CPG Management of Acute ST Segment Elevation Myocardial Infarction (2nd Edition)

MOH/P/PAK/127.
07(GU)
CLINICAL PRACTICE GUIDELINES
MANAGEMENT OF
ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
2007 - ( 2nd edition )
MINISTRY OF HEALTH NATIONAL HEART ASSOCIATION ACADEMY OF MEDICINE

MALAYSIA MALAYSIA MALAYSIA
Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
This guideline is meant to be a guide for clinical practice, based on the

best available evidence at the time of development. Adherence to this
guideline may not necessarily guarantee the best outcome in every case.
Every health care provider is responsible for the management of his/her
unique patient based on the clinical picture presented by the patient and
the management options available locally.
This guideline was issued in 2007 and will be reviewed in 2010 or sooner if
new evidence becomes available
CPG Secretariat
c/o Health Technology Assessment Unit
Medical Development Division
Ministry of Health Malaysia
4th floor, Block E1, Parcel E
62590, Putrajaya.
Electronic version available on the following website:

http:// www.moh.gov.my
http://www.acadmed.org.my
This is an update to the Clinical Practice Guideline on ST Elevated

MI (published 2001). This CPG supersedes the previous CPG on ST
Elevated MI (2001)
MESSAGE FROM THE DIRECTOR GENERAL OF HEALTH
In this new millennium, there has been an exponential increase of scientific

knowledge and publications. Indeed, one of the greatest challenges of
modern day medical practice is to keep pace with this information and
applying them into routine clinical practice.
The publication of the Malaysian CPG on STEMI by the National Heart

Association of Malaysia, Academy of Medicine and Ministry of Health
Malaysia is therefore very timely. Apart from the updates in the clinical
scientific knowledge, adaptations have been made for the local setting.
With this CPG, patients presenting to any of the health care institutions in
the country with STEMI will be assured of the latest standards of clinical
practice. However, for any CPG to be a success, it has to be utilized
optimally and updated from time to time.
I would like to commend to the expert panel for the time and effort taken
by them in updating this CPG and for health care practitioners to translate
knowledge in this CPG into routine clinical practice, for the benefit of our
fellow Malaysians.
Y.Bhg Tan Sri Datuk Dr Hj Mohd Ismail Merican

Director General of Health Malaysia
i
Clinical Practice Guidelines Development Expert Panel
Chairperson:
Dr Robaayah Zambahari Senior Consultant Cardiologist

Institute Jantung Negara, KL
Expert Panel Members (in alphabetical order):
Dr. Azlan Hussin (Secretary) Consultant Cardiologist and

Electrophysiologist
Institute Jantung Negara,KL
Dr Aris Chandran Consultant Physician
Ipoh General Hospital,Perak
Dr. Choo Gim Hooi Consultant Cardiologist
Selangor Medical Centre, Selangor
Dr. Jeyamalar Rajadurai Consultant Cardiologist
Subang Jaya Medical Centre, Selangor
Dr Khoo Kah Lin Consultant Cardiologist
Pantai Medical Centre, KL
Dr Omar Ismail Consultant Cardiologist
Penang General Hospital, Penang
Dr Rosli Mohd Ali Consultant Cardiologist
Institute Jantung Negara, KL
Dr Sim Kui Hian Consultant Cardiologist
Sarawak General Hospital, Sarawak
Dr Wan Azman Wan Ahmad Consultant Cardiologist
University Malaya Medical Centre, KL
Dr Zurkarnai Yusof Consultant Cardiologist
Hospital Universiti Sains Malaysia,
Kelantan
External Reviewers (in alphabetical order):

Dr Chan Hien Chuan Consultant Emergency Physician
Sarawak General Hospital, Sarawak
Dr K. Sree Raman Senior Consultant Physician
Hospital Tunku Jaa’far,
Negeri Sembilan
Dr Tee Lian Kim General Practitioner
Young and Newton Clinic, KL
Dr V. Paranthaman Family Medicine Specialist
Klinik Kesihatan Jelapang, Perak
ii
Rationale and Process of Development of this CPG
Rationale
Acute Myocardial Infarction is a major health problem, with relatively high

morbidity and mortality. Although mortality has been reduced, it is still
substantial. In the management of established acute myocardial infarction,
time is the essence.
The Clinical Practice Guidelines (CPG) in the Management of ST

Elevated Myocardial Infarction (STEMI) was developed to provide a
clear and concise approach to all clinicians on the current concepts in
the management of acute MI patients. In Malaysia, a significant number
of acute MI patients are managed by non-cardiologists. We feel that it is
important to summarise and adapt relevant clinical trial data and current
treatment strategies to our local practice.
The 1st CPG on STEMI was published in 2001. Since then, there have
been many new developments in the management of STEMI. Thus an
update on the latest and current guidelines in the 1st revision on the CPG
in STEMI would be most appropriate.
This CPG has been prepared by a panel of committee members appointed

by the National Heart Association of Malaysia (NHAM), Academy of
Medicine (AOM) and Ministry of Health (MOH). The committee members
comprise of cardiologists and general physicians from the government,
private sector and the Universities.
Objectives
These guidelines are intended to provide awareness and education in
• early recognition of STEMI

• evidence-based practice for the management of STEMI
• secondary prevention following STEMI
with the intention of reducing the morbidity and mortality associated with
STEMI
Process
Evidence was obtained by systematic review of current medical literature

on STEMI using search engines available online. The other international
guidelines on STEMI were also taken into consideration. After many
in-depth discussions, the draft was completed by the members of the
Expert Panel and submitted to key health personnel in major hospitals of
the Ministry of Health, Malaysia, universities and private sector for review
and approval.
The level of recommendation and the grading of evidence used in this

