CPG Ua Nstemi

June 2011
MOH/P/PAK/219.11(GU)
Clinical Practice Guidelines on

management of Unstable Angina/Non ST
Elevation Myocardial Infarction (UA/NSTEMI) 2011
STATEMENT OF INTENT
This guideline was developed to be a guide for best clinical practice
in the management of Unstable Angina/ Non ST Elevation Myocardial
Infarction (UA/NSTEMI). It is based on the best available evidence at the
time of development. Adherence to this guideline does not necessarily
lead to the best clinical outcome in individual patient care. Thus, every
health care provider is responsible for the management of his/her
unique patient, based on the clinical presentation and management
options available locally.
REVIEW OF THE GUIDELINE
This guideline was issued in 2011 and will be reviewed in 2016 or earlier
if important new evidence becomes available.
CPG Secretariat
Health Technology Assessment Unit
Medical Development Division
Level 4, Block EI, Parcel E
Government Offices Complex
62590 Putrajaya, Malaysia
Available on the following websites:

http://www.malaysianheart.org
http://www.moh.gov.my
http://www.acadmed.org.my

SUMMARY
1. Acute coronary syndrome is a spectrum of UA/NSTEMI and STEMI.
The clinical presentation will depend on the acuteness and severity
of coronary occlusion.
2. The diagnosis of UA/NSTEMI is based on history dynamic
ECG changes (without persistent ST elevation), raised cardiac
biomarkers.
3. In UA cardiac biomarkers are normal while in NSTEMI it is elevated.
4. Risk stratification is important for prognosis and to guide management
(Flowchart 1, pg 3).
5. Initial management of intermediate/high risk patients includes optimal
medical therapy with aspirin I,A and clopidogrel I,A (or ticagelor I,B),
UFH I,A or LMWH I,A or fondaprinux I,A. Prasugrel may be considered
as an alternative to clopidogrel in high risk patients after coronary
angiography if PCI is planned I,B. (Table 1, pg 4)
6. Patients with refractory angina and/or hemodynamically unstable
should be considered for urgent coronary angiography and
revascularization I,C.
7. Intermediate/high risk patients should be considered for early invasive
strategy (<72 hours). If admitted to a non-PCI centre, they should be
considered for transfer to a PCI centre I,A.
8. Low risk patients should be assessed non-invasively for ischemia I,A.
(Fig 1, pg 5)
9. All patients should receive optimal medical therapy at discharge.
This includes aspirin I,A, clopidogrel I,B (or ticagrelor I,B or prasugrel I,B if
given during PCI), -blockers I,B, ACE-I I,A or ARB (if ACE-I intolerant
I,B
) and statins I,A. If recurrent or residual ischemia is present, then
anti anginal therapy should also be given I,C. These include nitrates
I,C
, calcium channel blockers IIa, C and/or metabolic agents IIa, C (Table
1, pg 4)
10. These drugs should be uptitrated as outpatient to the recommended
tolerated doses I,C.
11. Cardiac rehabilitation and secondary prevention programs
which includes lifestyle modification is an integral component of
management I,A.

Flowchart 1: Risk Stratification of UA/NSTEMI
Flowchart 1: Risk Stratification of UA/NSTEMI
Low risk
Intermediate/High Risk
Patients with recurrent chest pain
Early post infarction unstable angina
Dynamic ST-segment changes
Elevated cardiac biomarkers
Diabetes
Hemodynamic instability
Depressed LV function (LVEF <40%)
Major arrhythmias (VF, VT)
no angina in the past

no ongoing angina
no prior use of
antianginal therapy
normal ECG
normal cardiac
biomarkers
normal LV function
younger age group
This includes (see Table 1, pg:4):

Aspirin
Clopidogrel or ticagrelor (or prasugrel after
coronary angiography)
Antithrombotics (UFH or LMWH or
Fondaparinux)
-blockers
Statins
ACE-I/ARB
Nitrates
+ CCB (if -blockers contraindicated and/or
unresponsive to above)
+ GP IIb/IIIa inhibitor
Medical therapy*
* This includes aspirin +
Coronary Angiography and Revascularization*
blockers + GTN
Risk stratify as
outpatient (Fig1, pg 5)
*If patient is admitted to a non-PCI centre and has

ongoing ischaemia despite optimal medical therapy, it is
recommended to transfer the patient for coronary
angiography with view to revascularization.
CCB : Calcium channel blockers

UFH : Unfractionated heparin
LMWH : Low Molecular Weight Heparin
GP : Glycoprotein
VF: Ventricular fibrillation
VT: Ventricular tachycardia

Table 1: Medications in Intermediate / High Risk Patients with UA/NSTEMI
Table 1: Medications in Intermediate / High Risk Patients with UA/NSTEMI
Drug
Aspirin
+ Clopidogrel
Initial and Inhospital

medication
I,A
I,A
Medication
at discharge
Comments
I,A
I,A
Continued long term if tolerating

Used in addition to aspirin as part of dual
antiplatelet therapy.
To be continued at least 1 month and
ideally for at least a year post
UA/NSTEMI and,
6-12months or longer post DES
implantation
antiplatelet therapy. This is a less
preferred alternative to clopidogrel.
antiplatelet therapy. Alternative to
clopidogrel in high risk patients
undergoing PCI.
antiplatelet therapy. Alternative to
clopidogrel.
Given for 2-8 days
Given for 2-8 days
Used in patients treated conservatively.
Given for 8 days or duration of
hospitalization
Used as an alternative to UFH and
GPIIb/IIIa inhibitors during PCI
Should be administered early if no
contraindications and continued
indefinitely if ischemia is present.
Continued indefinitely in the presence of
LV dysfunction (LVEF<40%)
Should be administered early in patients
with LV dysfunction (LVEF< 40%), heart
failure, diabetes, hypertension or CKD.
Should be considered long term to
prevent recurrent ischemia
As an alternative to ACE-I in intolerant
patients
I,B
I,C
or, Ticlopidine
IIa,B
IIa,B
or, prasugrel
I,B
I,B
or, ticagrelor
I,B
I,B
+ UFH
or, LMWH
I,A
I,A
I,A
or, fondaprinux
or, Bivalirudin
I,A
+ -blockers
1,B
I,B
I,A
+ ACE-I
I,A
I,A
IIa, A
I,B
I,B
+ Statins
I, A
I,A
+/- calcium
channel blockers
+/- nitrates
1,B
IIa,C
I,C
I,B
IIa,C
I,C
or ARB
High potency statins should be used

early till target LDL-C levels are achieved
and continued indefinitely.
If intolerant to -blockers
Indicated for residual/ recurrent ischemia.
Indicated for residual/ recurrent ischemia.

Figure 1: Non-invasive investigation of Low Risk Patients with
UA/NSTEMI*
Figure 1: Non-invasive investigation of Low Risk Patients with UA/

NSTEMI*
Low Risk patients with UA/NSTEMI
Abnormal ECG,
Limited exercise tolerance
Normal ECG,
Good Exercise Tolerance
Exercise stress test
Equivocal
Negative test
Positive
Exercise/Dobutamine Stress
Echocardiogram or
Radionuclear Perfusion
Scan
Equivocal / Positive Test
Risk Factor Reduction +

Medical Therapy for
CAD
Coronary Angiogram
* Low risk patients have :

no angina in the past
no ongoing angina
no prior use of antianginal therapy
normal ECG
normal cardiac biomarkers
younger age group
normal LV function
Patients who have undergone revascularization and with residual/recurrent or a

change in symptoms should be investigated as above.
All Intermediate/High Risk UA/NSTEMI patients should be considered for coronary
angiography and revascularization. (Flowchart 1, pg 3)

MESSAGE FROM THE DIRECTOR GENERAL OF HEALTH
In the last 8 years since the last CPG UA/NSTEMI was published, the
management of this most important of prodrome to a full blown STEMI has
changed significantly. However, like in 2002, despite the World Health Statistics
(2010) reporting a healthy rise in the number of doctors per population, Health
Facts 2008 from the Ministry of Health Malaysia still state that the main cause
of death in the country is cardiovascular disease.
It is now recognized that early, aggressive management of UA/NSTEMI can
improve clinical outcomes both in the short- and long-term. Mounting evidence
in the early use of antithrombotic agents, early access to revascularization,
and secondary prevention strategies, contribute to the significant reduction of
cardiovascular mortality and morbidity.
In the last few years, the establishment of the National Cardiovascular Database,
comprising of the Acute Coronary Syndrome (NCVD-ACS), Percutaneous
Coronary Intervention (NCVD-PCI), as well as the Malaysian Cardiac Surgery
Registry (MyCARE), has now provided us a unified tool to capture important
data on cardiovascular disease presentation and management in our country.
We now know that the incidence of ACS in Malaysia is approximately 141 per
100,000 population per year, and the inpatient mortality rate is approximately
7%, comparable to many developed countries. We have recorded over 8000
PCI performed in Malaysia over the last 3 years, with a very low rate of serious
complications, particularly in elective procedures (<1%).
Further, in the last few years, increasing numbers of Cardiology Units, as well as
well-run General Medicine Units, are participating in Phase I to III clinical trials.
More Malaysians are now being offered the opportunity to be directly involved
in new therapies and are also being provided stringent world-class care in the
context of a clinical trial setting.
In this rapidly evolving landscape of UA/STEMI management, and a definite
increase in patient load in the face of the rising prevalence of cardiovascular risk
factors published in the recent National Health and Morbidity Survey III, it is time
now to update this CPG UA/NSTEMI. We believe this will provide healthcare
providers with strategies, derived from contemporary evidence, to improve the
diagnosis and treatment of this unpredictable condition.
Dato Hasan Abdul Rahman,

Director General of Health,
Ministry of Health, Malaysia

FOREWARD FROM THE AMERICAN COLEGE OF CARDIOLOGY

On behalf of the American College of Cardiology I want to offer my hearty
congratulations to the National Heart Association of Malaysia in their creation
of this ACS NSTEMI clinical practice guideline update. Adherence to evidence
based medicine has conclusively been shown to improve clinical outcomes.
The field of cardiology in particular has been relatively blessed with a plethora
of many superb international randomized clinical trials (RCT) that form the
backbone of our cardiovascular clinical practice guidelines. The translation
and application of the RCT-generated evidence base to the Malaysian
bedside is the mission of clinical practice guidelines. In particular, NHAMs
Class 1 recommendations for the management of ACS/NSTEMIs represent
the must dos in the management of acute coronary syndromes as these care
measures directly lead to decrease in mortality and morbidity in cardiovascular
disease. In the United States over the past few decades a marked decrease
in the cardiovascular mortality and morbidity has been achieved. This
admirable accomplishment is directly due to increased adherence in clinical
practice guidelines for secondary and primary prevention of coronary disease
along with application of evidence based strategies in the management of
acute coronary syndromes. NHAMs clinical practice guideline reflects well
the local care environment here in Malaysia creating the potential of saving
thousands of lives though your promotion of evidence based ACS care. The
participation in a national acute coronary syndrome registry is an important
component of the cardiovascular quality cycle. If we dont measure it, we cant
manage it!! We applaud the leadership of the National Heart Association of
Malaysia with its enthusiasm and expertise manifested in NHAMs updated
ACS clinical practice guidelines along with your vigorous promotion of the
NCVD Malaysian Acute Coronary Syndrome Registry. The ACC looks forward
in future cardiovascular collaborations with the National Heart Association
of Malaysia in the areas of cardiovascular science, education and in the
promotion of cardiovascular quality.
Congratulations and a personal toast to Malaysian heart health!
Ralph Brindis, MD, MPH, FACC, FSCAI

Immediate Past President,
American College of Cardiology

Members of the Expert Panel

Members ofMembers
the Expert
of Panel
the Expert Panel
erson:
Chairperson:
amalar
Dr.Rajadurai
Jeyamalar Rajadurai
Consultant Cardiologist,
Sime DarbySime
Medical
Darby
Center
Medical Center
Subang Jaya,
Subang
Selangor
Jaya, Selangor
Members
ers (in
Members
(in alphabetical
order)
order)
(inalphabetical
alphabetical
order)
mad Nizar
Dr. Ahmad Nizar
Sime DarbySime
Medical
Darby
Center
Medical Center
Subang Jaya,Selangor
Subang Jaya,Selangor
uar Rapaee
Dr. Anuar Rapaee
Hospital Serdang
Hospital Serdang
Chandran
Dr. Aris Chandran
Consultant Physician,
Hospital Sultanah
Hospital
Bainun,
Sultanah
IpohBainun, Ipoh
ar Ismail
Dr. Omar Ismail
Hospital Besar
Hospital
PulauBesar
Pinang
Pulau Pinang
h Maskon
Dr. Oteh Maskon
Consultant Cardiologist
Consultant Cardiologist
Hospital UKM,
Hospital
KualaUKM,
Lumpur
Kuala Lumpur
e Raman
Dr. Sree Raman
Hospital Tuanku
Hospital
Jaafar,
Tuanku
Seremban
Jaafar, Seremb
(HTA trained)
(HTA trained)
Kui Dr.
Hian
Sim Kui Hian
Sarawak General
Sarawak
Hospital,Kuching
General Hospital,Kuchi
n Azman
Dr. Wan Azman
University Malaya
University
Medical
Malaya
Center
Medical Cente
bayaah
Dr.Zambahari
Robayaah Zambahari
Institute Jantung
Institute
Negara,
Jantung Negara,
Kuala Lumpur
Kuala Lumpur

External Reviewers (in alphabetical order):

External Reviewers
External Reviewers
(in alphabetical
(in alphabetical
order): order):
Dr. Chan Hiang

Dr. Chan
Chuan
Hiang Chuan
ConsultantConsultant
Physician Physician
Sarawak General
SarawakHospital,Kuching
General Hospital,Ku
Dr. Jeyaindran
Dr. Jeyaindran
SinnaduraiSinnadurai
Physician Physician
Head of Internal
Head of
Medicine,
Internal Medicine,
Ministry OfMinistry
Health, Of Health,
Hospital Kuala
Hospital
Lumpur
Kuala Lumpur
Dr. Lee Chuey

Dr. Lee
YanChuey Yan
Cardiologist
Cardiologist
Hospital Sultanah
HospitalAminah
Sultanah
Johor
Aminah Joh
Dr. Lee Fatt

Dr.Soon
Lee Fatt Soon
Geriatrician
Geriatrician
Hospital Kuala
Hospital
Lumpur,
KualaKL
Lumpur, KL
Dr. Kim Tan

Dr. Kim Tan
Cardiologist,
Cardiologist,
Sunway Medical
Sunway
Center,
Medical Center,
Sunway,Selangor
Sunway,Selangor
Dr. V Paranthaman
Dr. V Paranthaman
Family Medicine
FamilySpecialist,
Medicine Specialist,
Klinik Kesihatan
Klinik Kesihatan
Jelapang, Jelapang,
Ipoh, Perak
Ipoh, Perak
Dr. SanthaDr.
Kumari
Santha Kumari
Physician Physician
Hospital Sultanah
HospitalRahimah
SultanahKelang
Rahimah K
Dr. Tee Lian

Dr.Kim
Tee Lian Kim
General Practitioner,
Klinik Young,
Klinik
Newton
Young,
and
Newton
Partners
and Par
Kuala Lumpur/Petaling
Kuala Lumpur/Petaling
Jaya
Jaya
Dr. Wong Kai

Dr. Wong
Fatt Kai Fatt
LW Medical
LW
Associates
Medical Associates
Kuala Lumpur
Kuala Lumpur
Dr. Zurkarnai
Dr. Yusof
Zurkarnai Yusof
Cardiologist
Cardiologist
Hospital Universiti
Hospital Sains
Universiti
Malaysia
Sains Malay
Kota Baru,Kota
Kelantan
Baru, Kelantan

