb, B
patients, however, the relief is temporary.
• Short term infusions of parenteral inotropes - low dose dobutamine IIb, B
(5mcg/kg/min) or milrinone. These produce symptomatic
improvement but no survival benefit has been demonstrated.281-283
The prognosis of these patients is poor. They should be referred to
HF specialists to assess whether they may be potential candidates for
device therapy or heart transplantation.

53
 7.3.6 END OF LIFE CARE
It is important to recognize patients who appear to be approaching
the terminal phase of their illness. These patients have:
• no identifiable reversible cause
• been on optimum tolerated conventional drugs
• worsening renal function
• fail to respond to appropriate changes in diuretic and vasodilator
drugs
• sustained hypotension

In these patients it is important to :284-286

• explore their wishes in terms of options for care and place of care.
• provide symptom relief. Medications that may be useful include
analgesics, antiemetics, anxiolytics, opioids and diuretics etc.
• discuss with patient and family when it would be appropriate to
switch off devices such as ICD or CRT
• avoid inappropriate invasive procedures
• discuss issues of “Allow Natural Death (Do Not Resuscitate)” with
patient and family.
• provide physical, psychological, social and spiritual support of
patient and family support

7.3.7 TERMINAL HEART FAILURE –the last few days of life

As death approaches agitation, terminal restlessness, delirium and
death rattles are common. In these patients, it is important to manage
issues such as urinary retention, constipation, pain and uncomfortable
position in bed. Once patient is semi-conscious, nursing in coma
position will be most useful for drainage of retained secretions.285,286

8. ORGANIZATION OF CARE & MULTI DISCIPLINARY

APPROACH
8.1 Monitoring and follow-up
All patients with chronic HF require monitoring which includes:
• clinical assessment of functional capacity – NYHA functional class
or 6 min walk test
• fluid status and body weight
• blood pressure, heart rate and rhythm
• examination of cardiovascular and respiratory system
• cognitive status and nutritional status
• review of medications, including compliance, adjustment of doses, need
for up-titration and possible side effects including erectile dysfunction
• serum urea, electrolytes, creatinine and eGFR as necessary

54
More detailed monitoring will be required if the patient has significant
comorbidity such as diabetes mellitus, Chronic Kidney Disease (CKD) or if
their condition has deteriorated since the previous review.
The frequency of monitoring should depend on the clinical status and
stability of the patient. The monitoring interval should be short (days
to 2 weeks) if the clinical condition or medication has been changed.
It is required at least 6-monthly for stable patients with previously
documented episode(s) of HF.
Patients who wish to be involved in monitoring of their condition
should be provided with sufficient education and support from their
healthcare professional to do this, with clear guidelines as to what to
do in the event of deterioration (e.g. increasing dose of diuretics if
the weight increases by > 2 kg in 3 days).
HF is characterised by recurrent hospitalisations. Recent studies on
prevention of re-hospitalisation have focused on:
• home telemonitoring (the patient's status is assessed in the
patient's own home)
• natriuretic peptide-guided therapy- use of serum natriuretic peptide
levels to guide uptitration of drugs compared with 'usual' care.287
• formal follow-up by a HF team

8.2 Cardiology Referral

Most stable patients with HF can be managed by family care physicians
and GPs. We suggest referral to a cardiologist in the following situations:
1. At initial presentation to confirm the diagnosis, determine
the underlying cause of the HF and to advice on appropriate
intervention if indicated.
2. During episodes of acute decompensation.
3. Known HF not responding to treatment ie when symptoms are
recurrent or difficult to control
4. Known HF with symptomatic hypotension or excessive bradycardia
5. In the presence of acute coronary syndrome to determine the need
for revascularization by PCI or CABG.
6. In cases of near faints, syncope, resuscitated sudden death and
significant arrhythmias.
7. In any patient with significant valve disease not previously assessed
or with worsening valve disease.
8. Women with significant structural heart disease and past history
of HF or LV dysfunction who intent to get pregnant. This is for pre
conception counselling.
9. Pregnant women with complex cardiac lesions and/or Eisenmenger’s
syndrome.
10. Infants and children with HF

55
 8.3 Heart Failure Clinics
HF clinics enable focussed delivery of care by medical staff familiar with
the problems and needs of such patients.
The out patient management of patients with HF requires a multi-
disciplinary approach to provide patient education, optimization
of medical treatment, psychosocial support, consideration for more
advanced therapy including devices and heart transplantation, cardiac
rehabilitation and palliative care.This would involve medical experts
with interest and competence in the management of HF, supported
by HF nurses, pharmacists, dieticians, physiotherapists, primary care
providers, and social workers.
High risk and/or persistently symptomatic HF patients benefit from
these clinics. Such set ups can improve outcomes through structured
follow-up and better access to care.