CPG was adapted from the American Heart Association and the European
Society of Cardiology. The evidence supporting the recommendation was
iii
graded as A if the data was derived from multiple randomized clinical trials
involving a large number of individuals or meta-analyses. Evidence was
graded as B if the data was derived from a single randomized clinical trial
or limited to non randomized clinical trials or observational data registries.
Evidence was graded C if the recommendation was based on consensus
of expert opinion or case studies only.
In certain conditions where there are no clinical trials but nevertheless the
practice is recommended based on years of clinical experience and is thus
well supported even though the evidence is ranked as C. An example is
anticoagulation in the presence of a large mobile left ventricular thrombus.
The levels of recommendation were ranked as I, IIa, IIb or III as outlined in
page V.
Clinical Questions Addressed

• How do you diagnose STEMI?
• What is the best strategy to treat STEMI patients based on the current
evidence available?
• How to reduce the risk of a subsequent cardiovascular event?
• How to treat the following special groups?
- Elderly
- Diabetics
- Women
Target Group:
These guidelines are developed for all healthcare providers involved in the
management of STEMI in adults.
Target Population:
These guidelines are developed to treat all adults with STEMI
iv
LEVELS OF EVIDENCE AND GRADES OF RECOMMENDATION
LEVELS OF EVIDENCE
I Conditions for which there is evidence and/or general agreement
that a given procedure/therapy is beneficial, useful and/or
effective.
II Conditions for which there is conflicting evidence and/or
divergence of opinion about the usefulness/efficacy of a
procedure/therapy.
II-a Weight of evidence/opinion is in favor of its usefulness/efficacy.
II-b Usefulness/efficacy is less well established by evidence/opinion
III Conditions for which there is evidence and/or general agreement
that a procedure/therapy is not useful/effective and in some
cases may be harmful.
GRADES OF RECOMMENDATION
A Data derived from multiple randomized clinical trails or meta
analyses
B Data derived from a single randomized clinical trial or large
non randomized studies
C Only consensus of opinions of experts, case studies or standard
of care
(Adapted from the American Heart Association and the European Society of Cardiology)
v
TABLE OF CONTENTS
Message from the Director General of Health i

Members of the Expert Panel ii
Rationale and Process of Development of this CPG iii
Table of Contents vi
1. INTRODUCTION 1
2. TERMINOLOGY 1
2.1 Pathogenesis of STEMI 1
2.2 Clinical Diagnosis of STEMI 2
2.2.1 History 2
2.2.2 Electrocardiographic changes 3
2.2.3 Serum Cardiac Biomarkers 3
2.2.4 Other Diagnostic Modalitites 5
2.2.5 Difficult Diagnostics 5
3. PRE-HOSPITAL MANAGEMENT 7
3.1 For the general public 7
3.2 For Patients with known CHD 7
3.3 For the general practitioner/ family physician 7
3.4 For Allied Health Care Personnel 7
4. IN-HOSPITAL MANAGEMENT 9
4.1 Initial Recognition and Management 9
4.2 Reperfusion Strategies 10
4.2.1 Fibrinolytic Therapy 11
4.2.1.1 Indications 11
4.2.1.2 Contraindications 11
4.2.1.3 Choice of Fibrinolytic Agent 12
4.2.1.4 Indicators of Successful Reperfusion 13
4.2.1.5 Failed Fibrinolysis 14
4.2.2 Percutaneous Coronary Intervention (PCI) 14
4.2.2.1 Primary PCI 14
4.2.2.2 Facilitated PCI 14
4.2.2.3 Rescue PCI 14
4.2.2.4 Delayed PCI (>72 hours after fibrinolytic therapy) 14
4.3 Cardiac Care Unit Management 16
4.3.1 General Measures 16
4.3.2 Monitoring 16
4.3.3 Concomitant Therapy 16
4.3.3.1 Oxygen 16
4.3.3.2 Antiplatelet Agents 16
4.3.3.3 β-Blockers 17
4.3.3.4 Angiotensin Converting Enzyme Inhibitors (ACEI) and 17
Angiotensin Receptor Blockeres (ARB)
4.3.3.5 Nitrates 18
4.3.3.6 Calcium Channel Blockers 18
4.3.3.7 Antithrombotics 19
4.3.3.8 Glycoprotein IIb/IIIa Receptor Inhibitors 20
4.3.3.9 Statins 20
4.3.3.10 Aldosterone Antagonists 21
4.3.3.11 Others – Magnesium, Lignocaine, 21
Glucose-Insulin-Potassium Infusions
vi
4.4 Complications of STEMI 22