RATIONALE AND PROCESS OF GUIDELINE DEVELOPMENT

Rationale:
Coronary artery disease (CAD) is an important cause of morbidity and
mortality in Malaysia. Patients with CAD may present as stable angina or
as acute coronary syndromes (ACS). ACS is a spectrum of disease
ranging from unstable angina (UA), non ST elevation myocardial infarction
(NSTEMI) to ST elevation myocardial infarction depending on the
acuteness and severity of the coronary occlusion. The last CPG on
UA/NSTEMI was published in 2002. Thus the need for an update.
Objectives:
The objectives of this guideline are to:
provide guidance on the most effective evidence based therapeutic
strategies in patients with UA/NSTEMI to reduce in-hospital
morbidity and mortality.
reduce the risk of recurrent cardiac events in these patients
This Clinical Practice Guideline (CPG) has been drawn up by a committee
appointed by the National Heart Association of Malaysia, Ministry of
Health and the Academy of Medicine. It comprises cardiologists and
general physicians from the government and private sectors as well as
from the Universities.
Process:
Evidence was obtained by systematic review of current medical literature
on UA/NSTEMI using the usual search engines PubMed, Medscape and
Ovid. The other international guidelines (American and European) on the
subject were also studied. After much discussion, the draft was then
drawn up by the members of the Expert Panel 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.
The clinical questions were divided into major subgroups and members of
the Expert Panel were assigned individual topics. The group members met
several times throughout the development of the guideline. All retrieved
literature were appraised by individual members and subsequently
presented for discussion during group meetings. All statements and
recommendations formulated were agreed collectively by members of the
Expert Panel. Where the evidence was insufficient the recommendations
were derived by consensus of the Panel. The draft was then sent to local
external reviewers for comments. It was also sent to the American College
of Cardiology and the European Society of Cardiology for feedback.
10
10

The level of recommendation and the grading of evidence used in this
guideline was adapted from the American Heart Association and the
European Society of Cardiology (ACC/ESC) and outlined on page 13. In
the text, this is written in black on the left hand margin. In the Summary
and Key Recommendations, it is written as a superscript immediately after
the therapeutic agent or at the end of the statement as applicable.
Clinical Questions Addressed:
What is the current evidence on the best practice strategies to
reduce morbidity and mortality in patients with UA/NSTEMI?
Which of these strategies are applicable to our local setting
considering our limited health resources?
Target Group:
This guideline is directed at healthcare providers including general
practitioners, medical officers, general and family physicians and
cardiologists.
Target Population:
All patients (older than 18 years) presenting with chest pain.
Period of Validity of the Guidelines:
This guideline needs to be revised at least every 5 years to keep abreast
with recent developments and knowledge.
Applicability of the Guidelines:
This guideline was developed taking into account our local health
resources. The following are available at all state and district government
hospitals with physicians.
ECG machines, measurement of cardiac biomarkers (including
troponins), treadmill stress ECGs and echocardiograms.
Most of the medications that are recommended in this guideline are
already approved for use in Malaysia.
Intermediate/high risk patients should be identified early and
transferred to hospitals with existing catheterization facilities. In
accordance with the national health plan, the ministry has already
proposed the setting up of catheterization laboratories in most of
the state hospitals.
This guideline aims to streamline management of cardiac patients and
educate health care professional on strategies to optimize existing
resources. We do not anticipate barriers to its implementation.
11
11

Implementation of the Guidelines:
The implementation of the recommendations of a CPG is part of good
clinical governance. To ensure successful implementation of this CPG we
suggest:
increasing public awareness of CAD and its therapies.
continuing medical education and training of healthcare providers.
clinical audit This is done by monitoring :
o In-hospital mortality and morbidity in patients admitted with
ACS (NCVD registry)
o Readmission rates for a cardiac related event in patients
discharged with a diagnosis of ACS. Elective admissions for
cardiac procedure are excluded.
o Documentation of the following;
Risk stratification
Discharge medications to include, antiplatelets,
statins, ACE-inhibitors and Beta blockers.
Discharge plan with regards to cardiac
assessment/tertiary care referral.
12
12

GRADES OF RECOMMENDATIONS AND LEVELS OF EVIDENCE
GRADES OF RECOMMENDATION
I
II
Conditions for which there is evidence and/or general agreement

that a given procedure/therapy is beneficial, useful and/or
effective.
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.
LEVELS OF EVIDENCE
A
B
C
Data derived from multiple randomized clinical trials or meta

analyses
Data derived from a single randomized clinical trial or large non
randomized studies
Only consensus of opinions of experts, case studies or standard
of care
Adapted from the American Heart Association/American College of Cardiology

(AHA/ACC) and the European Society of Cardiology (ESC)
13
13

TABLE OF CONTENTS
Statement of Intent
Summary
Flowchart 1, Table 1, Figure 1
Message from Director General of Health, MOH
Foreward from President of American College of Cardiology
Members of the Expert Panel
External Reviewers
Rationale and Process of Guideline Development
1. Introduction
2. Definition of terms
3. Pathogenesis
4. Diagnosis
4.1 History
4.2 Physical Examination
4.3 Electrocardiography
4.4 Cardiac Biomarkers
4.5 Other Diagnostic Modalities
5. Risk Stratification
5.1 Assessment of Risk
5.2 Rationale for Risk Assessment
5.3 Risk Scores for Prognosis of UA/NSTEMI
5.4 Risk Assessment for Bleeding
6. Triage
7. Management of UA/NSTEMI
7.1 Pre hospital Management
7.2 In Hospital Management
7.2.1 Initial Management
7.2.2 Antiplatelet Agents
7.2.3 Anticoagulant Therapy
7.2.4 Anti Ischemic Drug Therapy
8. Revascularization strategies
8.1 Routine early invasive management
8.2 Routine early conservative management
9. UA/NSTEMI in special groups
9.1 UA/NSTEMI in Elderly
9.2 UA/NSTEMI in Women
9.3 UA/NSTEMI in Chronic Kidney Disease
9.4 UA/NSTEMI in diabetes
10. Post Hospital Discharge
10.1 Medications post discharge
10.2 Investigations during Follow Up
11. Cardiac Rehabilitation
12. References
13. Appendix
14. Acknowledgement
15. Disclosure Statements
16. Source of Funding
14
1
2
3-5
6
7
8
9
10-13
15
15-16
16
17-19
17
17
18
18-19
19
20-21
20
20
20
21
21-22
22-31
23
23-31
23
23-25
25-27
28-30
31-32
31
32
32-36
32-34
34
35
36
36-40
36-39
39-40
40-41
42-50
51-57
58
58
58

1. INTRODUCTION
Cardiovascular Disease (CVD) is one of the main causes of mortality and
morbidity in Malaysia. The estimated incidence of Acute Coronary
Syndrome (ACS) is 141 per 100,000 population per year, and the inpatient mortality rate is approximately 7%. This data is derived from the
National Cardiovascular Disease Database (NCVD) based on the ACS
2006 Annual report1. These figures are similar to that of many developed
countries. Unstable Angina/Non ST Elevation Myocardial Infarction
(UA/NSTEMI) which falls within the spectrum of ACS, is an important
cause of cardiac morbidity and mortality.
The last CPG on UA/NSTEMI was published in 2002. Since then, there
have been significant advances in the management of this important
condition. Thus, it is timely to update this CPG to keep abreast with
contemporary evidenced based state of the art management of this
condition.
2. DEFINITION OF TERMS
ACS is a clinical spectrum of ischemic heart disease. Depending upon the

degree and acuteness of coronary occlusion, it can present as (Figure 2,
pg 16):
Unstable angina (UA)
Non-ST elevation myocardial infarction (NSTEMI)
ST elevation myocardial infarction (STEMI)
These changes may be dynamic. A patient presenting with UA may
progress to NSTEMI or even STEMI.
The terms Q-wave myocardial infarction (QwMI) and non-Q wave
myocardial infarction (NQMI) are no longer preferred.
Unstable angina may be classified as2 (Appendix I, pg 51):
I.
II.
III.
New onset of severe angina or accelerated angina; no rest pain

Angina at rest within past month but not within preceding 48 hours
(angina at rest, subacute)
Angina at rest within 48 hours (angina at rest, acute)
It may be further classified according to clinical circumstances into either:

A)
B)
C)
Secondary develops in the presence of extracardiac disease

Primary develops in the absence of extracardiac disease
Post-infarct develops within 2 weeks of an acute MI
15
15

The diagnosis
of NSTEMI
is established
if a cardiac
biomarker
is detected.
The diagnosis
of NSTEMI
is established
if a cardiac
biomarker
is detected.
The diagnosis of NSTEMI is established if a cardiac biomarker is detected.
In NSTEMI,
ST/TST/T
changes
maymay
be present
in the
ECG,
whereas
in UA
In NSTEMI,
changes
be present
in the
ECG,
whereas
in UA
In NSTEMI, ST/T changes may be present in the ECG, whereas in UA
they they
are usually
absent
and and
eveneven
if they
are present,
are are
usually
transient.
are usually
absent
if they
are present,
usually
transient.
they are usually absent and even if they are present, are usually transient.
FIGURE
2: Pathogenesis
of ACS
FIGURE
2: Pathogenesis
of ACS
FIGURE 2: Pathogenesis of ACS
Adapted with modification from Antman EM, Anbe DT, Armstrong PW et al. ACC/AHA Guidelines
Adapted
with modification
from Antman
EM, Anbe
DT, Armstrong
PW et
al.etACC/AHA
Guidelines
Adapted
with modification
from Antman
EM, Anbe
DT, Armstrong
PW
al. ACC/AHA
Guidelines
for the management of patients with ST Elevation Myocardial Infarction at www.acc.org
for thefor
management
of patients
with ST
Elevation
Myocardial
Infarction
at www.acc.org
the management
of patients
with
ST Elevation
Myocardial
Infarction
at www.acc.org
3. PATHOGENESIS
3. PATHOGENESIS
3. PATHOGENESIS
ACS occurs due to atherosclerotic plaque rupture, fissure or ulceration
occurs
to atherosclerotic
plaque
rupture,
fissure
or ulceration
ACS ACS
occurs
due due
to atherosclerotic
plaque
rupture,
fissure
or ulceration
with superimposed thrombosis and coronary vasospasm. Depending on
superimposed
thrombosis
coronary
vasospasm.
Depending
with with
superimposed
thrombosis
and and
coronary
vasospasm.
Depending
on on
the acuteness, degree of occlusion and the presence of collaterals,
the acuteness,
degree
of occlusion
presence
of collaterals,
the acuteness,
degree
of occlusion
and and
the the
presence
of collaterals,
patients can present as UA, NSTEMI or STEMI.
patients
can present
as UA,
NSTEMI
or STEMI.
patients
can present
as UA,
NSTEMI
or STEMI.
The aetiology of the plaque fissure or rupture is still unclear. Possible
aetiology
of plaque
the plaque
fissure
or rupture
is still
unclear.
Possible
The The
aetiology
of the
fissure
or rupture
is still
unclear.
Possible
causes include inflammation, infection, uncontrolled blood pressure and
causes
include
inflammation,
infection,
uncontrolled
blood
pressure
causes
include
inflammation,
infection,
uncontrolled
blood
pressure
andand
smoking. ACS occurring de novo is called Primary UA/NSTEMI.
smoking.
occurring
de novo
is called
Primary
UA/NSTEMI.
smoking.
ACSACS
occurring
de novo
is called
Primary
UA/NSTEMI.
Occasionally UA/NSTEMI is secondary to a precipitating condition, which
Occasionally
UA/NSTEMI
is secondary
a precipitating
condition,
which
Occasionally
UA/NSTEMI
is secondary
to atoprecipitating
condition,
which
is extrinsic to the coronary arterial bed. This is called secondary
is extrinsic
to the
coronary
arterial
is called
secondary
is extrinsic
to the
coronary
arterial
bed.bed.
ThisThis
is called
secondary
UA/NSTEMI and can occur due to:
UA/NSTEMI
and occur
can occur
UA/NSTEMI
and can
due due
to: to:
increased myocardial oxygen demand as occurring in fever,
increased
myocardial
oxygen
demand
occurring
fever,
increased
myocardial
oxygen
demand
as as
occurring
in in
fever,
tachycardia
and thyrotoxicosis
tachycardia
and
thyrotoxicosis
tachycardia
and
thyrotoxicosis
reduced coronary blood flow due to hypotension
reduced
coronary
blood
flow
due
to hypotension
reduced
coronary
blood
flow
duedelivery
to hypotension
reduced
myocardial
oxygen
in anaemia or hypoxemia
reduced
myocardial
oxygen
delivery
in anaemia
or hypoxemia
reduced myocardial
oxygen
delivery
in anaemia
or hypoxemia
Secondary UA/NSTEMI is an important cause of ACS in the elderly.
Secondary
UA/NSTEMI
an important
cause
of ACS
in the
elderly.
Secondary
UA/NSTEMI
is anisimportant
cause
of ACS
in the
elderly.
1616
16
16

4. DIAGNOSIS
4.1
History
The symptoms of UA/NSTEMI may be indistinguishable from that of

STEMI. These include:
Chest pain - This is the presenting symptom in most
patients. Chest pain or discomfort is usually retrosternal,
central or in the left chest and may radiate to the jaw or
down the upper limb. It may be crushing, pressing or burning
in nature. The severity of the pain is variable.
A significant number of patients, especially women, diabetics and
the elderly, present with atypical symptoms3. These include :
Dyspnoea without any history of chest pains.
Unexplained sweating, nausea and vomiting, syncope and
presyncope, fatigue and epigastric discomfort.
In patients with these presentation(s) and with a prior history of
coronary artery disease (CAD), a family history of premature
CVD, diabetes and other cardiovascular risk factors, the index
of suspicion of ACS should be high. Prior history of diabetes
and renal disease will influence management4,5.
4.2
Physical Examination
The objective of the physical examination is to identify:

possible causes,
precipitating causes and
consequences of UA/NSTEMI
Uncontrolled hypertension, anaemia, thyrotoxicosis, severe aortic
stenosis, hypertrophic cardiomyopathy and other co-morbid
conditions such as lung disease should be identified.
Presence of left ventricular failure (hypotension, respiratory
crackles or S3 gallop) and arrhythmias carry a poor prognosis.
Carotid bruits or peripheral vascular disease indicates extensive
atherosclerosis and a higher likelihood of concomitant CAD.
17
17

4.3
Electrocardiography
The ECG adds support to the diagnosis and provides prognostic

information6-11. A recording made during an episode of chest pain is
particularly valuable.
I, C
It should be performed within 10 minutes of the patients arrival at

the Emergency Department.
Features suggestive of UA/NSTEMI are:
Dynamic ST/T changes
ST depression > 0.5 mm in 2 or more contiguous leads
T-wave inversion deep symmetrical T-wave inversion
Other ECG changes include new or presumed new onset bundle
branch block (BBB)* and cardiac arrhythmias, especially sustained
ventricular tachycardia. Evidence of previous infarctions such as Q
waves may be present.
I, C
However, a completely normal ECG does not exclude the diagnosis

of UA/NSTEMI. Serial ECGs should be done as the ST changes
may evolve.
* New LBBB should be treated as STEMI
4.4. Cardiac Biomarkers

I, A
Cardiac troponins (troponin T or I) are the recommended

biomarkers. (Figure 3, pg 19) They are highly specific and sensitive
for myocardial injury and/or necrosis (infarction), and also provide
important prognostic information, there being a correlation between
the level of troponin and cardiac mortality and other adverse
cardiac events12-16. The troponin level may not be elevated if the
test is done early (<6 hours). To confidently exclude myocardial
necrosis (infarction), a repeat test needs to be done 612 hours
after admission. Troponin testing can be done in the laboratory
(quantitative) or with a hand held rapid semi-quantitative assay.
Blood levels may persist for 514 days after the acute event.
17
Non coronary
rare
Non
coronary causes
causes for
forelevated
elevatedtroponins
troponinsare
areextremely
extremely
rare . 17It. It may o
may occur
in acute
myocarditis,
pulmonary
embolism,
acute
myocarditis,
acute
pulmonaryacute
embolism,
a dissecting
aorticaaneurysm
dissecting
aortic
heartshock.
failureSevere
and sometimes
in
heart
failure
and aneurysm,
sometimesacute
in septic
renal dysfunction
ma
septic
shock.
Severe
renal
dysfunction
may
also
cause
raised
cause raised troponins in the absence of ACS. A raised level is however asso
troponins
in thein absence
of ACS. inAthese
raised
level (Appendix
is however
with
an increase
all cause mortality
patients.
II, pg 52)
associated with an increase in all cause mortality in these patients.
(Appendix II, pg 52)
18
18