9. FUTURE DEVELOPMENT
Future developments may focus on:
• novel pharmacological therapies (e.g. serelaxin, LCZ 696)
A recent large trial compared an angiotensin receptor neprilysin
inhibitor ( LCZ 696) with the ACE-I enalapril on top of other standard
therapy in patients with HF and reduced LV function. LCZ 696 was
found to be superior to enalapril, with a significant reduction in death
and in hospitalizations for HF.288
• Genetic and molecular research may provide further insight into
diagnosis, classification and treatment of HF.
• Cell-based therapies to repair or restore the myocardium. To date,
these have demonstrated modest benefit and phase III trials are on-
going.289
• Advances in device therapy that can support the patient until the
heart recovers.
• Effective programs to prevent new onset HF and re-hospitalisations
eg usage of natriuretic peptide-guided treatment of HF.287

10. PERFORMANCE MEASURES

Performance measures should be used with the goal of improving
quality of care for HF.290,291
Process performance measures focus on the aspects of care that are
delivered to a patient, while outcome measures focus on the end-
points such as mortality or hospitalisation.
Process Performance indicators includes:
- % of patients who had documentation of NYHA Functional Class
- % of patients who had LVEF measurement
- % of patients discharged with ACE-I/ARB
- % of patients discharged on β-blockers
- % of patients given a post discharge appointment
56
 Outcome Measures indicators include:
- In hospital mortality
Refer to Appendix IV for calculation of these measures.

11. IMPLEMENTING THE GUIDELINES AND RESOURCE

IMPLICATIONS
Both acute and chronic HF are common problems encountered at all
levels of healthcare, both in district and general hospitals and in family
medicine clinics. To ensure that patients receive good evidence-based
care, the information in this CPG must be successfully disseminated.
This can be done by ensuring:
– Continuous medical education via regular seminars, lectures
and roadshows particularly at the district hospital and family
medicine clinics. There is generally a lack of knowledge of
evidenced based therapy of HF. Thus education and training is
the most important aspect of the implementation of this CPG.
– Availability of the drugs mentioned in this CPG. Most of these
are already easily available in the Ministry Of Health Drug
formulary. Healthcare personnel need however, to be educated
on their appropriate and timely usage.
– Coordinated linkages between primary healthcare personnel
and tertiary cardiac centres to allow easy and appropriate
referrals. Guidelines for referral are in section 8.2.
– Widespread availability of this CPG to healthcare providers via
printed copies, electronic websites, etc.

57
 Appendix

Appendix I
The New York Heart Association Functional Classification
1 Years
Class
Mortality

No limitation.Ordinary physical activity

CLASS I does not cause undue fatique,dyspnoea or 5 - 10%
palpitation.

Slight limitation of physical activity. Such

CLASS II patients are comfortable at rest. Ordinary
10 - 15%
physical activity results in fatique, palpitation,
dyspnoea or angina.

Marked limitation of physical activity.

Although patients are comfortable at 15 - 20%
CLASS III rest, less than ordinary activity will lead to
symptoms.

Inability to carry on any physical activity

without discomfort. Symptoms of congestive
CLASS IV 20 - 50%
failure is present at rest. With any physical
activity, increased discomfort is experienced.

Appendix II
Important Drug Interactions With Heart Failure Medications
Non-Steroidal These cause vasoconstriction, fluid retention and renal
Anti- dysfunction. The latter is more likely to occur in the
Inflammatory presence of ACEI. NSAIDs should not be prescribed to
Drugs (NSAID) patients in HF unless absolutely necessary.

Calcium Channel Short-acting nifedipine and diltiazem depress

Blockers (CCB) myocardial contractility.

These may impair cardiac contractility and increase

Tricyclic vulnerability to arrhythmias. If indicated, a selective
Antidepressants serotonin reuptake inhibitor may be preferable.

58
Appendix III
Salt Content In Common Malaysian Foods
Content Of Sodium In Foods

Low Content Moderate High Content

Content

Fruit Meat Flavouring Agents Sauces : Soya Tomato

Vegetables Fish Egg Barbeque
Pure Oil Milk Tauchioh
Natural Fats
Sugar Extract Vegetable (Marmite)
Plain Flour Meat (Bovril)
Rice
Most Cereals Enhancers Monosodium
Legumes Glutamate
Rice Flavouring cubes

Rising Agents Bicarbonate of Soda
Baking Powder

Dressing Salad Cream

Moyonnaise

Processed Food Tinned or Canned Food

• Salted Crisps
• Salted Nuts
• Cheese
• Packed Soup
• Raising Agents

Preserved Food Salted Fish /Eggs Cured

Meat Preserved
Sausages
Vegetables /Fruits
Belacan

Medication EffervescentsSalts
Bicarbonate Powder

59
 Appendix IV

Calculation Of Performance And Outcome Measures

Number of patients who

% of patients had documentation of
who had NYHA Functional Class
= X 100
documentation of Number of HF patients
NYHA Functional who were seen during
Class that time period

Number of patients who

% of patients = had LVEF measurement X 100
who had LVEF Number of HF patients
measurement who were seen during
that time period

Number of patients who

were on ACE-I/
% of patients
ARB at discharge
discharged with = X 100
Number of HF patients
ACE-I / ARB
who were seen during
that time period

Number of patients who

were on β-blockers at
% of patients of
= discharge X 100
discharged on
Number of HF patients
β-blockers
who were seen during
that time period

Number of patients who

% of patients were given a post
given a post discharge appointment
discharge = Number of HF patients X 100
appointment who were seen during
that time period

60
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 Acknowledgements
The committee would like to thank the following for their patience,
time and effort :
• Technical Advisory Committee, Clinical Practice Guidelines, Ministry
of Health
• Panel of experts who reviewed the draft
• Secretariat

Disclosure Statement
None of the members of the Expert Committee had any potential conflicts
of interest to disclose.

Sources Of Funding
This CPG was made possible by an educational grant from Novartis,
Malaysia. Views and interests of the funding body have not influenced
final recommendations

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