4.4.1 Arrhythmias 22
4.4.2 Left Ventricular Dysfunction and Shock 23
4.4.2.1 Presentation 23
4.4.2.2 Differential diagnoses of LV dysfunction and shock 23
4.4.2.3 Investigations 24
4.4.2.4 Management 24
4.4.3 Mechanical complications 24
4.4.4 Right Ventricular Infarction (RVI) 25
4.4.5 Others 25
4.4.5.1 Chest pain post STEMI 25
4.4.5.2 LV Thrombus and Arterial Embolism 26
4.4.5.3 Deep Venous Thrombosis (DVT) 26
4.5 Urgent/ Emergent CABG surgery 26
5. RISK STRATIFICATION POST-STEMI 27
6. DURATION OF HOSPITALIZATION 28
7. SECONDARY PREVENTION 29
7.1 Cessation of Smoking 29
7.2 Diet 29
7.3 Regular Exercise 29
7.4 Control of Hypertension 29
7.5 Good Glycemic control 29
7.6 Antiplatelet Agents 30
7.7 β-Blockers 30
7.8 ACE Inhibitors and ARB 30
7.9 Lipid-lowering therapy 30
7.10 Oral Anticoagulant (warfarin) 30
7.11 Others 30
8. SPECIAL GROUPS 31
8.1 STEMI in elderly 31
8.2 STEMI in diabetics 31
8.3 STEMI in women 31
9. CARDIAC REHABILITATION IN STEMI 32
10. FUTURE DEVELOPMENTS 32
11. CHECK LISTS FOR FOLLOW-UP VISIT 32
12. SUMMARY 33
Flow Chart 1: Management of Patients Presenting with STEMI 34
Algorithm 1: Pulseless Arrhythmias 35-36
Algorithm 2: Stable Ventricular Tachycardia 37
Algorithm 3: Atrial Fibrillation 37
Algorithm 4: Bradyarrythmias 38
Appendix 1: Grades of recommendation and level of evidence for
acute therapy of STEMI 39
Appendix 2: Grade of recommendation and level of evidence for
secondary prevention post STEMI 40
Appendix 3: Pharmacokinetics of Phosphodiesterase 5 inhibitors 41
References 42
Acknowledgments 52
Disclosure Statement 52
Sources of funding 52
vii
1. INTRODUCTION
Cardiovascular disease remains an important cause of death in Malaysia

accounting for 20-25% of all deaths in government hospitals from 2000-
2005. Following an acute myocardial infarction (AMI) the mortality rate was
about 20% in 2004.1 This high rate could have been due to late
presentation and diagnosis, leading to delayed treatment. Occasionally the
diagnosis could have been missed. In developed countries the mortality
rate following an AMI had decreased to less than 9% by the early 2000’s2.
Much progress has been made in the management of AMI, especially

in the last two decades with the discovery that early reperfusion therapy
results in myocardial salvage and a significant reduction in morbidity and
mortality. The majority of deaths occur soon after the onset of symptoms,
the “pre-hospital phase”. To reduce these deaths, the public needs to be
educated of the symptoms of an infarct and on the need to seek
medical attention immediately. Healthcare personnel should be sensitized
and trained to deal with these patients urgently and appropriately.
Emergency Departments in hospitals need to develop critical pathways
and management strategies to maximize treatment benefits.
Guidelines help in the management of patients. All the recommendations

stated in this guideline may not be available to all eligible patients. Patient
care should be individualized and sound clinical judgement plays an
important role in decision making.
2. TERMINOLOGY
Acute coronary syndrome is a clinical spectrum of ischemic heart disease

ranging from unstable angina, non-ST-elevation myocardial infarction
(NSTEMI) to ST-elevation myocardial infarction (STEMI) depending upon
the degree and acuteness of coronary occlusion.(see Figure 1)
STEMI: Myocardial infarction due to acute total occlusion of the

coronary artery
NSTEMI: Myocardial infarction due to acute sub-total occlusion of the
coronary artery
2.1 Pathogenesis of STEMI
STEMI is necrosis of heart muscle due to inadequate blood supply following

an acute total coronary occlusion. This occlusion is usually due to
atherosclerotic plaque rupture, fissuring or ulceration with superimposed
thrombosis and coronary vasospasm. Rarely, it may result from non-
atherosclerotic arterial disease such as coronary vasospasm alone,
coronary embolism or vasculitis3.

Figure 1: Adapted with modification from Antman EM, Anbe DT, Armstrong PW et al. “ACC/AHA
Guidelines for the management of patients with ST Elevation Myocardial Infarction” at www.acc.org
2.2 Clinical Diagnosis of STEMI
It is diagnosed by:
i. Clinical history of ischaemic type chest pain
ii. ECG changes – The following are integral to the diagnosis of
STEMI:
New onset ST-segment elevation of:
- ≥ 0.1 mV in 2 contiguous limb leads, or V4 to V6
and/or
- ≥ 0.2 mV in 2 contiguous precordial leads V1 to V3
Presumed new left-bundle branch block
iii. Evidence of myocardial injury or necrosis as indicated by
elevated serum cardiac biomarkers

2.2.1 History
A good history is vital in raising the clinical suspicion and making a

diagnosis of STEMI. Chest pain of STEMI is typically retrosternal, severe,
crushing, squeezing or pressing in nature, lasting more than 30 minutes,
associated with profuse sweating, nausea, vomiting and shortness of
breath. It is sometimes described as chest tightness only. The pain may
radiate to the jaw or down the left upper limb. It may occur at rest or with
activity. Occasionally the pain may be burning in nature and of lesser
severity. It may be in the epigastric region and be misinterpreted as
indigestion or heart burn. Rarely may it be localized to the back in the
interscapular region only resulting in a misdiagnosis.
Other atypical presentations include unexplained nausea and vomiting,

weakness, dizziness, lightheadedness and syncope, which may occur in
the presence or absence of chest pain.