Creatinine kinase (CK) and its MB fraction (CKMB) are also important
Creatinineofkinase
(CK) and
its MB
fraction (CKMB)
also important
indicators
myocardial
necrosis
(infarction).
They areare
however,
less
indicatorsand
of specific
myocardial
necrosis
(infarction).
They
however,
sensitive
compared
to cardiac
troponins.
CK are
and CKMB
haveless
compared
to cardiac
troponins.
and CKMB
have
asensitive
shorter and
halfspecific
life and
hence are
more useful
thanCK
troponins
when
a shorter reinfarction.
half life and hence are more useful than troponins when
diagnosing
diagnosing reinfarction.
All patients with NSTEMI have raised troponins, however, the CKMB may
18,19
be
normal in
10-20%
of have
theseraised
patients
. Ahowever,
raised CKMB
in the
All patients
with
NSTEMI
troponins,
the CKMB
may
18,19
18,19
presence
of ainnormal
troponin
level has
no prognostic
. A significance
raised CKMB . in the
be normal
10-20%
of these
patients
presence of a normal troponin level has no prognostic significance 18,19.
Myoglobin is not cardiac specific. It can be detected as early as 2 hours
after
the onset
of chest
pain.
A negative
testbewithin
4-8 hours
of chest
Myoglobin
is not
cardiac
specific.
It can
detected
as early
as 2pain
hours
is
useful
in ruling
out pain.
myocardial
necrosis
(infarction).
It should
not
after
the onset
of chest
A negative
test within
4-8 hours
of chest
pain
however
as the
biomarker necrosis
to identify (infarction).
patients with It
NSTEMI.
is usefulbeinused
ruling
outonly
myocardial
should not
however be used as the only biomarker to identify patients with NSTEMI.

FIGURE 3: Time course of elevation of serum cardiac biomarkers in ACS
FIGURE 3: Time course of elevation of serum cardiac biomarkers in ACS
(Adopted from Clinical Implications of the new definition of myocardial infarction. John K French,
Harvey D White; Heart 2004;90:99106)
(Adopted
from Clinical
Implications of the new definition of myocardial infarction. John K French,
4.5 Other
diagnostic
modalities
4.5 Other diagnostic
Harveymodalities
D White; Heart 2004;90:99106)
IIa, B
Echocardiogram LV systolic function is an important

Echocardiogram LV systolic function is an important
prognostic indicator in patients with UA/NSTEMI. Transient
prognostic indicator in patients with UA/NSTEMI. Transient
reversible regional wall motion abnormalities may be detected
reversible regional wall motion abnormalities may be detected
during ischemia.
during ischemia.
IIa, B
Key message:
Key message:
The diagnosis of UA/NSTEMI is based on history + dynamic ECG changes

The diagnosis of UA/NSTEMI
is based on history + dynamic ECG
19
(without persistent ST elevation), + raised cardiac biomarkers.
(without persistent ST elevation), + raised cardiac biomarkers.
In UA cardiac biomarkers are normal while in NSTEMI it is elevated.
In UA cardiac biomarkers are normal while in NSTEMI
it is elevate
A raised troponin level has diagnostic
19 and prognostic significance I,A.
A raised troponin level has diagnostic and prognostic significance
19

5.
RISK STRATIFICATION
5.1 Assessment of Risk

The initial evaluation should be used to provide information about the
diagnosis and prognosis. An attempt should be made to simultaneously
answer 2 questions:
What is the likelihood that the signs and symptoms represent ACS?
(Appendix III, pg 53)
What is the likelihood of an adverse clinical outcome death, MI (or
recurrent MI), stroke, HF, recurrent symptomatic ischemia, and
serious arrhythmia?
In making a diagnosis of ACS one should consider the symptoms, ECG
abnormalities and cardiac biomarkers. The absence of risk factors does
not exclude a diagnosis of ACS.
5.2 Rationale for Risk Stratification
Patients with UA/NSTEMI have an increased risk of death, recurrent MI,
recurrent symptomatic ischemia, serious arrhythmias, heart failure and
stroke.
Early assessment would help in determining the:
prognosis of the patient
management strategies
- selection of the site of care (coronary care unit, monitored
step-down ward or outpatient setting)
- selection of appropriate therapy and the need for coronary
angiogram and revascularization
5.3 Risk Scores for prognosis of UA/NSTEMI
Several risk stratication scores have been developed and validated in
large patient populations. In clinical practice, 2 risk scores that are
commonly used are:
TIMI Risk Score 20,21 - it is less accurate in predicting events, but is
simple and widely accepted. ( Appendix IV, pg 54)
GRACE risk scores 22 (Appendix V, pg 55)
21
20

Both risk scores confer additional important prognostic value beyond
Both risk scores confer additional important prognostic value beyond
global risk assessment by physicians. These validated risk scores may
global risk assessment by physicians. These validated risk scores may
rene risk stratication, thereby improving patient care in routine clinical
rene risk23 stratication, thereby improving patient care in routine clinical
practice 23. We have proposed a simplified risk stratification model as
practice . We have proposed a simplified risk stratification model as
outlined in Flowchart 1, pg 3.
outlined in Flowchart 1, pg 3.
Hemorrhagic complications are an independent risk factor for subsequent
Hemorrhagic complications are an independent risk factor for subsequent
mortality in ACS patients and in those undergoing PCI. These patients can
mortality in ACS patients and in those undergoing PCI. These patients can
be identified by:
be identified by:
ACUITY HORIZONS-AMI24 Bleeding Risk Score
Risk Score
ACUITY HORIZONS-AMI24 Bleeding
CRUSADE Bleeding Risk Score25
CRUSADE Bleeding Risk Score25
These scores are calculated based on age, clinical status and
These scores are calculated based on age, clinical status and
hemodynamics at presentation, serum creatinine and hematocrit level and
hemodynamics at presentation, serum creatinine and hematocrit level and
the use and combinations of antiplatelets and anticoagulants.
the use and combinations of antiplatelets and anticoagulants.
Key messages
Key messages
Risk stratification is important for prognosis and to guide
Risk stratification
is important for prognosis and to guide
management I,A
.
management I,A.
6.
6.
TRIAGE
TRIAGE
Triage helps in identifying patients who need urgent care. Rapid

Triage helps in identifying patients who need urgent care. Rapid
assessment and aggressive management of high risk patients may result
assessment and aggressive management of high risk patients may result
in an improvement in outcome and a reduction in mortality.
in an improvement in outcome and a reduction in mortality.
Rapid assessment includes:
Rapid assessment includes:
evaluation of patients clinical status:
evaluation of patients clinical status:
- mental status
- mental status
- comfort status
- comfort status
- respiration
- respiration
- peripheral perfusion
- peripheral perfusion
vital signs:
vital signs:
- blood pressure
- blood pressure
- rate and volume of pulse
- rate and volume of pulse
- respiratory rate
- respiratory rate
history:
history:
-
presence and severity of chest pains

presence and severity of chest pains
21
22
22

-
past history of coronary and vascular events, interventions

and surgery
risk factors
hypertension
diabetes mellitus
dyslipidaemia
previous medications eg anti-anginals, antiplatelets
family history of premature CAD
ECG
cardiac biomarkers
- troponins
- CK-MB
Based on the above clinical assessment, patients can be risk stratified to
(Flowchart 1, pg 3) :
I.
II.
Intermediate/high risk
Low risk
The TIMI Risk Score and the Grace Risk Score (see 5.3) are also used to
provide additional prognostic information.
The appropriate management, which includes the rapidity and the degree
of invasiveness, is generally guided by the risk status of the patient. There
is evidence that high risk patients have increasing benefit from therapies
(like low molecular weight heparin (LMWH), glycoprotein (GP) IIb/IIIa
inhibitors) and an invasive strategy.
The recommended therapy based on risk-stratification is as in Flowchart
1, pg 3.
Key messages
Intermediate/high risk patients benefit from early angiography and
revascularization I,A.
7. Management of UA/NSTEMI
The goals of management are:
Immediate relief of ongoing ischemia and angina
Prevention of recurrent ischemia and angina
Prevention of serious adverse cardiac events
23
22

7.1 Pre-hospital Management
7.1 Pre-hospital Management
Based
on the triage:
7.1 Pre-hospital
Management
Based on the triage:
Ifonthe
Based
thehistory
triage: is suggestive of ACS :
- history
Give soluble
aspirin 300
crushed
stat
If the
is suggestive
of mg
ACS
:
- history
Give sublingual
GTN300
If the
is suggestive
of mg
ACS
:
soluble
aspirin
crushed
stat
lead ECG
and300
cardiac
biomarkers
soluble
aspirin
mg crushed
stat
- Do
Give12sublingual
GTN
Give12sublingual
- Do
lead ECGGTN
and cardiac biomarkers
- Do 12 lead ECG and cardiac biomarkers
If the ECG and cardiac biomarkers are suggestive of ACS
Give and
clopidogrel
mg stat if are
available.
If the- ECG
cardiac300
biomarkers
suggestive of ACS
-- ECG
Sendand
the cardiac
patient300
to
the
healthcare
facility
where
If the
biomarkers
suggestive
of ACS
Give
clopidogrel
mgnearest
stat if are
available.
definitive
be
given.
mgnearest
stat
if available.
-- Give
Sendclopidogrel
the treatment
patient300
to can
the
healthcare facility where
- Send
the treatment
patient to can
the nearest
definitive
be given.healthcare facility where
definitive
treatment
can be given.
If the ECG
and cardiac
biomarkers
are inconclusive for ACS
Lowand
riskcardiac
patients
: they canare
be inconclusive
referred as outpatient
If the- ECG
biomarkers
for ACS
for
cardiac
assessment.
(Fig
1,are
pginconclusive
5)
If the- ECG
and
biomarkers
for ACS
Low
riskcardiac
patients
: they
can
be
referred as outpatient
Intermediate
/ High: Risk
patients
: shouldasbeoutpatient
admitted
- Low
risk patients
they
can
referred
for cardiac
assessment.
(Fig
1, be
pg 5)
.Intermediate
cardiac assessment.
(Fig
1, pg 5): should be admitted
- for
/ High Risk
patients
- - Intermediate
/ High Risk patients : should be admitted
.
7.2 In-Hospital
Management (Table1, pg 4)
- .
7.2 In-Hospital
Management (Table1, pg 4)
7.2.1 In-Hospital
Initial management
General
Measures
7.2
Management
(Table1,
pg 4)
7.2.1 Initial management General Measures
Following
risk stratification:
7.2.1 Initial
management
General Measures
Following risk stratification:
low
risk patients
may be treated as outpatient.
Following
risk stratification:
low risk patients may be treated as outpatient.
High
riskpatients
patients
preferably
should
be admitted to CCU/HDU
low risk
may
be treated
as outpatient.
I, C
High
risk
patients
preferably
should
be admitted to CCU/HDU
with
continuous
ECG
monitoring.
I, C
High
risk patients
preferably
should be admitted to CCU/HDU
with continuous
ECG
monitoring.
I, C
supplemental
oxygen
should be given to maintain SpO2 >90%,
with continuous
ECG monitoring.
supplemental
oxygen
should be failure,
given torespiratory
maintain SpO
in
patients with
left ventricular
distress
or
2 >90%,
I, B
supplemental
oxygen
should
be failure,
given torespiratory
maintain SpO
2 >90%,
in
patients
left ventricular
distress
or
having
high with
risk
features
for hypoxemia.
I, B
in
patients
left ventricular
failure, respiratory distress or
I, B
having
high with
risk features
for hypoxemia.
for painhigh
relief,
(intravenous
having
riskmorphine
features for
hypoxemia.2 mg to 5 mg) together
IIa,B
for pain
relief, morphine
(intravenous
2 mg
mg) together
with
concomitant
intravenous
anti-emetic
maytobe5given.
IIa,B
for
pain
relief, morphine
(intravenous
2 mg
tobe5given.
mg) together
with
concomitant
intravenous
anti-emetic
may
IIa,B
7.2.2. Medications
- Antiplatelet
agents
with concomitant
intravenous
anti-emetic may be given.
7.2.2. Medications - Antiplatelet agents
7.2.2.1
Oral antiplatelet
agents
7.2.2. Medications
- Antiplatelet
agents
7.2.2.1
Oral antiplatelet agents
7.2.2.1.1
Acetylsalicylic
(ASA)
7.2.2.1
Oral
antiplateletacid
agents
7.2.2.1.1 Acetylsalicylic acid (ASA)
Recommended
loading
dose: 300 mg of soluble/chewable
Acetylsalicylic
acid (ASA)
I, A 7.2.2.1.1
26,27
. Enteric
coated
aspirin
for
aspirin
Recommended
loading
dose:
300 is
mgnotof recommended
soluble/chewable
I, A
26,27
initial
loading
dose
because
ofaspirin
its300
slowis
onset
of
action.
Recommended
loading
dose:
mg
soluble/chewable
. Enteric
coated
notof recommended
for
aspirin
I, A
26,27
. Enteric
coatedofaspirin
isonset
not recommended
for
aspirinloading
initial
dose because
its slow
of action.
24
initial loading dose because of its slow onset of action.
24
24
23

Maintenance dose: 75-150 mg daily of soluble or enteric
coated aspirin 26,27
I, A
Aspirin in excess of 300-325 mg per day is associated with

increased risk of minor bleeding without greater efficacy 27.
7.2.2.1.2
Adenosine
Antagonists
Diphosphate
(ADP)
Receptor
These include:
I, A
Clopidogrel loading dose: 300 to 600 mg, maintenance dose:

75 mg/day 28,29
IIa, B
Ticlopidine dose: 250 mg b.i.d. It is associated with

neutropenia in 1% of patients 30. Due to this safety reason, it is
not preferred. Patients on ticlopidine should have their total
white cell count monitored regularly for the initial 3 months.
I, B
Prasugrel loading dose 60 mg, maintenance dose: 10 mg/day
I, B
To date, outcome data is only available in ACS patients

undergoing PCI 31. It is recommended to be given after
coronary angiography in patients planned for PCI.
Its use in other subsets of patients is still being evaluated.
It is not recommended for patients >75 years old, <60 kg

weight, past history of transient ischemic attack or stroke
due to a higher risk of major bleeding.
Ticagrelor loading dose : 180 mg, maintenance dose : 90 mg

bid.
-
Ticagrelor was shown to significantly reduce cardiovascular

endpoints when compared to clopidogrel in patients with
ACS 32.
This agent is short acting and thus can be used in patients

who may need surgery without increasing the risk of
bleeding.
Potential drawback is dyspnoea and transient ventricular

pauses during the first week. This was rarely associated
with symptoms or need for a pacemaker. There was also a
small increase in non CABG related major bleeding32.
25
24
with symptoms or need for a pacemaker. There was also a
management of Unstable Angina/Non 32