Diabetics, the elderly and females may not present with typical chest
pains. Common presenting symptoms in these patients are dyspnoea and
atypical chest pains.
Other important points to note in the history are the presence of:
- previous history of ischemic heart disease, percutaneous coronary
intervention (PCI) or coronary artery bypass surgery (CABG)
- risk factors for atherosclerosis
- symptoms suggestive of previous transient ischemic attack or other
forms of cerebrovascular disease
- symptoms suggestive of peripheral vascular disease
2.2.2 Electrocardiographic changes
The diagnosis of STEMI depends upon the presence of characteristic ECG
changes. These evolving ECG changes are hyperacute changes of a tall
peaked T-wave, ST segment elevation followed by the development of
Q-wave, return of the ST segment to isoelectric and T-wave inversion. The
cut off points for new or presumed new ST segment elevation are ≥ 0.2mV
in leads V1, V2, or V3 and ≥ 0.1mV in other leads. This should be present
in 2 or more contiguous leads. The presence of new onset or presumably
new left bundle branch block (LBBB) in a patient with typical type chest
pain indicates an infarct.
However in some cases especially when the patient presents early, the
ECG may be normal or equivocal. In patients with ongoing chest pain and
in whom the clinical index of suspicion of STEMI is high, 12 lead ECG
tracings repeated at close intervals of at least 15 minutes might show
evolving changes. Comparison with previous ECG’s may also be helpful in
such situations.
In patients with an inferior infarct, one should look for associated
posterior, lateral and RV infarct. The latter requires right sided chest leads
for diagnosis.
For localization of infarct see Table 1.
Table 1: ECG patterns of various STEMI locations
Location Leads ECG findings
Anteroseptal V1 – V3 ST elevation, Q wave
Extensive anterior V1 – V6 ST elevation, Q wave
Posterior V7 – V8 T elevation, Q wave
Posterior V1 – V2 ST depression, Tall R wave
Anterolateral I, AVL, V5 – V6 ST elevation, Q wave
Inferior II, III, AVF ST elevation, Q wave
Right Ventricular V4R, V5R ST elevation, Q wave
2.2.3 Serum Cardiac Biomarkers

A rise and fall in the levels of serum cardiac biomarkers support the
diagnosis of STEMI. One should not, however, wait for the results of these
biomarkers before initiating reperfusion therapy. These cardiac biomarkers
include4 :-
• Cardiac troponins (cTnT and cTnI)

• Creatine kinase-Myocardial Band (CK-MB)

• Creatine kinase (CK)
• Myoglobin
• Fatty Acid Binding Proteins
For the relative timing, rate of rise, peak value, duration of elevation and
properties of these cardiac biomarkers following STEMI, see Figure 2 and
Table 2.
Cardiac troponins and CK-MB are the most specific cardiac biomarkers.
It takes about 3-8 hours after STEMI for them to rise. Thus, too early a
measurement may result in a misleadingly low level.
For the diagnosis of STEMI, the value of CK-MB should be twice the upper
limit of normal. Persistently elevated values of CK-MB are almost never
due to myocardial necrosis. CK-MB rises early and falls early. Hence, CK-
MB measurements are useful for the diagnosis of reinfarction. CK is not
as sensitive or as specific as CK-MB. Nevertheless, it is also useful for the
diagnosis of STEMI and reinfarction.
A single measurement of a raised Troponin T or I (99th percentile of the
values for a reference control group) is sufficient to indicate myocardial
necrosis5. They are useful in detecting myocardial infarction in patients
presenting with atypical histories and non diagnostic ECG’s. Elevated
troponin levels are more important for the diagnosis of NSTEMI than
STEMI. Troponins may remain elevated for up to 14 days. Therefore it is
not useful for the diagnosis of reinfarction.
It is recommended that measurement of cardiac biomarkers be done at
periodic intervals, at hospital admission and again at 12-24 hours. This
would help to establish or exclude the diagnosis and may be useful for an
estimation of infarct size.
AST and LDH levels are not sensitive or specific for AMI with frequent false
positive elevations.
Figure 2: Time Course of Elevation of Serum Cardiac Biomarkers after STEMI
(Reproduced with permission from “Clinical Implications of the new definition of myocardial infarction”.
John K French, Harvey D White; Heart 2004;90:99–106)

Table 2: Properties of Serum Cardiac Biomarkers

Protein First detection* Duration of detection Sensitivity Specificity
Fatty acid binding protein 1.5 – 2 hours 8 – 12 hours +++ ++
Myoglobin 1.5 – 2 hours 8 – 12 hours +++ +
CK-MB 2 – 3 hours 1 – 2 days +++ +++
Troponin I 3 – 4 hours 7 – 10 days ++++ ++++
Troponin T 3 – 4 hours 7 – 14 days ++++ ++++
CK 4 – 6 hours 2 – 3 days ++ ++
Aspartate Transaminase 6 – 10 hours 3 – 5 days ++ +
LDH 6 –10 hours 5 – 7 days ++ +
* Hours after symptom onset.
CK, creatine kinase; LDH, lactate dehydrogenase
(Reproduced with permission from “Clinical Implications of the new definition of myocardial infarction”.
John K French, Harvey D White; Heart 2004;90:99–106)
2.2.4 Other Diagnostic Modalities.

Imaging techniques such as chest radiography, echocardiography6, multi-
slice computed tomography (MSCT)7 and radionuclide techniques8 are
useful investigations in the patient presenting with acute chest pain. They
help to:
• Rule out or confirm the presence of acute infarction or ischaemia.
• Identify non-ischaemic conditions causing chest pain such as valvular
heart disease, pulmonary embolism, aortic dissection and
pneumothorax.
• Identify mechanical complications of acute infarction.
• Provide prognostic information.
Echocardiography is a particularly useful bedside imaging technique in

difficult diagnostic situations.
2.2.5 Difficult Diagnosis
Sometimes the diagnosis of myocardial infarction is difficult. About 2-8%

of patients presenting with chest pains to the emergency department have
been misdiagnosed and sent home. The morbidity and mortality in these
patients is high. To reduce this misdiagnosis, we suggest the following
measures be taken in all patients presenting with chest pains:
• They should be given priority in the emergency department and attended

to urgently.
• Myocardial ischemia or infarction should be excluded in all these
patients.
• Clinical suspicion should be high in all patients with predisposing risk
factors for atherosclerosis.
• A careful history will often help in making the diagnosis.
• An ECG should be done as soon as possible in all patients with chest
pains especially when the clinical suspicion of AMI is high. The threshold
for doing an ECG in a patient presenting with chest pain should be low.
• Where the initial ECG is non diagnostic, it should be repeated and
compared with old ECG’s. Thus it is important to maintain good clinical
records that can be rapidly retrieved.