ST
small increase in non CABG related major bleeding .
Elevation
Infarction
(UA/NSTEMI)
2011
withMyocardial
symptoms or need
for a pacemaker.
There was
also a
7.2.2.2 Intravenous
Antiplatelet
Therapy
Glycoprotein
small increase
in non CABG
related major
bleeding 32. (GP)
IIb/IIIa Inhibitors
7.2.2.2 Intravenous Antiplatelet Therapy Glycoprotein (GP)
include:
IIb/IIIa These
Inhibitors
Abciximab
These
include:
Tirofiban
Abciximab
Eptifibatide
Tirofiban
TheseEptifibatide
agents may be used in high risk patients awaiting transfer
to a PCI facility for an early invasive strategy. Its routine use as
33,34
These agents
may be
used
in high
riskno
patients
upstream
therapy
prior
to PCI
is now
longer awaiting
practicedtransfer
.
to a PCI facility for an early invasive strategy. Its routine use as
33,34
therapy
prior to PCI is now no longer practiced
.
7.2.3.upstream
Anticoagulant
Therapy
7.2.3. Anticoagulant
Therapy
These include: (Table
2, pg 27)
I, A
I, A
I, A
I, A
I, A
I, A
I, B
I, B
I, A
I, A
These
include: (Table
2, pg(UFH)
27)
Unfractionated
heparin
Unfractionated heparin (UFH)
Low Molecular Weight Heparin (LMWH)-Enoxaparin 35,36,37
Anti Xa inhibitor-Fondaparinux
Low Molecular Weight Heparin (LMWH)-Enoxaparin 35,36,37
Anti- XaItinhibitor-Fondaparinux
is best used in UA/NSTEMI patients treated
conservatively 38,39.
- It isis associated
best usedwith
in an
UA/NSTEMI
treated
increase in patients
catheter-related
38,39
.
conservatively
thrombus
and coronary
angiographic complications.
- It is
with an increase
in catheter-related
is associated
not recommended
as the sole
anticoagulant
38,39 coronary angiographic complications.
thrombus
during
PCIand
.
is notin recommended
as the
the patient
sole anticoagulant
- It
If used
UA/NSTEMI and
requires an
38,39
during
PCI
. UFH should be given during the
invasive
strategy,
- If
used in UA/NSTEMI
the itpatient
requireswith
an
procedure.
When used and
in PCI,
is associated
38,39,40
invasive
strategy,
UFH
given
lower
bleeding
rates
thanshould
LMWHbe
. during the
procedure. When used in PCI, it is associated with
38,39,40
lower
bleeding
. undergoing
Presently
newer
oralrates
antithan
Xa LMWH
inhibitors are
evaluation for ACS.
Presently newer oral anti Xa inhibitors are undergoing
evaluation
for ACS.
Anti
IIa inhibitors
Bivalirudin
Anti- IIaItinhibitors
Bivalirudin
may be used
as a substitute for heparin in patients
with heparin-induced thrombocytopenia (HIT) 41.
may
be used as
a substitute
foras
heparin
in patients
- It is
reasonable
to use
bivalirudin
an alternative
to
41
.
with
thrombocytopenia
(HIT)
UFHheparin-induced
and GP IIb/IIIa inhibitors
in patients
undergoing
42-45
- PCI
It is reasonable
to use bivalirudin as an alternative to
.
and GP IIb/IIIa
inhibitors
in patients undergoing
- UFH
It is associated
with less
bleeding.
42-45
- PCI
To date .it is not yet available in Malaysia.
- It is associated with less bleeding.
- To date it is not yet available
26 in Malaysia.
26
25

Key messages
High risk patients preferably should be continuously monitored in
CCU/HDU I,C.
Intermediate/high risk patients should be given ASA I,A,clopidogrel I,A
(or prasugrel I,B or ticagrelor I,B) and UFH I,A or LMWH I,A or
fondaparinux I,A. Prasugel may be given after coronary angiography in
high risk patients undergoing PCI I,B. (Table 1, pg 4)
Low risk patients should be given aspirin I,A and risk stratified as
outpatient with non invasive tests for reversible ischemia. (Fig 1, pg 5)
27
26

TABLE 2: Doses of Anticoagulant Agents in UA/NSTEMI and during PCI*35-39,42-45
AGENT
UFH
UA/NSTEMI
During PCI
Enoxaparin
UA/NSTEMI
During PCI
Bivalirudin
UA/NSTEMI
During PCI
DOSING REGIMEN
Initial IV bolus : 60 IU/kg (max 4000 IU) followed by infusion of 12
IU/kg/hour (max 1000 IU/hour) adjusted to maintain aPTT 1.5-2.0x
normal. Duration of therapy : 2-8 days35-37
Loading Dose :
Empirical loading dose: 5000-10000 IU, or
Weight adjusted loading dose:
- Not receiving GP IIb/IIIa inhibitors: 70-100 IU/kg
- Receiving GP IIb/IIIa inhibitors : 50-70 IU/kg
Further doses if procedure is > 1 hour may be by:
Empirical weight adjusted doses :
- Not receiving GP IIb/IIIa inhibitors: 60 IU/kg
- Receiving GPIIb/IIIa inhibitors: 50 IU/kg
Guided by ACT monitoring
- Not receiving GP IIb/IIa inhibitors maintain ACT:
250-300 secs
- Receiving GP IIb/IIIa inhibitors maintain ACT: 200 secs
Initial 30 mg IV bolus and then 15 minutes later by:
sc 1.0 mg/kg every 12 hours if age less than 75 years
sc 0.75 mg/kg every 12 hours if age 75 years and above
Duration of therapy : 2-8 days 35-37
Depends on prior enoxaparin use:
No prior use : 0.5-0.75 mg/kg IV bolus
Prior use within 8 hours of PCI: no additional dose
Prior use between 8-12 hours of PCI: 0.3 mg/kg IV.
Supplemental UFH may also be given during PCI
0.1 mg/kg bolus and 0.25 mg/kg/hour infusion
Depends on prior bivalirudin/UFH use:
Prior treatment with bivalirudin: additional 0.5 mg/kg bolus
and increase infusion rate to 1.75 mg/kg/hour
Prior treatment with UFH: wait 30 mins then 0.75 mg/kg
bolus and infusion of 1.75 mg/kg/hour
No prior treatment: 0.75 mg/kg bolus and infusion of 1.75
mg/kg/hour
Fondaparinux
UA/NSTEMI
2.5 mg sc daily for 8 days or duration of hospitalization 38,39
During PCI
If used during PCI, additional 50-60 IU/ kg UFH is recommended.
* For doses in renal impairment see section 9.3, Table 6, pg 35

28
27

7.2.4 Anti-Ischemic Drug Therapy
These agents may be given either for relief of ischemia (symptoms)
or for prognosis.
7.2.4.1
I, C
I, C
Nitrates (Table 3, pg 29)
Sublingual glyceryl trinitrate (GTN 0.5 mg) Patients with

UA/NSTEMI with ongoing chest pain should receive sublingual
GTN 0.5 mg every 5 minutes for a total of 3 doses. If symptoms still
persist, intravenous GTN should be considered.
Intravenous nitrates may be administered in the following
situations:
No symptom relief after 3 doses of sublingual GTN
Presence of dynamic ECG changes
Presence of left ventricular failure
Concomitant high blood pressure.
Oral nitrates may be given after 12 to 24 hours of pain free period.
Rebound angina may occur with abrupt cessation of nitrates 46.
Contraindications to nitrate therapy:
Hypotension (SBP< 90 mmHg)
RV infarction
History of phospho-diesterase 5 inhibitors
(depending upon the half-life of the agent)
7.2.4.2
I, B
ingestion
-blockers (Table 4, pg 29)
In the absence of contraindications, -blockers should be

administered early.
Contraindications for -blockers in UA/NSTEMI 47 :
Patients with marked first-degree AV block (PR interval
greater than 0.24s).
Second- or third-degree AV block.
History of bronchial asthma
Severe peripheral arterial disease
Acute decompensated LV dysfunction
Cardiogenic shock.
29
28

Table 3: Recommended dosages of Nitrates in UA/NSTEMI*
Compound
Route
Dosage
Time of Onset
Table 3: Recommended dosages of Nitrates in UA/NSTEMI*

Compound
Nitroglycerine,
Glyceryl
trinitrate
Nitroglycerine,
Glyceryl
trinitrate
Isosorbide
dinitrate
Isosorbide
Isosorbide
dinitrate
mononitrate
0.3 - 0.6 mg, can repeat up

to 3 times
at 5 minute
Dosage
intervals
0.3 - 0.6 mg, can repeat up
200 g/min*
to53times
at 5 minute
intervals
0.4 0.8 mg
per metered
Sublingual
Route
Intravenous
Sublingual
Intravenous
GTN
Spray
GTN Spray
Transdermal patch
Intravenous
Transdermal patch
Oral
Intravenous
Oral (LA)
Oral
dose, no more than 3

5 200 g/min*
sprays at 5 minute
intervals
0.4 0.8
mg per metered
dose, no more than 3
2.5 20 mg over 12 hours
sprays at 5 minute
on, then 12 hours off
intervals
2 12 mg / hour
2.5 20 mg over 12 hours
off
10 on,
20then
mg,12
2 hours
3 times
daily
2 12 mg / hour
2 minute
Time
of Onset
12
minute
minute
minute
2 1minute
2 minute
1 2 hours
1 minute
1 2 hours
30 60 minutes
1 minute
mg 2
daily,
10 30-60
20 mg,
3 times
( max 120
dailymg )
30 60 minutes
*The dose of IV nitrates should be titrated every 5 10 minutes until symptoms and/or
Isosorbide
30-60 mg daily,
ischaemia is relieved
the desired haemodynamic
response is obtained
Oraland
(LA)
mononitrate
( max 120 mg )
*As stated in MIMS Malaysia
*The dose of IV nitrates should be titrated every 5 10 minutes until symptoms and/or
ischaemia
is relieved and thedosages
desired haemodynamic
is obtained
Table 4: Recommended
of -blockersresponse
in UA/NSTEMI*
Type
Initiation dose
Target dose
Table 4: Recommended dosages of -blockers in UA/NSTEMI*
Metoprolol
Type
Atenolol
25 mg bd
100 mg bd
Initiation
25 mg oddose
Target
100
mg dose
od
Metoprolol
Bisoprolol
25 mg
mg od
bd
1.25
100
10
mgmg
odbd
Atenolol
Carvedilol
25 mg
3.125
mg od
bd
100
25
mgmg
bdod
Bisoprolol
*As
stated in MIMS Malaysia
Carvedilol
1.25 mg od
10 mg od
3.125 mg bd
25 mg bd
30
30
29

7.2.4.3
7.2.4.3
Calcium
Calcium
Channel
Channel
Blockers
Blockers
5, pg
5, 30)
pg 30)
7.2.4.3
Calcium
Channel
Blockers
(Table(Table
5, (Table
pg 30)
Calcium
Calcium
channel
channel
blockers
blockers
(CCB)
(CCB)
may
may
be in
be
used
used
in UA/NSTEMI
in UA/NSTEMI
in the
Calcium
channel
blockers
(CCB)
may
be
used
UA/NSTEMI
in the in the
following
following
situations:
situations:
following
situations:
Verapamil
Verapamil
or diltiazem
or diltiazem
an
as an
alternative
alternative
to patients
towho
patients
areare
not not
Verapamil
or diltiazem
as anasalternative
to patients
arewho
notwho
48 48
able
to tolerate
to tolerate
or who
or who
have
have
contraindication
contraindication
to toblockers.
48blockers.
able
toable
tolerate
or who
have
contraindication
to blockers.
Continuing
Continuing
or recurring
or or
recurring
recurring
angina
angina
despite
angina
despite
adequate
despite
adequate
adequate
doses of
doses
doses
of of
IIa,C
IIa,CIIa,C Continuing
nitrates
nitrates
nitrates
andand
-blockers
and
-blockers
-blockers
verapamil,
verapamil,
verapamil,
diltiazem,
diltiazem,
diltiazem,
slow release
slow
slow
release
release
nifedipine
nifedipine
nifedipine
andand
amlodipine.
and
amlodipine.
amlodipine.
Prinzmetals
Prinzmetals
Prinzmetals
angina
angina
(variant
angina
(variant
angina)
(variant
angina)
angina)
I, BI, B I, B
Short-acting
Short-acting
Short-acting
dihydropyridine
dihydropyridine
dihydropyridine
CCB CCB
should
CCB
should
beshould
avoided
be avoided
be avoided
III,III,
A AIII, A
Table
Table
Table
5: 5:
Recommended
Recommended
5: Recommended
dosages
dosages
dosages
of Calcium
of Calcium
of Channel
Calcium
Channel
Blockers
Channel
Blockers
inBlockers
UA/NSTEMI*
in UA/NSTEMI*
in UA/NSTEM
Drug
Drug
Drug
Diltiazem
Diltiazem
Diltiazem
Dose Dose
Dose
Immediate
Immediate
release
release
30-90
30-90
mg mg
tds tds
Immediate
release
30-90
mg
tds
Slow Slow
release
Slow
release
100-200
release
100-200
mg
100-200
od mg mg
od od
Verapamil
Verapamil
Verapamil
Immediate
Immediate
release
release
40-80
40-80
mg mg
tds tds
Immediate
release
40-80
mg
tds
Slow
release
release
120-240
120-240
od od
Slow Slow
release
120-240
mg
od mg mg
Amlodipine
Amlodipine
Amlodipine
2.5-10
2.5-10
od od
2.5-10
mg
odmg mg
Nifedipine
Nifedipine
Nifedipine
Slow Slow
release
Slow
release
30-90
release
30-90
mg 30-90
od mg mg
od od
*As
stated
in MIMS
inMalaysia
MIMS
Malaysia
Malaysia
*As*As
stated
instated
MIMS
7.2.5
7.2.5
Lipid
Lipid
Modifying
Modifying
Drugs
Drugs
7.2.5
Lipid
Modifying
Drugs
Current
Current
data
data
indicate
indicate
that
early
early
initiation
initiation
high
of high
dose
dose
statin
statin
therapy
therapy
Current
data
indicate
that that
early
initiation
of
highofdose
statin
therapy
I,A A I, A soon
soon
after
admission
for for
UA/NSTEMI
cancan
reduce
major
adverse
soon
after
admission
UA/NSTEMI
reduce
major
adverse
after
admission
for UA/NSTEMI
can reduce
major
adverse
49-54
49-5449-54
cardiac
events
topleotropic
its
cardiac
events
due due
to its
effectseffects
cardiac
events
due
to pleotropic
its pleotropic
effects
. Patients
. Patients
.with
Patients
ACS
withwith
ACS
ACS
undergoing
undergoing
undergoing
PCI,PCI,
have
PCI,
have
also
have
also
been
also
been
found
been
found
to found
benefit
to to
benefit
with
benefit
thewithwith
the the
administration
administration
administration
of high
of high
of
dose
high
dose
statins
dose
statins
before
statins
before
and
before
within
andand
10
within
days
within
10
of days
10
the days
of the
of the
55-5755-5755-57
. . .
procedure
procedure
procedure
The
The
statins
The
statins
statins
thatthat
have
that
have
been
have
been
studied
been
studied
instudied
UA/NSTEMI
in UA/NSTEMI
in UA/NSTEMI
to date to
are:
date
to date
are:are:
Atorvastatin
Atorvastatin
Atorvastatin
80mg
80od
mg
80 mg
od od
Simvastatin
Simvastatin
Simvastatin
40mg
40od
mg
40 mg
od od
31
30
31 31

7.2.6Angiotensin
AngiotensinConverting
ConvertingEnzyme
EnzymeInhibitor
Inhibitor(ACE-I)/ARB
(ACE-I)/ARB(Table
(Table
7.2.6
7,7,pgpg39)
39)
I, A
I, A
These
Theseshould
shouldbebeconsidered
consideredearly
earlyforforpatients
patientswith
withLV
LVdysfunction
dysfunction
55
. .
and
anddiabetes
diabetes 55
Key
Keymessages
messages
Patients
Patientsshould
shouldbebetreated
treatedwith
withoptimal
optimalmedical
medicaltherapy.
therapy.
(Table
(Table1,1,pgpg4)4)
I,C
I,B
I,C
Nitrates
, ,-blockers
Nitrates I,C
-blockers I,B+ +CCBs
CCBs I,Care
aregiven
givenforforrelief
reliefofof
ischemia.
ischemia.
Statins I,AI,Aand ACE-I (for LV dysfunction, LVEF < 40%) I,AI,Aare