• Cardiac biomarkers especially the troponins, are helpful in ruling in or

ruling out a myocardial infarction.
• Where the diagnosis is unclear but the clinical suspicion is high, these
patients should be observed in the emergency department for a few
hours and the resting ECG and cardiac biomarkers repeated to look for
serial changes. If these remain stable, then the patient may be sent home
but asked to return for an early review in the outpatient clinic.
In addition, the hospital needs to:
• educate all medical staff on the importance of early detection and

treatment of AMI because this results in myocardial salvage and
improved patient outcomes.
• have regular refresher courses on ECG interpretation.
• implement critical pathways for patients presenting with chest pains to the
emergency department.
Recommendations:
• The public and allied health care personnel should be

educated on the importance of early diagnosis and the benefits
of early reperfusion therapy.
• STEMI is diagnosed by the clinical history of chest pain, ECG

changes of ST elevation/ LBBB and elevated serum cardiac
biomarkers.
• Atypical presentations can occur in the elderly, women and in

diabetic patients.
• If the initial ECG is non-diagnostic, it may need to be repeated

at frequent intervals to detect evolving changes of STEMI.
• Too early a measurement can sometimes result in a

misleadingly low level of serum cardiac biomarkers.

3. PRE-HOSPITAL MANAGEMENT
Immediate measures to be taken in suspected cases of STEMI
3.1 For the general public:

• Seek immediate medical attention at the nearest hospital.
• Call for an ambulance (dial 991 or hospital direct line if known) or
get someone to take you immediately to the nearest hospital.
• Do not drive yourself.
• If not on regular aspirin and with no history of allergy, chew and
swallow one 300mg tablet of aspirin immediately.
3.2 For Patients with known CHD:

• If the pain is suggestive of STEMI (see section 2.2.1), take one
dose of sublingual GTN and be rapidly transported to the hospital.
• If the pain is not severe, take one tablet of GTN and repeat every
5 minutes for a maximum of 3 doses. If the pain still persists after
15 minutes, go to the hospital.
3.3 For the general practitioner / family physician:

I, A • Ask patient to chew and swallow one 300mg tablet of aspirin9.
I, C • Give sublingual GTN.
I, A • If the ECG shows ischemic changes, give 300mg of clopidogrel if

available.10,11
I, C • Wherever possible, set up intravenous access.
I, C • Pain relief with intravenous opiates (IV morphine 3-5mg slowly).
I, C • Avoid intramuscular injections since this could result in

intramuscular hematomas if fibrinolytic agents are subsequently
administered.
I, C • Call an ambulance or ask the patient’s relative or friend to send

the patient immediately to the nearest hospital.
• Wherever possible, contact the doctor at the hospital so that the

patient can be treated promptly on arrival.
3.4 For Allied Health Care Personnel:
Immediate measures to be taken when there is an ambulance call:-

• Note nature of complaint.
• Obtain name of caller, address and telephone number.
• If possible, request that a relative or friend wait at a strategic place
to help locate the patient.
• Dispatch an adequately equipped ambulance with trained
paramedics immediately.
• Patient should be given oxygen and aspirin (if he has not taken)
and transported to hospital.

• Upon reaching the hospital, the patient should be taken directly to

the Emergency Department.
An ECG should be done as soon as possible. In hospitals where

networking facilities are available, allied health care personnel in the
ambulance should relay/transmit the ECG to the call centre for review by
the Specialist, for consideration of pre-hospital fibrinolysis or primary PCI.
Allied Health care personnel should be trained:-

• to identify patients at high risk of developing CHD.
• to identify patients presenting with AMI.
• on the importance of early referral and treatment.
• in basic and advanced cardiopulmonary resuscitation (CPR).
Recommendations:
• Patients with suspected STEMI should be given sublingual GTN,

aspirin and clopidogrel.
• These patients should be rapidly transported to the hospital.

4. IN-HOSPITAL MANAGEMENT
Early management of STEMI is directed at:
• Pain relief
• Establishing early reperfusion
• Treatment of complications - arrhythmias
4.1 Initial Recognition and Management
I, A When the patient with suspected STEMI reaches the emergency

department, evaluation and initial management should take
place promptly (FAST TRACK - RED ZONE) because the
benefits of reperfusion therapy is greater the earlier it is initiated 12.
I, C A quick targeted history should be taken and vital signs noted. The
diagnosis should be confirmed with an ECG, which should be done
as soon as possible, preferably within 10 minutes of the patient’s
arrival in the emergency department. It is important to relieve pain
and quickly assess the patient’s suitability for reperfusion by either
fibrinolytic therapy or primary PCI.
The following should be done immediately and concomitantly in the

emergency department (see flow chart 1, page 44):-
I, C • Assessment and stabilization of the patient’s haemodynamics.
I, C • Sublingual GTN if chest pain persists (unless systolic blood

pressure (SBP) < 90 mmHg).
I, C • Continuous ECG monitoring.
I, A • 300mg of aspirin chewed and swallowed if not given earlier 9.
I, A • Clopidogrel at a dose of 300mg should be given if not given

earlier 10,11.
I, C • Oxygen by nasal prongs / facemask.
I, C • Venous access established and blood taken for cardiac

biomarkers, full blood count, renal profile, glucose and lipid profile.
Preferably 2 intravenous lines should be set up.
I, C • Pain relief - morphine should be administered intravenously at

2-5mg every 5-15 minutes until pain is relieved. Watch for
evidence of toxicity – hypotension and respiratory depression.
Anti-emetics ( IV metoclopromide 10mg or promethazine 25mg )
should be given.
I, C • Intramuscular injections should be avoided.
I, C • Assessment for reperfusion strategy.