Statins and ACE-I (for LV dysfunction, LVEF < 40%) are
given for prognosis.
given for prognosis.
8. Revascularization Strategies
8. Revascularization Strategies
There is a strong rationale for early revascularization in
There is a strong rationale for early revascularization in
. (Flowchart 1,
intermediate/high risk patients with UA/NSTEMI 56,57
intermediate/high risk patients with UA/NSTEMI 56,57. (Flowchart 1,
pg 3, Appendix IV, pg 54) Contemporary antiplatelet and
pg 3, Appendix IV, pg 54) Contemporary antiplatelet and
anticoagulant therapies have reduced the early hazard of PCI.
anticoagulant therapies have reduced the early hazard of PCI.
With increasing procedure experience, technological improvements
procedure experience,
technological
improvements
inWith
PCI increasing
and the development
of new antiplatelet
and anticoagulant
in
PCI
and
the
development
of
new
antiplatelet
and
anticoagulant
regimens there is a general trend for early revascularization
in
regimens
there
is a general
trend for
early revascularization in
these
patients
following
optimal medical
therapy.
these patients following optimal medical therapy.
8.1. Routine early invasive management 58-61
8.1. Routine early invasive management 58-61
Urgent (as soon as possible after hospital presentation) 62
I, B
62
Urgent (as
soon as possible after hospital
coronary
angiography/revascularization
for presentation)
patients with
I, B
coronary orangiography/revascularization
with
refractory
recurrent angina associated for
with patients
dynamic ST
refractoryheart
or recurrent
angina
associated
with dynamic
ST
deviation,
failure, life
threatening
arrhythmias
and/ or
deviation, heart
failure, life threatening arrhythmias and/ or
hemodynamic
instability
hemodynamic instability
Early (<72 hours) coronary angiography/revascularization- in
I, A
patients
with hours)
high-risk
features
as predicted by a positivein
Early (<72
coronary
angiography/revascularizationI, A
biomarker
assay,
ST segment
changes
or a high
score
patients with
high-risk
features
as predicted
by risk
a positive
58-61
according
to assay,
the TIMIST
scale
or equivalent
. a high risk score
biomarker
segment
changes or
according to the TIMI scale or equivalent 58-61.
Routine invasive evaluation is not recommended in low risk
IIb, B
58-61
.
patients
Routine invasive
evaluation is not recommended in low risk
IIb, B
patients 58-61.
However these patients are recommended to have non-invasive
assessment
for inducible
ischemia. to have non-invasive
However these
patients or
aresilent
recommended
assessment for inducible or silent32
ischemia.
32
31

8.2 8.2Routine
Routine
earlyearly
conservative
conservative
management
management
(selective
(selective
invasive
invasive
63,64,65
63,64,65
therapy)
therapy)
TheThe
use use
of aggressive
of aggressive
anticoagulant
anticoagulant
and antiplatelet
and antiplatelet
agentsagents
has has
alsoalso
reduced
reduced
the incidence
the incidence
of adverse
of adverse
outcomes
outcomes
in patients
in patients
63,64,6563,64,65
managed
managed conservatively
conservatively
.
. Selective
Selectivecoronary
coronary
is indicated
is indicated
for those
for those
who cannot
who cannot
be be
stabilized
stabilized
medically
medically
or inor whom
in whom
objective
objective
evidence
evidence
of
of
significant
significant
ischemia
ischemia
is provoked
is provoked
in theinsub
theacute
sub acute
phase.phase.
I, A I, A
IIa, AIIa, A
A conservative
A conservative
strategy
strategy
is recommended
is recommended
for women
for women
who are
who are
66
stabilized
stabilized
and and
remain
remain
biomarker
biomarker
negative
negative
. 66.
IIa, AIIa, A
An early
An early
invasive
invasive
or conservative
or conservative
therapy
therapy
is a reasonable
is a reasonable
option option
66
66
.
.
for men
for men
who who
are stabilized
are stabilized
and remain
and remain
biomarker
biomarker
negative
negative
Patients
Patients
with with
UA/NSTEMI
UA/NSTEMI
treated
treated
conservatively
conservatively
are atare
riskatofrisk of
developing
developing
recurrent
recurrent
adverse
adverse
cardiac
cardiac
events.
events.
Thus Thus
these these
patients
patients
needneed
to be
to evaluated
be evaluated
periodically
periodically
for reversible
for reversible
ischemia
ischemia
usingusing
non non
invasive
invasive
tests.tests.
If ischemia
If ischemia
is present,
is present,
they they
should
should
be be
considered
considered
for for
coronary
coronary
angiography
angiography
and and
revascularization.
revascularization.
KeyKey
messages
messages
Patients
Patients
with with
refractory
refractory
angina
angina
and/ and/
or hemodynamically
or hemodynamically
unstable
unstable
should
considered
for urgent
coronary
angiography
should
be be
considered
for urgent
coronary
angiography
and and
I,C
revascularization
revascularization
. I,C.
Intermediate/high
Intermediate/high
risk risk
patients
patients
should
should
be considered
be considered
for early
for early
I,A
I,A
invasive
invasive
strategy
strategy
(<72(<72
hours)
hours)
. If admitted
. If admitted
to a non-PCI
to a non-PCI
centre,centre,
they they
I,B
I,B
should
should
be considered
be considered
for transfer
for transfer
to a PCI
to a centre
PCI centre
. (Flowchart
. (Flowchart
1,
1,
pg 3)
pg 3)
I,C
I,C
LowLow
risk risk
patients
patients
should
should
be assessed
be assessed
non-invasively
non-invasively
for ischemia
for ischemia
.
.
(Fig(Fig
1, pg1,5)pg 5)
9 UA/NSTEMI
UA/NSTEMI
IN SPECIAL
IN SPECIAL
GROUPS
GROUPS
All patients
All patients
should
should
receive
receive
optimal
optimal
medical
medical
therapy.
therapy.
(Table(Table
1, pg 4)
1, pg 4)
9.1 9.1UA/NSTEMI
UA/NSTEMI
in the
in Elderly
the Elderly
Cardiovascular
Cardiovascular
morbidity
morbidity
and mortality
and mortality
increases
increases
by 70%
by for
70%
every
for every
10
10
.
.
yearyear
increase
increase
in age
in 18,67-68
age18,67-68
33
32
33

9.1.1
9.1.1
Clinical
Clinicalpresentation:
presentation:
AA high
high index
index ofof suspicion
suspicion isis necessary
necessary to make a diagnosis
diagnosis of
of
UA/NSTEMI
UA/NSTEMI inin elderly
elderly patients.
patients. Atypical
Atypical presentations
presentations occur more
more
frequently.
frequently.These
Theseinclude:
include:
dyspnoea
dyspnoea
diaphoresis
diaphoresis
nauseaand
andvomiting
vomiting
nausea
neurological
neurological symptoms
symptoms such
such as
as acute
acute confusional states
states and
and
syncope
syncope
ACS
ACSfrequently
frequentlydevelops
develops as
as aa secondary
secondary coronary
coronary event in the setting
setting
ofofanother
anotheracute
acute illness
illness e.g.
e.g. pneumonia.
pneumonia. The
The elderly often are in heart
heart
69
.. The
diagnostic.
failure
failureatatthe
thetime
timeofofpresentation
presentation 69
The ECGs
ECGs may be non diagnostic.
9.1.2.
9.1.2. Management
Management
There
especially
Thereisislimited
limitedtrial
trial data
data to
to guide
guide management
management in the elderly especially
ininthe
significant cocothesetting
setting ofof advanced
advanced age
age (more
(more than
than 75 years) or significant
morbidity
consider the
the
morbidity(e.g.
(e.g.prior
prior stroke,
stroke, renal
renal impairment).
impairment). One should consider
biological
when
biological age
age rather
rather than
than the
the chronological
chronological age of the patient when
making
group
makingmanagement
management decisions.
decisions. The
The elderly
elderly are a heterogenous group
and
individualized.
andthe
therisk
risk benefit
benefit ratio
ratio of
of each
each intervention
intervention should be individualized.
Creatinine
drug
Creatinine clearance
clearance should
should be
be calculated
calculated to enable appropriate drug
dosing.
dosing.(Appendix
(AppendixVI,pg
VI,pg56)
56)
I, I,AA
Bothaspirin
aspirinand
and clopidogrel
clopidogrel (especially
(especially in those undergoing
Both
undergoing PCI)
PCI)
70,71
confergreater
greaterabsolute
absolute and
and relative
relative benefits
benefits in the elderly 70,71
..
confer
I, I,BB
Prasugrel should
should be
be avoided
avoided in
in patients
patients older than 75 years
Prasugrel
years in
in
31
view
viewofofthe
thebleeding
bleedingrisk
risk 31
..
I, I,AA
InInaameta-analysis,
effective in
in
meta-analysis,both
both UFH
UFH and
and LMWH
LMWH were equally effective
However bleeding
bleeding risk
risk is
is higher with both agents.
agents.
the
theelderly
elderly7272. .However
I, I,BB
Elderly
use of
of
Elderlypatients
patientshave
have more
more bleeding
bleeding complications
complications with the use
73,74
GPIIb/IIIa
.. IfIf required,
required, the
the dose should be adjusted
adjusted
GPIIb/IIIainhibitors
inhibitors 73,74
according
accordingtotothe
therenal
renalfunction.
function.
I, I,AA
The
benefits with
with
The elderly
elderly have
have greater
greater in-hospital
in-hospital and long term benefits
75-79
.. In
In some
some trials, all the benefits of
of an
an
an
anearly
earlyinvasive
invasivestrategy
strategy 75-79
early invasive strategy were in the elderly rather than in younger
risk of major bleeding 80.
patients 75. However there is an increased
34
34
When selecting patients for an early invasive strategy, the risk
benefit ratio must be considered. For patients with multi vessel
33
disease and not suitable for CABG, partial revascularization of the

Elevation
Myocardial
Infarction
(UA/NSTEMI)
2011
early
early
earlyinvasive
invasive
invasive
strategy
strategy
strategywere
were
were
in
ininthe
the
theelderly
elderly
elderly
rather
rather
ratherthan
than
thaninin
in
younger
younger
7575
.. However
.However
Howeverthere
there
thereisisisan
an
anincreased
increased
increasedrisk
risk
riskof
of
ofmajor
major
majorbleeding
bleeding
bleeding8080. .
patients
patients
patients75
When
When
Whenselecting
selecting
selectingpatients
patients
patientsfor
for
foran
an
anearly
early
earlyinvasive
invasive
invasivestrategy,
strategy,
strategy, the
the risk
risk
benefit
benefit
benefitratio
ratio
ratiomust
must
mustbe
be
beconsidered.
considered.
considered.For
For
Forpatients
patients
patientswith
with
withmulti
multi
multivessel
vessel
disease
disease
diseaseand
and
andnot
not
notsuitable
suitable
suitablefor
for
forCABG,
CABG,
CABG,partial
partial
partialrevascularization
revascularization
revascularizationofofthe
the
culprit
culprit
culpritlesion
lesion
lesionmay
may
maybe
be
beaaaconsideration.
consideration.
consideration.
Long
Long
Long term
term
term management
management
management post
post
post discharge
discharge
discharge should
should
should include
include
medications
medications
medications that
that
that have
have
have been
been
been proven
proven
proven beneficial
beneficial
beneficial inin
in secondary
secondary
secondary
prevention.
prevention.
prevention.
9.2
9.2
UA/NSTEMI
UA/NSTEMI
UA/NSTEMIin
ininWomen
Women
Women
Women
Womendevelop
develop
developCAD
CAD
CADabout
about
aboutaaadecade
decade
decadelater
later
laterthan
than
thanmen
men
menat
at
ataaatime
time
timewhen
when
they
theyare
areolder
older
olderand
and
andhave
have
havemore
more
moreco-morbidity
co-morbidity
co-morbiditysuch
such
suchas
as
asobesity,
obesity,
obesity,diabetes,
diabetes,
diabetes,
81
81
.. . However
However
However gender
gender
gender isis
is not
not
not an
an
hypertension
hypertension
hypertension and
and
and osteoarthritis
osteoarthritis
osteoarthritis 81
independent
independent
independentpredictor
predictor
predictorof
ofof111year
year
yearsurvival.
survival.
survival.
9.2.1
9.2.1 Clinical
Clinical
ClinicalPresentation
Presentation
Presentation
Women
Women
Womenpresenting
presenting
presentingwith
with
withACS
ACS
ACSoften
often
oftenhave
have
haveatypical
atypical
atypicalsymptoms
symptoms
symptomssuch
such
asasneck
neck
neckand
and
andshoulder
shoulder
shoulderache
ache
acheand
and
anddyspnoea.
dyspnoea.
dyspnoea.Often,
Often,
Often,women
women
women have
have
non
nonspecific
specific
specificECG
ECG
ECGchanges
changes
changessuch
such
suchas
as
asTTTwave
wave
wavechanges
changes
changeseven
even
eveninin the
the
absence
absence
absenceof
ofofheart
heart
heartdisease,
disease,
disease,thus
thus
thusmaking
making
making the
the
the diagnosis
diagnosis
diagnosis ofof
of CAD
CAD
difficult.
difficult.
difficult.
9.2.2
9.2.2
9.2.2
Management
Management
Management
InIngeneral,
general,
general,there
there
thereare
are
areno
no
nogender
gender
genderspecific
specific
specificdifferences
differences
differencesinin
inthe
the
theefficacy
efficacy
efficacy
ofofthe
the
thecommonly
commonly
commonlyused
used
useddrugs
drugs
drugsin
ininACS.
ACS.
ACS.The
The
Thefollowing
following
following are
are
are some
some
important
important
importantdifferences:
differences:
differences:
I, BI, B
Prasugrelis
associatedwith
withmore
morebleeding
bleedinginin
inindividuals
individualswho
Prasugrel
Prasugrel
isisassociated
associated
with
more
bleeding
individuals
who
31
31
areless
lessthan
than60kg
60kgin
weight31
.. .
are
are
less
than
60kg
ininweight
weight
I, BI, B
meta-analysis indicates
indicates aaa lack
lack of
of benefit
benefit of
of GPIIb/IIIa
GPIIb/IIIa
A A meta-analysis
meta-analysis
indicates
lack
of
benefit
of
GPIIb/IIIa
8282
inhibitorsin
women82
.. The
.The
Thebleeding
bleeding
bleedingrisk
risk
riskisisisalso
also
alsohigher.
higher.
higher.
inhibitors
inhibitors
ininwomen
women
IIa,IIa,
AA
Thereis
conflictingdata
data regarding
regarding the
the benefits
benefits ofof
of an
an early
There
There
isisconflicting
conflicting
data
regarding
the
benefits
an
early
66,84-86
66,84-86
invasivestrategy
strategyin
womenwith
withUA/NSTEMI
UA/NSTEMI66,84-86
invasive
invasive
strategy
ininwomen
women
with
UA/NSTEMI
. ..Until
Until
Untilthis
this
issue
issue
issueis
isisresolved
resolved
resolvedin
ininrandomized
randomized
randomizedcontrolled
controlled
controlledtrials,
trials,
trials, an
an
an invasive
invasive
invasive
strategy
strategy
strategyis
isisbest
best
bestreserved
reserved
reservedfor
for
forwomen
women
womenwith
with
withongoing
ongoing
ongoingischemia
ischemia
ischemiaand
and
raised
raised
raisedtroponins.
troponins.
troponins.
9.3
UA/NSTEMI in Chronic Kidney Disease (CKD)

In patients with ACS, the presence of CKD is an additional high35
35
35
risk feature associated with increased mortality, the more severe
87-90
the CKD, the higher the mortality
.
I, B
The creatinine clearance can be calculated using the Cockroft34 pg 56). Drug doses should be
Gault formula (Appendix VI,
adjusted according to renal function.
9.3
Clinical
UA/NSTEMI
in Practice
Chronic KidneyGuidelines
Disease (CKD) on

In patients with ACS, the presence of CKD is an additional highElevation
Myocardial Infarction (UA/NSTEMI) 2011
risk feature associated with increased mortality, the more severe
the CKD, the higher the mortality.87-90
The creatinine clearance can be calculated using the CockroftGault formula (Appendix VI, pg 56). Drug doses should be
adjusted according to renal function.
I, B
Patients with renal impairment were excluded from most clinical

trials. In general, the management of patients with CKD is similar
to those with normal renal function except for the following
differences:
I, B
IIa, B
Patients with CKD have more co-morbidity.

ACE-I and ARB may cause worsening renal function and
hyperkalemia.
They are at increased bleeding risks. The doses of
antithrombotic agents need to be adjusted accordingly to avoid
excessive bleeding (Table 6, pg 35). Bivalirudin and
fondaparinux seem to be associated with less bleeding than
heparin or enoxaparin 45,91.
A recent meta-analysis showed that patients with CKD
presenting as UA/NSTEMI and treated with an early invasive
strategy had better outcomes particularly in patients with mild to
moderate renal insufficiency 92,93.
PCI in patients with CKD is associated with increased risks of:
bleeding
worsening renal function and acute on chronic renal failure due
to contrast nephropathy and/or cholesterol embolisation.
Strategies should be taken to reduce this risk. (Appendix VII, pg
56 and VIII, pg 57)
Table 6: Dosages of Anti-thrombotics in CKD*

Table 6: Dosages of Anti-thrombotics in CKD*
LOADING DOSE
LOADING DOSE
UFH
UFH
Enoxaprin
Enoxaprin
MAINTENANCE DOSE
MAINTENANCE DOSE
No change
No change
30
mg IV
30 mg IV
No change
No change
1 mg/kg sc every 24 hours if
1 mg/kg sc every 24 hours if
CrCl < 30 ml/min
CrCl < 30 ml/min
Fondaparinux Avoid if Cr Cl < 30 ml/min Avoid if Cr Cl < 30 ml/min
Fondaparinux Avoid if Cr Cl < 30 ml/min Avoid if Cr Cl < 30 ml/min
Eptifibatide
180 mcg/kg
IV Infusion 1.0 mcg/kg/min if
Eptifibatide
180 mcg/kg
IV Infusion 1.0 mcg/kg/min if
CrCl
Cl<<50
50ml/min
ml/min
Cr
36
Tirofiban
IV
0.4 mcg/kg/min
mcg/kg/min IV
IVinfusion
infusion0.05
0.05mcg/kg/min
mcg/kg/min
Tirofiban
IV infusion
infusion 0.4
if if
for
CrCl
Cl<30
<30ml/min
ml/min
for 30
30 mins
mins
Cr
* *Modified
for the
theManagement
ManagementofofPatients
Patientswith
with
UA/NSTEMI.
Modifiedfrom
fromACC/AHA
ACC/AHA 2007
2007 Guidelines
Guidelines for
UA/NSTEMI.
J JAm
AmColl
CollCardiol
Cardiol2007;
2007; 50:1-157.
50:1-157.
9.4
9.4
UA/NSTEMI
UA/NSTEMI in
in Diabetes
Diabetes
94,95
Diabetics
mortality
followingan
anACS
ACS94,95
. The
Diabetics have
have an
an increased mortality
following
. The
35
glucose
has been
been shown
shown toto be
beaasignificant
significant
glucose level
level at
at admission
admission has
Fondaparinux
Avoid
if Cr Cl < 30 ml/min Avoid
if Cr Cl
30 ml/min if
Eptifibatide
180 mcg/kg
IV Infusion
1.0<mcg/kg/min
Eptifibatide
180 mcg/kg
IV
Infusion
1.0
mcg/kg/min
if
Clinical
Practice Guidelines
on
Cr Cl < 50 ml/min
Cr
Cl < 50 ml/min
Tirofiban
IV infusion
0.4 mcg/kg/minAngina/Non
IV infusion
0.05 mcg/kg/min
if
management
of
Unstable
ST
Tirofiban
IV
mcg/kg/min IV
infusion
0.05 mcg/kg/min if
for infusion
30 mins0.4Infarction
Cr
Cl <30 ml/min
Elevation Myocardial
(UA/NSTEMI)
2011
for 30
mins
Cr Cl <30 ml/min
* Modified from ACC/AHA
2007 Guidelines for the Management of Patients with UA/NSTEMI.
*J Am
Modified
from ACC/AHA
2007 Guidelines for the Management of Patients with UA/NSTEMI.
Coll Cardiol
2007; 50:1-157.
J Am Coll Cardiol 2007; 50:1-157.
9.4
9.4
UA/NSTEMI in Diabetes
UA/NSTEMI in Diabetes
Diabetics have an increased mortality following an ACS 94,95
94,95. The
Diabeticslevel
haveatanadmission
increased has
mortality
. The
glucose
been following
shown toanbeACS
a significant
glucose
level
at
admission
has
been
shown
to
be
a
significant
predictor of 1 year mortality with a predictive value equivalent to LV
96,97
predictor
of 1 year mortality
with a predictive value equivalent to LV
systolic dysfunction
.
systolic dysfunction 96,97.
Diabetics should be treated aggressively with:
Diabetics should be treated aggressively with:
Antiplatelet agent aspirin and clopidogrel or prasugrel.
Antiplatelethas
agent
aspirin
or prasugrel.
Prasugrel
been
found toand
be clopidogrel
more effective
in diabetics 31
31.
. a
Prasugrel
has
been
found
to
be
more
effective
diabeticsonly
GP IIb/IIIa inhibitors a contemporary trial in
indicated
GP IIb/IIIa
inhibitors
a contemporary
trial indicated only a
modest
reduction
in adverse
events 98,99
.
modest
reduction
in adverse
events 98,99
Early
invasive
approach
diabetics
are. however at higher risk
Early
invasive
approach
diabetics
are however at higher risk
of contrast nephropathy than non diabetics.
of contrast nephropathy than non diabetics.
I, B
I, B
IIb, B
IIb, B
I, A
I, A
There is still a lack of consensus on the optimal management of

There sugars
is still aduring
lack of
on the
optimalinsulin
management
blood
theconsensus
acute event.
Intensive
therapy of
to
blood sugars
during theinacute
event.
Intensive
insulin
to
achieve
normoglycemia
the acute
setting
has not
beentherapy
shown to
achievemortality
normoglycemia
in the acute
setting
has not in
been
to
reduce
and is associated
with
an increase
the shown
episodes
reduce
mortality 100
and is associated with an increase in the episodes
of
hypoglycemia
100. A general consensus is to keep blood sugars
of
hypoglycemia
general
is to
keep
sugars
less
than 8mmol/l .inA the
acuteconsensus
setting and
then
aimblood
for optimal
less than
8mmol/l
in the acute setting and then aim for optimal
control
following
discharge.
control following discharge.
I, B
I, B

The acute phase of UA/NSTEMI is usually 1 to 3 months. The
The
phase of of
UA/NSTEMI
usually STEMI
1 to 3 months.
risk acute
of recurrence
ischaemic isevents,
or deathThe
is
risk
of during
recurrence
of ischaemic
events,
STEMI
or death
is
highest
this period.
Following
this, most
patients
assume
highest
thissimilar
period.toFollowing
this, most
patients
a clinicalduring
course
that of patients
with
chronicassume
stable
a
clinical course similar to that of patients with chronic stable
angina.
angina.
Several lifestyle modification measures and drug therapies have
Several
lifestyle
and drug
therapies
have
been shown
to modification
be effective measures
in improving
long-term
outcome.
been shown to be effective in improving long-term outcome.
However they are underutilized. Therefore
health care providers
37
should ensure that patients 37
with UA/NSTEMI receive
appropriate treatment post hospital discharge and ensure that
patients remain compliant to treatment.
Important discharge instructions should include:
education on medication
Patients given sublingual nitrates should be instructed in its
proper and safe use.
lifestyle change and CV risk factors modification
scheduling of timely follow-up appointment and dates for
further investigations
referral to a cardiac rehabilitation program where appropriate
10.1
Medications post-discharge (Table1, pg 4)
10.1.1 Antiplatelet agents

36
I, A
ASA should be prescribed at 75-150 mg daily unless
Patients given sublingual nitrates should be instructed in its
proper and safe

use.
Clinical
Practice
Guidelines on
lifestyle change and CV risk factors modification

scheduling of timely follow-up appointment and dates for
Elevation
Myocardial Infarction (UA/NSTEMI) 2011
further investigations
referral to a cardiac rehabilitation program where appropriate
10.1
Medications post-discharge (Table1, pg 4)
10.1.1 Antiplatelet agents

I, A
ASA should be prescribed at 75-150 mg daily unless

contraindicated 26,27.
I, A
In patients who cannot tolerate ASA, clopidogrel is an

alternative. It has better risk reduction 101. When clopidopgrel is
not available, ticlopidine can be given.
I, A
The combination of ASA and clopidogrel 75 mg daily should be

continued for at least one month and ideally up to 9 to 12
months after UA/NSTEMI treated medically 71,102 and in patients
who have undergone PCI with bare metal stents.
I, A
If patients received drug eluting stents during PCI then dual

antiplatelet treatment is recommended 71,102,103.
I, C
The duration of dual antiplatelet therapy following DES

implantation is for 6 to 12 months or longer 103.
There are no recent clinical trial data on the use of triflusal in
ACS.
10.1.2 -blockers (see section 7.2.4.2)

I, B
-blockers should be continued for patients with ischemia unless

contraindicated.
I, B
Long term treatment following UA/NSTEMI may lead to

significant mortality reduction104.
I, A
-blockers should be continued indefinitely in patients with

38
reduced LV function, with or without
symptoms of heart
failure105,106.
10.1.3 Lipid Modifying Therapy

I, A
There is a large body of evidence that early initiation of statin

therapy improves outcome regardless of baseline LDL-C
levels in patient with ACS 49-51,07-109.
I, A
More aggressive lipid lowering further lowers cardiovascular

event rates 110.
Lipid management includes:
I, C
37
Assessment of a fasting lipid profile for all patients, within 24
Clinical
Practice
Guidelines
-blockers
should
be continued
indefinitely in on
patients with
reduced LV function,
with or without
symptoms ofSTheart
management
of Unstable
Angina/Non
failure105,106
.
Elevation
Myocardial
Infarction (UA/NSTEMI) 2011
10.1.3 Lipid Modifying Therapy

I, A
There is a large body of evidence that early initiation of statin

therapy improves outcome regardless of baseline LDL-C
levels in patient with ACS 49-51,07-109.
I, A
More aggressive lipid lowering further lowers cardiovascular

event rates 110.
Lipid management includes:
I, C
Assessment of a fasting lipid profile for all patients, within 24

hours of hospitalization.
I, A
Statins, in the absence of contra-indications, regardless of

baseline LDL-C and diet modifications, should be initiated
soon after admission and continue indefinitely to provide life
long benefits 111,112. This also applies to patients post PCI.
I, A
LDL-C level should be targeted <2.0 mmol/L for most patients

111,112
.
I, B
Patients with low HDL-C may benefit from fibrates or nicotinic

acid 113,114.
10.1.4 Angiotensin-converting enzymes inhibitors (ACE-Is) (Table
7, pg 39)
I, A
IIa, A
IIa, A
ACE-Is have shown long term benefit in all patients with

evidence of LV dysfunction (LVEF 40%) 115-117 and in
patients with diabetes, hypertension or CKD unless
contraindicated 1018-120.
For all other patients ACE-Is should be considered to prevent
recurrence of ischaemic events 121-124.
For patients with reduced LV systolic function, ACE-I should
be initiated early, during the course of hospitalization. Agents
and doses of proven efficacy are recommended.
39
38

Table
Table 7:
7: Recommended
Recommended dosages
dosages of
of ACE-I
ACE-I in
in UA/NSTEMI
UA/NSTEMI
Table 7: Recommended dosages of ACE-I in UA/NSTEMI
Type
Initiation
Target
Type
Initiation dose
dose
Target dose
dose
Type
Initiation dose
Target dose
Captopril
6.25
mg
bd-tds
25-50
mg
Captopril
6.25 mg bd-tds
25-50 mg tds
tds
Captopril
6.25 mg bd-tds
25-50 mg tds
Ramipril
2.5
mg
bd
10
mg
od
Ramipril
2.5 mg bd
10 mg od
Ramipril
2.5 mg bd
10 mg od
Enalapril
2.5-5
mg
od
20
mg bd
Enalapril
2.5-5
20
Enalapril
2.5-5 mg
mg od
od
20 mg
mg bd
bd
Enalapril
2.5-5 mg od
20 mg bd
Lisinopril
5
mg
od
40
mg
od
Lisinopril
5
mg
od
40
mg
od
Lisinopril
5 mg od
40 mg od
Lisinopril
5 mg od
40 mg od
Perindopril
2-2.5 mg
mg od
od
8-10 mg
mg od
Perindopril
2-2.5
8-10
Perindopril
2-2.5 mg od
8-10 mg od
od
Perindopril
2-2.5 mg od
8-10 mg od
10.1.5
Angiotensin-Receptor
Blockers
(ARBs)
(Table
8,
pg
39)
10.1.5 Angiotensin-Receptor
Angiotensin-Receptor Blockers
Blockers (ARBs)
(ARBs) (Table
(Table 8,
8, pg
pg 39)
39)
10.1.5
10.1.5 Angiotensin-Receptor Blockers (ARBs) (Table 8, pg 39)
I, A
ARBs
should
be
substituted
for
patients
with
ACE-I
I,
ARBs
be substituted
125-127 be
I, A
A
ARBs should
should
substituted for
for patients
patients with
with ACE-I
ACE-I
intolerance
125-127.
I, A
ARBs should
substituted for patients with ACE-I
125-127. be
intolerance
intolerance 125-127.
intolerance
.
Table
8: Recommended
dosages of ARB in UA/NSTEMI
Table
Table 8:
8: Recommended
Recommended dosages
dosages of
of ARB
ARB in
in UA/NSTEMI
UA/NSTEMI
Table 8:
Recommended
dosagesdose
of ARB in UA/NSTEMI
Type
Initiation
Target dose
Type
Initiation
Target
Type
Initiation dose
dose
Target dose
dose
Type
Initiation
dose
Target
Valsartan
40-80 mg od
160 mgdose
od
Valsartan
40-80
mg
od
160
mg
Valsartan
40-80 mg od
160 mg od
od
Valsartan
40-80
mg
od
160
mg
od
10.1.6 Aldosterone receptor antagonist
10.1.6
10.1.6 Aldosterone
Aldosterone receptor
receptor antagonist
antagonist
10.1.6 Aldosterone
receptor antagonist
Long-term aldosterone
receptor blockade should be considered
I, B
Long-term
blockade
considered
Long-term
aldosterone
receptor
blockade
should
betreated
considered
in patients aldosterone
who are inreceptor
heart failure
and should
alreadybe
with
I,
B
I, B
Long-term
aldosterone
receptor
blockade
should betreated
considered
in
patients
who
heart
failure
and
ACE-I
and -blockers.
spironolactone
and
in
patients
who are
are in
inThese
heartagents
failureinclude
and already
already
treated with
with
I, B
in
patients
who are inThese
heartagents
failureinclude
and already
treated with
128,129
ACE-I
and
spironolactone
and
.
epleronone
ACE-I
and -blockers.
-blockers.
These
agents
include
spironolactone
and
128,129
ACE-I
and -blockers.
These agents include spironolactone and
..
epleronone
epleronone 128,129
128,129
Care
should be .taken in patients with renal dysfunction and
epleronone
Care
hyperkalaemia.
Care should
should be
be taken
taken in
in patients
patients with
with renal
renal dysfunction
dysfunction and
and
Care should be taken in patients with renal dysfunction and
hyperkalaemia.
hyperkalaemia.
10.1.7 hyperkalaemia.
Anti Anginal Therapy
10.1.7
10.1.7 Anti
Anti Anginal
Anginal Therapy
Therapy
Anti anginals are not required for patients with successful
I, C10.1.7 Anti Anginal Therapy
Anti
not
for
revascularization
no required
residual ischaemia.
Anti anginals
anginals are
areand
not
required
for patients
patients with
with successful
successful
I,
I, C
C
Anti anginals areand
not
required
for patients with successful
revascularization
no
residual
ischaemia.
I, C
revascularization
and
no
residual
ischaemia.
10.2 Follow-up
investigations
(Fig
1,
pg
5)
revascularization and no residual ischaemia.
10.2
Follow-up
investigations (Fig
1, pg
5)
10.2
Follow-up
pg UA/NSTEMI
5)
In
the
outpatient investigations
evaluation of (Fig
low 1,
risk
patients, the
10.2 Follow-up
investigations
(Fig
1,
pg 5)
following
investigations
maybe
considered:
In
the
outpatient
evaluation
of
low
risk
UA/NSTEMI
In the outpatient evaluation of low risk UA/NSTEMI patients,
patients, the
the
In the outpatient
evaluation
of
low risk UA/NSTEMI patients, the
following
investigations
maybe
considered:
following
investigations
maybe
considered:
Echocardiogram
to
assess
LV
function
following investigations maybe considered:
Treadmill stress test
Echocardiogram
to
LV
Echocardiogram
to assess
assess
LV function
function
Stress echocardiogram
treadmill
or pharmacological stress
Echocardiogram
to assess
LV function
Treadmill
stress
test
Treadmill
stress
test
Nuclear
perfusion
study
Treadmill
stress
test
Stress
echocardiogram
treadmill
or pharmacological
stress
Stress
echocardiogram
treadmill
pharmacological
stress
MRI
stress
MRI for ischaemia
andorperfusion
MRI for viability
Stress
Nuclear
perfusion
Nuclearechocardiogram
perfusion study
study treadmill or pharmacological stress
40
Nuclear
perfusion
study
MRI
MRI
ischaemia
MRI
stress
stress
MRI for
for
ischaemia and
and perfusion
perfusion MRI
MRI for
for viability
viability
MRI stress MRI for ischaemia and
40perfusion MRI for viability
39
40
40