4.2 Reperfusion Strategies
A Early and prompt reperfusion is crucial as TIME LOST is

equivalent to MYOCARDIUM LOST 12,13,14.
A Despite overwhelming data showing that prompt reperfusion therapy

improves survival 12,13 it is still widely underutilized and delayed.
A Most studies indicate that primary PCI is superior to fibrinolytic
therapy as a reperfusion strategy15,16.
A However in patients who present within 3 hours of symptom onset
and are at low risk, both treatment strategies appear to have similar
benefits17,18.
In the majority of our hospitals, fibrinolytic therapy is more readily

available and constitutes the main reperfusion strategy. If both
choices are available, the following factors help guide the choice of
reperfusion strategies:
• Time from symptom onset to first medical contact

• Time delay to PCI (time from hospital arrival to balloon dilatation –
door to balloon time)
• Time to hospital fibrinolysis (time from hospital arrival to
administration of fibrinolytic therapy – door to needle time)
• Contraindications to fibrinolytic therapy
• High risk patients
The best reperfusion strategy will depend upon:
A) Time from onset of symptoms
• Early presentation (within 3 hours)

I,A
If both treatment options are readily available, they have been
shown to be equally effective17,18 except for the following situations
where primary PCI is the preferred strategy:
- fibrinolytic therapy is contraindicated
- in high-risk patients
- PCI time delay [(door-to-balloon time) – (door-to-needle time)] is
less than 60 minutes19
• Late presentation (3 to 12 hours)

I,A Primary PCI is preferred 15,16. The door to balloon time should be
within 90 min if the patient presents at a PCI capable facility19.

IIa,B If transferred from a center with no PCI facilities, it should be less
than 2 hours. (including transfer delay)20
If the time delay to primary PCI is longer than as mentioned,
then fibrinolytic therapy should be given.
• Very late presentation (> 12 hours)

III, A Both primary PCI and fibrinolytic therapy are not routinely
recommended in patients who are asymptomatic and
haemodynamically stable 12.
10
However, reperfusion therapy would still be beneficial in patients

with persistent ischaemic symptoms, haemodynamic or electrical
instability. In this subgroup, primary PCI is the preferred strategy.
B) Contraindications to fibrinolytic therapy
See section 4.2.1.2
C) High risk patients
These include patients with:

• Large infarcts
• Anterior infarcts
• Cardiogenic shock
• Elderly patients
• Post revascularization (post CABG and post PCI)
• Post infarct angina
I,A Primary PCI is the preferred strategy in these patients 21,22,23.
I,A The goals of time to reperfusion therapy should be within:

• 30 minutes door to needle time12,13
I,B
• 90 minutes door to balloon time 19
4.2.1 Fibrinolytic Therapy

I,A Fibrinolytic therapy has been shown to reduce mortality when given
within the appropriate time frame. When given within 1 hour from time
of onset of symptoms, it is most beneficial and has been shown to be
able to abort the infarction and reduce mortality by up to 50%12,17.
I,A The door-to-needle time should be within 30 mins. Strategies should

be put in place to achieve this target. Fibrinolytic therapy should be
made available in all hospitals and there should be protocols to
initiate it in the emergency department.
I,A Pre-hospital fibrinolytic therapy has been shown to achieve faster

reperfusion17,24.
I,C Patients presenting with a low blood pressure (SBP < 90mm Hg)
should receive inotropic support prior to fibrinolytic therapy.
4.2.1.1 Indications
I,A Fibrinolytic therapy should only be given to patients with STEMI. It
has no role and may even be detrimental in patients with NSTEMI12,25.
4.2.1.2 Contraindications
Absolute contraindications
Risk of Intracranial haemorrhage
Any history of intracranial haemorrhage
Ischaemic stroke within 3 months
11
Known structural cerebral vascular lesion (e.g. arteriovenous

malformation)
Known intracranial neoplasm
Risk of bleeding
Active bleeding or bleeding diathesis (excluding menses)
Significant head trauma within 3 months
Suspected aortic dissection
Relative contraindications
Risk of intracranial haemorrhage
Severe uncontrolled hypertension on presentation (BP > 180/110
mm Hg)*
Ischaemic stroke more than 3 months ago
History of chronic, severe uncontrolled hypertension
Risk of Bleeding
Current use of anticoagulation in therapeutic doses (INR > 2)
Recent major surgery < 3 weeks
Traumatic or prolonged CPR >10 minutes
Recent internal bleeding (e.g. gastrointestinal or urinary tract
haemorrhage) within 4 weeks
Non-compressible vascular puncture
Active peptic ulcer
Others
Pregnancy
Prior exposure (>5 days and within 12 months of first usage) to
streptokinase (if planning to use same agent)
* The blood pressure should be reduced prior to institution of fibrinolytic

therapy.
4.2.1.3 Choice of Fibrinolytic Agent
Presently the agents available in Malaysia are:
Streptokinase
I, A This is the most widely used agent. It is not fibrin specific and is
less efficacious than fibrin selective agents 26,27. Despite
having a lower risk of intracranial haemorrhage, the reduction in
mortality is less than with fibrin specific agents26,28.
I, B Streptokinase is antigenic and promotes the production of

antibodies. Thus the utilization of this agent for re-infarction is
less effective if given again 5 days after the first administration 29.
PCI or fibrin specific agents should then be considered.
Regimen:
- 1.5 mega units in 100 ml normal saline or 5% dextrose over 1 hour.
Other regimens are:

- 1.5 mega units over 20 minutes, or
- 0.75 mega unit bolus and then repeated at the same dose after an
interval of 50 minutes if there is no clinical reperfusion.
12
The last 2 regimens achieve a higher coronary artery patency rate

and are associated with lower in-hospital mortality. However they are
associated with a higher incidence of hypotension30.
Alteplase
I,A This agent is fibrin specific and achieves better reperfusion at 90
min as compared to streptokinase 26,31.
I,A However there is a higher rate of reocclusion. Thus heparin
needs to be given for 48 hours 31,32,33.
Regimen: For patients > 65 kg

15 mg bolus; then 50 mg over 30 min and 35 mg over the
next 60min
For patients < 65 kg

15 mg bolus; then 0.75 mg/kg over 30 min and 0.5 mg/kg
over the next 60min
Second generation fibrin specific agents: Tenecteplase, Reteplase

B Tenecteplase has been recently introduced in Malaysia. These
second generation fibrin specific agents are as efficacious as
alteplase 34. Tenecteplase has been shown to have a slightly lower
bleeding risk as compared to alteplase 34. The mainadvantage of
using these agents is that they are easier to administer. They are
given as single or double bolus injections and also do not induce
antibody production.
Regimen: Tenecteplase (TNK-tPA) single i.v. bolus
30mg if < 60kg
35mg if 60 to < 70kg
50mg if >90kg
Heparin needs to be given for 48 hours
4.2.1.4 Indicators of Successful Reperfusion
There is no sensitive bedside clinical method to reliably detect
successful reperfusion35. Some useful guides are:
• resolution of chest pain (may be confounded by the use of narcotic
analgesics).
• early return of ST segment elevation to isoelectric line or a decrease
in the height of the ST elevation by 50% in the lead that records the
highest ST elevation therapy within 60-90mins of initiation of
fibrinolytic therapy.
• early peaking of CK and CK-MB levels.
• restoration and/or maintenance of haemodynamic and/or electrical
stability
The occurrence of ‘reperfusion arrhythmias’ is not a reliable indicator of
successful reperfusion. An exception is accelerated idioventricular rhythm
and sudden sinus bradycardia which have been correlated with a patent
infarct related coronary artery after fibrinolytic therapy or primary PCI35.
13
4.2.1.5 Failed Fibrinolysis
Failure of fibrinolytic agents to open up the occluded infarct related

artery is manifested as continuing chest pain, persistent ST segment
elevation and hemodynamic instability. These patients are more likely
to develop complications such as heart failure and arrhythmias.
I,B The treatment of choice for these patients is rescue PCI36.

They should not be given a second dose of a fibrinolytic agent. This is
because there has been no difference in event free survival
demonstrated if these patients are given a repeat dose of a
fibrinolytic agent or if they are treated conservatively36.
4.2.2. Percutaneous Coronary Intervention (PCI)
4.2.2.1 Primary PCI
I,A Primary PCI is the reperfusion strategy of choice as indicated earlier

(section 4.2)15,16 It should be performed promptly by experienced
operators and in centers performing a sufficient number of primary
PCI procedures.
4.2.2.2 Facilitated PCI
IIa,A Current evidence indicates that strategies combining fibrinolytic

therapy is associated with higher reperfusion rates and TIMI flow.
However, it is associated with higher mortality and bleeding rates. It is
therefore not recommended37,38 .
4.2.2.3 Rescue PCI
Rescue PCI may be considered in patients who have failed

fibrinolytic therapy or have recurrent chest pain and/or ischaemic
complications. Those who may benefit are patients with:
• ongoing chest pains
• haemodynamic and electrical instability
• cardiogenic shock in patient < 75 years old, within 36 hours of
STEMI and <18 hours of shock whose coronary anatomy is
suitable for revascularization
• heart failure and onset of chest pain within 12 hours
• cardiogenic shock – In these high risk patients, those who are <75
years of age and who present within 36 hours of STEMI and <18
hours of shock may be considered for rescue PCI if their coronary
anatomy is suitable for revascularization
This strategy is associated with high mortality and morbidity rates. As

such, patients should be individually evaluated.
4.2.2.4 Delayed PCI (> 72 hours after fibrinolytic therapy)
Routine angiography and PCI in asymptomatic and stable patients

post fibrinolytic therapy is controversial 39,40.
14
Recommendations:
• Patients presenting to the hospital need to be rapidly evaluated

for prompt reperfusion therapy.
• Reperfusion therapy with either primary PCI or fibrinolytic therapy

reduces mortality and is useful in patients presenting within 12
hours from onset of symptoms.
• We should aim to achieve a door-to-needle time of less than 30

min and a door-to-balloon time of less than 90 min.
• Fibrinolytic therapy if given within 3 hours of onset of symptom

gives equivalent results as primary PCI.
• The preferred strategy is primary PCI if the time of onset of

symptoms is between 3-12 hours.
• The treatment of choice for failed fibrinolysis is rescue PCI.
15
4.3 CARDIAC CARE UNIT MANAGEMENT
4.3.1 General Measures

A period of at least 12 hours of complete bed rest is recommended
following admission to CCU. Patients with uncomplicated infarcts are
encouraged to ambulate early. Those with haemodynamic instability
will need a longer period of monitoring.
Sedatives may be useful.
Use of bedside commodes and assisted bedside washing should be

safe in most patients.
The Valsalva maneuver has been shown to precipitate dangerous

haemodynamic and electrocardiographic changes particularly in the
young 41 and thus prevention of constipation with stool softeners is
encouraged.
4.3.2 Monitoring
The general condition of the patient, vital signs, pulse oximetry and
the ECG should be continuously monitored following STEMI, looking
for complications.
4.3.3 Concomitant Therapy