Low risk patients with significant demonstrable ischaemia and all
Low
risk
with significant
demonstrable
ischaemia and
Low
risk patients
patients
significant
demonstrable
and all
all
intermediate/high
riskwith
patients
should be
considered forischaemia
revascularization.
intermediate/high
intermediate/high risk
risk patients
patients should
should be
be considered
considered for
for revascularization.
revascularization.
Key
messages
Key
Key messages
messages
Patients
should
be
Patients
should
be on
on optimal
optimal medical
medical therapy
therapy at
at discharge.
discharge. This
This
I,A be on optimal medical therapy at discharge. This
Patients
should
I,A, clopidogrel (for at least a month and ideally for
includes
ASA
includes
ASA
I,A, clopidogrel (for at least a month and ideally for
I,Bclopidogrel (for
I,B at least aI,Cmonth and
I,A ideally for
I,B
includes
at least
least a
aASA
year) ,I,B
, -blockers I,B
+ CCBs I,C, ACE-I I,A
or ARB I,B
at
year)
I,B, -blockers I,B + CCBs I,C, ACE-I I,A or ARB I,B
I,A
at
least
a year)
, -blockers + CCBs , ACE-I or ARB
I,A. (Table 1, pg 4)
and
statins
and statins I,A. (Table 1, pg 4)
and statins . (Table 1, pg 4)
These
These drugs
drugs should
should be
be uptitrated
uptitrated during
during outpatient
outpatient visits
visits to
to the
the
I,C
These
drugs should
be doses
uptitrated
I,C. during outpatient visits to the
recommended
tolerated
recommended tolerated doses I,C.
recommended tolerated doses .
Low
Low risk
risk patients
patients should
should be
be assessed
assessed non-invasively
non-invasively for
for
Low
risk I,C
patients
should
be assessed non-invasively for
I,C
ischaemia
.
(Fig
1,
pg
5)
ischaemia
.
(Fig
1,
pg
5)
I,C
ischaemia . (Fig 1, pg 5)
11. Cardiac Rehabilitation/Secondary prevention
11. Cardiac Rehabilitation/Secondary prevention
Cardiac rehabilitation is aimed at improving the physical and psychological
Cardiac rehabilitation is aimed at improving the physical and psychological
well being of the patient. It has been shown to reduce mortality by
well
being of 20%-25%
the patient.
It .has
been
reduce
mortality
by
130-132
approximately
There
wasshown
also a to
trend
towards
reduction
130-132
133reduction
There was
also aoftrend
towards
approximately
20%-25%
.
MI over a .median
follow-up
12 months
in non-fatal recurrent
in non-fatal recurrent MI over a median follow-up of 12 months 133.
11.1
11.1
Cardiac rehabilitation programs include:

Cardiac rehabilitation programs include:
Counselling and educating the patient and family members on CAD
Counselling
educating
the patient and family members on CAD
Beginning
anand
exercise
program
Beginning
exercise
program
Helping
theanpatient
modify
risk factors such as high blood pressure,
Helping thehigh
patient
modify
risk factors
such as
high blood
pressure,
smoking,
blood
cholesterol,
physical
inactivity,
obesity
and
smoking, high blood cholesterol, physical inactivity, obesity and
diabetes
diabetes
Providing vocational guidance to enable the patient to return to work
Providing
to enable
the patient to return to work
Supplying
information
on
limitations
Supplying vocational
informationguidance
on physical
physical
limitations
Supplying
oncompliance
physical limitations
Educating
and
to
Educating information
and ensuring
ensuring
compliance
to medications
medications
Educating
and ensuring
compliance to medications
Providing
support
Providing emotional
emotional
support
Providing emotional support
Cardiac
Cardiac rehabilitation/secondary
rehabilitation/secondary prevention
prevention programs
programs are
are generally
generally
Cardiacinto
rehabilitation/secondary
prevention programs are generally
divided
3
divided
into
3 main
main phases:
phases:
divided into 3 main phases:
Phase
Phase 1:
1: Inpatient
Inpatient CR
CR (also
(also known
known as
as Phase
Phase 1
1 CR):
CR): a
a program
program that
that
Phase
Inpatient CR
known as
Phase to
1 CR):
a program
that
delivers
and
rehabilitative
services
hospitalized
patients
delivers1:preventive
preventive
and (also
rehabilitative
services
to
hospitalized
patients
following
ACS
delivers
and rehabilitative services to hospitalized patients
followingpreventive
ACS
following ACS
Phase
Phase 2:
2: Early
Early outpatient
outpatient CR
CR (also
(also known
known as
as Phase
Phase 2
2 CR):
CR): generally
generally
within
first 3outpatient
continuing
upPhase
Phase
2: Early
CRbut
(also
known as
2 CR): generally
within the
the
first 3 to
to 6
6 months
months
but
continuing
up to
to 1
1 year
year
within the first 3 to 6 months but continuing up to 1 year
Phase 3: Long-term outpatient CR (also known as Phase 3 or Phase
41
4 CR): beyond 1 year
41
41
11.2
Return to physical activity 40

Elevation
Myocardial
(UA/NSTEMI)
2011
Phase 3: Long-term
outpatientInfarction
CR (also known
as Phase 3 or
Phase
4 CR): beyond 1 year
11.2
Return to physical activity
Physical activity can be resumed at 50% of maximal exercise capacity in a

patient with preserved LV function without inducible ischemia within 1
week post-discharge. This should be gradually increased over time
preferably guided by treadmill stress test.
11.3
Risk factor modification:

Smoking cessation Patients who quit smoking can reduce the
rate of reinfarction and death as early as 1 year.
Weight Achieve or maintain optimal body weight.
Exercise Encourage a minimum of 3060 minutes of moderate
activity 3-4 times weekly (walking, cycling, swimming or other
equivalent aerobic activities).
Diet To consume low cholesterol or low saturated fat diet.
Lipids Aim for an LDL-C < 2.0 mmol/l.
Hypertension Aim for a blood pressure of <140/85 mmHg. In
diabetics the target is <130/80 mmHg. In elderly patients, a higher
BP target may be acceptable.
Diabetes Mellitus Optimal glycemic control in diabetes. (Refer
CPG on Diabetes)
11.4 Discharge Instructions

Therapeutic lifestyle changes should be initiated in all patients and
reemphasized during follow up.
Patients should be on optimal medical therapy. (Table 1, pg 4).
They should be educated on the importance of adherence to drug
therapy to ensure optimal outcomes. Patients with DES should be
warned of the consequences of non compliance to anti platelet drug
therapy.
The doses of ACE-I/ARB and -blockers should be uptitrated to the
maximal tolerated doses.
Patients should be instructed on how to use GTN. If the chest pain
does not subside after 2 GTNs or if there is a change in the usual
pattern of angina, they should go to the nearest health facility.
42
41

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121. Fox KM. Efficacy of perindopril in reduction of cardiovascular events among
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2005; 143 : 659-672
52
50

APPENDIX I: Braunwalds Classification of Unstable Angina*
CLINICAL CIRCUMSTANCES
A
Severity
INew onset of
severe angina or
accelerated
angina; no rest
pain
IIAngina at rest
within past month
but not within
preceding 48 hours
(angina at rest,
subacute)
IIIAngina at rest
within 48 hours
(angina at rest,
acute)
Develops in
Presence of
Extracardiac
Condition That
Intensifies
Myocardial
Ischemia
(Secondary UA)
Develops in
Absence of
Extracardiac
Condition (Primary
UA)
Develops
Within 2 weeks
of MI
(Postinfarction
UA)
IA
IB
IC
IIA
IIB
IIC
IIIA
IIIB-Tneg IIIB-Tpos
IIIC
UA : Unstable angina; T : Troponins

*Hamm CW, Braunwald E. A classification of unstable angina revisited. Circulation.
2000 ;102 :118-22.
53
51

Appendix
Elevationsof
of cardiac
cardiac troponin
absence
of of
Appendix
II:II:Elevations
troponinininthe
the
absence
overt ischaemic
ischaemic heart
overt
heartdisease*
disease*
Damage
related
secondarymyocardial
myocardial ischaemia
2) 2)
Damage
related
to to
secondary
ischaemia(MI
(MItype
type
Tachy- or bradyarrhythmias
Tachy- or bradyarrhythmias
Aortic dissection and severe aortic valve disease
Aortic dissection and severe aortic valve disease
Hypo- or hypertension, e.g. haemorrhagic shock, hypertensive emergency
Hypo- or hypertension, e.g. haemorrhagic shock, hypertensive emergency
Acute and chronic heart failure without significant concomitant coronary artery
Acute
and chronic
disease
(CAD) heart failure without significant concomitant coronary artery
disease
(CAD) cardiomyopathy
Hypertrophic
Hypertrophic
cardiomyopathy
Coronary vasculitis,
e.g. systemic lupus erythematosus, Kawasaki syndrome
Coronary
vasculitis,
e.g.dysfunction
systemic without
lupus erythematosus,
Coronary
endothelial
significant CAD, Kawasaki
e.g. cocainesyndrome
abuse
Coronary endothelial dysfunction without significant CAD, e.g. cocaine abuse
Damage not related to myocardial ischaemia
Damage not related to myocardial ischaemia

Cardiac contusion
Cardiac
incisions with surgery
Cardiac
contusion
Radiofrequency
or cryoablation
Cardiac incisions with
surgery therapy
Rhabdomyolysis with cardiac involvement
Radiofrequency
or cryoablation therapy
Myocarditis
Rhabdomyolysis with cardiac involvement
Cardiotoxic agents, e.g. anthracyclines, herceptin, carbon monoxide poisoning
Myocarditis
Severe burns affecting >30% of body surface
Cardiotoxic agents, e.g. anthracyclines, herceptin, carbon monoxide poisoning
Severe
burns affecting >30% of body surface
Indeterminant or multifactorial group
Indeterminant
or multifactorial
Apical ballooning
syndrome group
Severe pulmonary embolism or pulmonary hypertension
Apical
ballooning
syndrome
Peripartum
cardiomyopathy
Severe
pulmonary
embolism or pulmonary hypertension
Renal
failure
Severe acute
neurological diseases, e.g. stroke, trauma
Peripartum
cardiomyopathy
Infiltrative
Renal
failure diseases, e.g. amyloidosis, sarcoidosis
Extreme
exertion
Severe
acute
neurological diseases, e.g. stroke, trauma
Sepsis
Infiltrative diseases, e.g. amyloidosis, sarcoidosis
Acute respiratory failure
Extreme
exertion
Frequent defibrillator shocks
Sepsis
Acute respiratory failure
*Thygesen
K, Mair J,Katus
H et al for Study Group on Biomarkers in Cardiology of the ESC
Frequent
defibrillator
shocks
Working Group on Acute Cardiac Care. Recommendations for the use of cardiac troponin
measurement in acute cardiac care. Eur Heart J 2010; 31 : 2197-2204.
54
*Thygesen K, Mair J,Katus H et al for Study Group on Biomarkers in Cardiology of the ESC
Working Group on Acute Cardiac Care. Recommendations for the use of cardiac troponin
measurement in acute cardiac care. Eur Heart J 2010; 31 : 2197-2204.
54
52

Appendix
AppendixIII:
III: Likelihood
Likelihood That
That Signs and Symptoms
SymptomsRepresent
Representan
anACS
ACS
secondary
secondary to CAD
CAD
Greater
GreaterLikelihood
Likelihood
Lower Likelihood
Likelihood
Lower
History
History
Chest
Chestor
orleft
leftarm
armpain
pain or
or discomfort
discomfort as
chief
chiefsymptom
symptomreproducing
reproducing prior
prior
documented
documentedangina
angina
Chest pains
painsininthe
theabsence
absenceofof
Chest
any of
of the
the greater
greaterlikelihood
likelihood
any
characteristics
characteristics
Known
Knownhistory
historyof
of CAD,
CAD, including
including MI
Recent cocaine
cocaineuse
use
Recent
New
Newchest
chestor
orleft
leftarm
arm pain
pain or
or discomfort
as
aschief
chiefsymptom
symptom
Age
Agegreater
greaterthan
than70
70 years
years
Male
Malesex
sex
Diabetes
Diabetesmellitus
mellitus
Examination
Examination
Transient
TransientMR
MRmurmur,
murmur, hypotension,
hypotension,
diaphoresis,
diaphoresis,pulmonary
pulmonary edema,
edema, or rales
Chest discomfort
discomfortreproduced
reproduced
Chest
by palpation
palpation
by
Extracardiac
Extracardiacvascular
vascular disease
disease
ECG
ECG
New,
New,ororpresumably
presumably new,
new, transient
transient STT-wave
T-wave attening
atteningor
orinversion
inversion
segment
segmentdeviation
deviation (1
(1 mm
mm or
or greater)
greater) or T- less
less than
than 11mm
mmininleads
leadswith
with
wave
waveinversion
inversionin
in multiple
multiple pre-cordial
pre-cordial
dominant
dominant RRwaves
waves
leads
leads
Normal ECG
ECG
Normal
Cardiac
CardiacBiomarkers
Biomarkers
Elevated
Elevatedcardiac
cardiacTnI,
TnI, TnT,
TnT, or
or CK-MB
markers
markers
Normal
Normal
Modified
Modifiedfrom
fromBraunwald
BraunwaldE,
E, et
et al.
al. Unstable
Unstable Angina: Diagnosis
Diagnosisand
andManagement.
Management.1994;3-11994;3-1AHCPR
AHCPRPublication
PublicationNo
No94-0602:1-154.
94-0602:1-154.
55
55
53

APPENDIX IV : TIMI RISK SCORE FOR UA/NSTEMI
APPENDIX IV : TIMI RISK SCORE FOR UA/NSTEMI
TIMI Risk Score
All-Cause Mortality, New or Recurrent
TIMI Risk Score
All-Cause Mortality, New or Recurrent
MI, or Severe Recurrent Ischemia
MI, or Severe Recurrent Ischemia
Requiring Urgent Revascularization
Requiring Urgent Revascularization
Through 14 d After Randomization, %
Through 14 d After Randomization, %
0-1
4.7
0-1
4.7
2
8.3
2
8.3
3
13.2
3
13.2
4
19.9
4
19.9
5
26.2
5
26.2
6-7
40.9
6-7
40.9
The TIMI risk score is determined by the sum of the presence of 7 variables at
The TIMI risk score is determined by the sum of the presence of 7 variables at
admission:
admission:
1 point is given for each of the following variables:
1 point is given for each of the following variables:
Age 65 y or older
Age3 65
or olderfor CAD ( family history of premature CAD,
At least
risky factors
At least 3 risk factors
for CAD (active
familysmoker,
history of
premature CAD,
hypertension,elevated
cholesterols,
diabetes)
hypertension,elevated
cholesterols,
Known
CAD (coronary stenosis
of > 50%)active smoker, diabetes)
Known
CAD
(coronary
Use of
aspirin
in prior
7 daysstenosis of > 50%)
Use
of
aspirin
in
prior
7 dayson ECG
ST-segment deviation (>0.5mm)
ST-segment
deviation in
(>0.5mm)
At least
2 anginal episodes
prior 24 on
h ECG
At least
2 anginal
in prior 24 h
Elevated
serum
cardiacepisodes
biomarkers
Elevated serum cardiac biomarkers
Total Score = 7 points
Total Score = 7 points
Low Risk : < 2 point
2 point
Low Risk
< points
Moderate
Risk: :3-4
HighModerate
Risk : >5Risk:
points3-4 points
High Risk : >5 points
Adapted from :
Adapted
Antmanfrom
EM,: Cohen M, Bernink PJ, et al. The TIMI risk score for unstable
Antman EM,
Cohen
Bernink
et al. The and
TIMItherapeutic
risk scoredecision
for unstable
angina/non-ST
elevation
MI: M,
a method
forPJ,
prognostication
angina/non-ST
elevation
MI: a. method for prognostication and therapeutic decision
making.
JAMA 2000; 284
: 83542
making.
2000;
284Giugliano
: 83542 . RP, et al. Implications of upstream
Sabatine
MS,JAMA
Morrow
DA,
SabatineIIb/IIIa
MS, inhibition
Morrow DA,
al. Implications
of upstream
glycoprotein
and Giugliano
coronary RP,
arteryet stenting
in the invasive
glycoprotein
IIb/IIIa inhibition
stentinginfarction.
in the invasive
management
of unstable
angina/nonandSTcoronary
elevationartery
myocardial
A
management
of unstable inangina/non
elevation
myocardial
infarction.
A
comparison
of the Thrombolysis
Myocardial ST
Infarction
(TIMI)
IIIB trial and
the
comparison
of
the
Thrombolysis
in
Myocardial
Infarction
(TIMI)
IIIB
trial
and
Treat angina with Aggrastat and determine Cost of Therapy with Invasive or the
Treat
angina
with
Aggrastat
and
determine
Cost
of
Therapy
with
Invasive
or
56
54
56

APPENDIX
V: V:
GRACE
PREDICTION
SCORE
CARD
AND AND
NOMOGRAM
APPENDIX
GRACE
PREDICTION
SCORE
CARD
NOMOGRAM
FOR
ALLALL
CAUSE
MORTALITY
FROM
DISCHARGE
TO 6 TO 6
FOR
CAUSE
MORTALITY
FROM
DISCHARGE
MONTHS*
MONTHS*
*Eagle KA,Lim MJ,Dabbous OH et al for the Grace Investigators. A Validated Prediction Model for All
Forms of Acute Coronary Syndrome.Estimating the Risk of 6-Month Postdischarge Death in an
International Registry JAMA. 2004;291:2727-2733.
*Eagle KA,Lim MJ,Dabbous OH et al for the Grace Investigators. A Validated Prediction Model for
Forms of Acute Coronary Syndrome.Estimating the Risk of 6-Month Postdischarge Death in an
57
International Registry JAMA. 2004;291:2727-2733.
57
55

APPENDIX
APPENDIX
VI: VI:
Calculation
Calculation
Of Creatinine
Of Creatinine
Clearance
Clearance
APPENDIX
APPENDIX
VI: Calculation
VI: Calculation
Of Creatinine
Of Creatinine
ClearanceClearance
Estimated
Estimated
GFRGFR
(ml/min)
(ml/min)
= (140-age)
= (140-age)
x weight
x weight or or1.2 (140-age)
1.2 (140-age)
Estimated Estimated
GFR (ml/min)
GFR= (ml/min)
(140-age)
= (140-age)
x weight x weight
or 1.2 (140-age)
or 1.2 (140-age)
(0.814
(0.814
x SCrx [mol/L
SCr [mol/L
]) ])
SCr [mol/L
SCr [mol/L
]
]
]) [mol/LS])Cr [mol/LSCr
] [mol/L ]
(0.814 x S(0.814
x SCr
Cr [mol/L
SCr : S
serum
creatinine
creatinine
Cr : serum
SCr : serumScreatinine
Cr : serum creatinine
For women
For women
multiply
multiply
by 0.85
by 0.85
For women
For
multiply
women
bymultiply
0.85 by 0.85
Severity
Severity
Of CKD*
Of CKD*
Severity Of
Severity
CKD* Of CKD*
SEVERITY
SEVERITY
OF CKD
OF CKD
CREATININE
CREATININE
CLEARANCE
CLEARANCE
SEVERITYSEVERITY
OF CKD OF CKD
CREATININE
CREATININE
CLEARANCE
CLEARANCE
Normal
Normal
to mild
to mild
>60 >60
ml/min
ml/min
Normal toNormal
mild
to mild
>60 ml/min>60 ml/min
Moderate
Moderate
30-59
30-59
ml/min
ml/min
Moderate Moderate
30-59 ml/min
30-59 ml/min
Severe
Severe
<30 <30
ml/min
ml/min
Severe Severe
<30 ml/min<30 ml/min
* National
* National
Kidney
Kidney
Foundation.
Foundation.
K/DOQI
K/DOQI
clinical
clinical
practice
practice
guidelines
guidelines
for chronic
for chronic
kidney
disease:
disease:
evaluation,
evaluation,
classification,
classification,
and
and
stratification.
stratification.
Jchronic
Kidney
J Kidney
* kidney
National
*Kidney
National
Foundation.
Kidney
Foundation.
K/DOQI
clinical
K/DOQI
practice
clinical
guidelines
practiceAm
guidelines
forAm
for chronic
Dis.2002;
Dis.2002;
39 (suppl
39evaluation,
(suppl
1): S1S226
1): S1S226
kidney
disease:
kidney
disease:
evaluation,
classification,
classification,
and stratification.
and stratification.
Am J Kidney
Am J Kidney
Dis.2002; 39
Dis.2002;
(suppl 1):
39S1S226
(suppl 1): S1S226
APPENDIX
APPENDIX
VII: Prevention
VII: Prevention
of Contrast
of Contrast
Induced
Induced
Nephropathy
Nephropathy
APPENDIX
APPENDIX
VII: Prevention
VII: Prevention
of Contrast
of Induced
ContrastNephropathy
Induced Nephropathy
ACC/ESC
ACC/ESC
Classification
Classification
ACC/ESC
ACC/ESC
Classification
Classification
Contrast
Contrast
Agent
Agent
- Isomolar
- Isomolar
agent
agent
I, A I, A
Contrast
Agent
Contrast
Agent
- Low
- Low
osmolar
osmolar
agents
agents
IIa,
- Isomolar
-agent
Isomolar
agent
I, A BIIa, B I, A
- use-osmolar
use
minimal
minimal
volume
volume
- Low
- Low
agents
osmolar
agents
IIa, I,B C I, C
IIa, B
- use minimal
- usevolume
minimal volume
I, C
I, C
Avoid
Avoid
nephrotoxic
nephrotoxic
agents
agents
eg eg
I, C I, C
NSAIDS,metformin
NSAIDS,metformin
Avoid nephrotoxic
Avoid nephrotoxic
agents egagents eg
I, C
I, C
NSAIDS,metformin
NSAIDS,metformin
Saline
Saline
Infusion
Infusion
I, C I, C
Saline Infusion
Saline Infusion
I, C
I, C
Sodium
Sodium
Bicarbonate
Bicarbonate
IIa, BIIa, B
Sodium Bicarbonate
Sodium Bicarbonate
IIa, B
IIa, B
Acetylcysteine
Acetylcysteine
IIb, BIIb, B
Acetylcysteine
Acetylcysteine
IIb, B
IIb, B
58
58
56
58
58

APPENDIX
VIII:
ofofContrast
APPENDIX
VIII:Prevention
Prevention
ContrastInduced
InducedNephropathy
Nephropathy
AGENT
AGENT
CONCENTRATION DOSE
DOSE/ FLOW
/ FLOWRATE
RATE
CONCENTRATION
Sodium
Chloride* 0.9%
0.9%
solution
Sodium
Chloride*
solution
Rateofof1.0-1.5
1.0-1.5ml/kg/hr
ml/kg/hrfor
for
Rate
3h-12hbefore
beforeand
and6h-24h
6h-24h
3h-12h
afterthe
theprocedure
procedureensuring
ensuring
after
urineflow
flowrate
rateofof150
150
a aurine
ml/hour
ml/hour
Reducerate
ratetoto0.5
0.5ml/kg/hr
ml/kg/hrifif
Reduce
LVEF<40%
LVEF<40%
Sodium
Sodium
Bicarbonate**
Bicarbonate**
3 ml/kg/hr for 1 hour before

3 ml/kg/hr for 1 hour before
the contrast followed by an
the contrast followed by an
infusion of 1 ml/kg/hr for 6
infusion
of 1 ml/kg/hr for 6
hours after the procedure
hours after the procedure
NN-acetylcysteine***
acetylcysteine***
154 mEq/L in 5%
154 mEq/L in 5%
dextrose in water
dextrose in water
(154 ml of
(154
ml of
1000 mEq/l of
1000
mEq/l
of
sodium
bicarbonate
sodium
+ 850 bicarbonate
ml of 5%
+ 850
ml of 5%
Dextrose)
Dextrose)
1200 mg twice daily, one day

1200
mgand
twice
daily,
before
one
day one
afterday
the
before
and one day after the
contrast
contrast
* McCullough PA, Bertrand ME, Brinker JA, Stacul F. A meta-analysis of the renal safety of
isosmolar iodixanol
compared
with low-osmolar
media. J of
Am
Cardiol.
PA, Bertrand
ME, Brinker
JA, Stacul F.contrast
A meta-analysis
theColl
renal
safety 48:
of
* McCullough
2006; 6929.
isosmolar
iodixanol compared with low-osmolar contrast media. J Am Coll Cardiol. 48:
2006; 6929.
** Briguori C, Colombo A, Violante A et al. Standard vs double dose of N-acetylcysteine to
prevent contrast
agentA,associated
J 2004;
: 206-211.
C, Colombo
Violante Anephrotoxicity.
et al. StandardEur
vsHeart
double
dose 25
of N-acetylcysteine
to
** Briguori
prevent contrast agent associated nephrotoxicity. Eur Heart J 2004; 25 : 206-211.
*** Tepel M, Van der Giet M, Schwarzfeld C et al. Prevention of radiographic-contrastin renal
functionCbyetacetylcysteine.
J Med. 2000; 343:
Tepel M, Vanreductions
der Giet M,
Schwarzfeld
al. Prevention NofEngl
radiographic-contrast*** agent-induced
180184.
agent-induced reductions in renal function by acetylcysteine. N Engl J Med. 2000; 343:
180184.
59
59
57

ACKNOWLEDGMENTS
ACKNOWLEDGMENTS
The committee of this guideline would like to express their gratitude and
The
committee
of this
guideline
would
like to express their gratitude and
appreciation
to the
following
for their
contribution:
appreciation to the following for their contribution:
Technical Advisory Committee, Clinical Practice Guidelines, Ministry of
Technical
Committee,
Clinical
Practice Guidelines, Ministry of
Health for Advisory
their valuable
input and
feedback
Health
their valuable
input
and
feedback
Panel offorexternal
reviewers
who
reviewed
the draft
Panel
of external
reviewers
reviewed the draft
Secretarial
assistance
from who
sanofi-aventis
Secretarial assistance from sanofi-aventis
DISCLOSURE STATEMENT
DISCLOSURE STATEMENT
The panel members have no potential conflict of interest to disclose.
The panel members have no potential conflict of interest to disclose.
SOURCES OF FUNDING
SOURCES OF FUNDING
This CPG was made possible
This
CPG was (M)
madeSdn
possible
Sanofi-Aventis
Bhd.
Sanofi-Aventis
(M)
Sdn
content of this guideline. Bhd.
content of this guideline.
by an unrestricted educational grant from

by
unrestricted
grant from
Theanfunding
body educational
did not influence
the
The funding body did not influence the
60
60
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June 2011

Clinical Practice Guidelines on

Available on the following websites:

Clinical Practice Guidelines on

Clinical Practice Guidelines on

no angina in the past

This includes (see Table 1, pg:4):

Coronary Angiography and Revascularization*

*If patient is admitted to a non-PCI centre and has

CCB : Calcium channel blockers

Clinical Practice Guidelines on

Initial and Inhospital

Continued long term if tolerating

High potency statins should be used

Clinical Practice Guidelines on

Figure 1: Non-invasive investigation of Low Risk Patients with UA/

Exercise stress test

Equivocal / Positive Test

Risk Factor Reduction +

* Low risk patients have :

Patients who have undergone revascularization and with residual/recurrent or a

Clinical Practice Guidelines on

Dato Hasan Abdul Rahman,

Clinical Practice Guidelines on

FOREWARD FROM THE AMERICAN COLEGE OF CARDIOLOGY

Congratulations and a personal toast to Malaysian heart health!

Ralph Brindis, MD, MPH, FACC, FSCAI

Clinical Practice Guidelines on

Members of the Expert Panel

Clinical Practice Guidelines on

External Reviewers (in alphabetical order):

Dr. Chan Hiang

Dr. Lee Chuey

Dr. Lee Fatt

Dr. Kim Tan

Dr. Tee Lian

Dr. Wong Kai

Clinical Practice Guidelines on

RATIONALE AND PROCESS OF GUIDELINE DEVELOPMENT

Clinical Practice Guidelines on

Clinical Practice Guidelines on

Clinical Practice Guidelines on

Conditions for which there is evidence and/or general agreement

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

Usefulness/efficacy is less well established by evidence/opinion

Conditions for which there is evidence and/or general agreement

Data derived from multiple randomized clinical trials or meta

Adapted from the American Heart Association/American College of Cardiology

Clinical Practice Guidelines on

Clinical Practice Guidelines on

ACS is a clinical spectrum of ischemic heart disease. Depending upon the

New onset of severe angina or accelerated angina; no rest pain

It may be further classified according to clinical circumstances into either:

Secondary develops in the presence of extracardiac disease

Clinical Practice Guidelines on

Clinical Practice Guidelines on

The symptoms of UA/NSTEMI may be indistinguishable from that of

The objective of the physical examination is to identify:

Clinical Practice Guidelines on

The ECG adds support to the diagnosis and provides prognostic

It should be performed within 10 minutes of the patients arrival at

However, a completely normal ECG does not exclude the diagnosis

4.4. Cardiac Biomarkers