4.3.3.1 Oxygen
I,C Oxygen is indicated in the presence of hypoxemia. In uncomplicated
cases, its use should probably be limited to the first 24 hours.
Oxygen, via nasal prongs, at 2 - 4 litres/min is usually adequate. One
should aim to maintain the oxygen saturation above 95%.
4.3.3.2 Antiplatelet Agents

A) Aspirin
I,A Aspirin is indicated in all patients at diagnosis and should be
continued indefinitely unless contraindicated. The initial dose of 100-
300mg should be followed by a maintenance dose of 75 - 150mg
daily9.
B) Clopidogrel
I,A Clopidogrel, when given together with aspirin and fibrinolytic therapy
in STEMI, has been shown to reduce the odds of an occluded infarct
related artery, death or reinfarction without increasing the risk of
bleeding or cerebrovascular accidents. 10,11 A loading dose of 300 mg
should be given followed by a maintenance dose of 75 mg daily.
We recommend treatment for at least 1 month after fibrinolytic
therapy. Following PCI, a longer period of dual antiplatelet therapy
(up to 12 months) is necessary particularly when drug-eluting stents
are used.
16
4.3.3.3 β-blockers
I,A Current recommendations are to use oral β-blockers early in all

patients without specific contraindications 42,43.
I,B In patients with asymptomatic LV dysfunction (LV ejection fraction
on echocardiogram < 40%) and not in overt heart failure, carvedilol
has been shown to reduce the frequency of death and recurrent
AMI44. When indicated, it should be started in patients who are
hemodynamically stable after 48 hours.

Contraindications to β - blockers:
1) Bradycardia < 60/minute
2) SBP < 100mmHg
3) Pulmonary congestion with crepitations beyond the lung
bases
4) Signs of peripheral hypoperfusion
5) Second or third degree atrio-ventricular (AV) block
6) Asthma or chronic obstructive airway disease ( COAD)
7) Severe peripheral vascular disease
Table 3: Recommended dosages of β -blockers in STEMI
Type Initiation dose Target dose

Metoprolol 25mg bd 100mg bd
Atenolol 25mg od 100mg od
Propranolol 5mg tds 80mg tds
Carvedilol 3.125mg bd 25mg bd
4.3.3.4 Angiotensin Converting Enzyme Inhibitors (ACEI) and

Angiotensin Receptor Blockers (ARB)
I,A Early use of ACEI (within 24 hours) following STEMI has been shown
to improve survival 45. ACEI should be started when the blood
pressure is stable and systolic blood pressure (SBP) remains above
100mmHg.
The benefits of ACEI are greatest in patients with:

I,A • Heart failure45,46

I,A • Anterior infarcts45,47

I,A • Asymptomatic left ventricular dysfunction ( LV ejection
fraction < 40% on echocardiography)48,49
I,B In patients who cannot tolerate ACEI, the ARB, valsartan, has been
shown to have a similar survival benefit 50.
Contraindications to ACEI and ARB therapy:

1) Systolic BP < 100mmHg
2) Established contraindications e.g. bilateral renal artery
stenosis, worsening renal function.
17
Table 4: Recommended dosages of ACEI and ARB in STEMI
Type Initiation dose Target dose

Captopril 6.25mg bd –tds 25 - 50mg tds
Ramipril 2.5mg bd 10mg od
Enalapril 2.5 - 5mg od 10mg od
Lisinopril 5mg od 10mg od
Perindopril 2mg od 4mg od
Valsartan 80mg od 160mg bd
4.3.3.5 Nitrates
III,A The routine use of nitrates has not been shown to have a survival
benefit51,52.
I,C Nitrates can be considered in patients with:

• Continuing chest pain and / or ischemia
• Heart failure
• Hypertension
In the acute stage, IV nitrates are recommended because of their

rapid onset of action, ease of titration and potential for prompt
termination in the event of side effects. After the first 48 hours, oral
or topical nitrates may be continued in patients with persisting
ischemia and/or heart failure.
Contraindications to nitrate therapy:

1) Hypotension (SBP< 90mmHg)
2) RV infarction
3) History of phospho-diesterase 5 inhibitors ingestion
depending upon the half-life of the agent. (Appendix 3)
4.3.3.6 Calcium Channel Blockers
III,A There is no data to support the routine use of calcium channel

blockers post STEMI53,54.
However they may be used as adjunctive therapy in patients with
hypertension and/or on-going ischaemia despite β-blockers and
nitrates.

II-a,B In patients who cannot tolerate β-blockers, verapamil or diltiazem
may be used for secondary prevention .
55
Calcium channel blockers should be avoided in patients with LV

dysfunction, pulmonary congestion, bradycardia and AV block.
18
Table 5: Recommended doses of Nitrates in STEMI
Compound Route Dosage Time of Onset

Intravenous 5 - 200µg/min* 1 minute
Nitroglycerine,
Sublingual 0.3 - 0.6mg, can repeat up to 2 minute
Glyceryl 3 times at 5 minute intervals
trinitrate GTN Spray 0.4 - 0.8mg per metered dose,
no more than 3 sprays 2 minute
at 5 minute intervals
Transdermal patch 0.2 - 0.8mg over 12 hours on, 1 - 2 hours
then 12 hours off
Isosorbide
dinitrate Intravenous 1.25 - 5mg / hour 1 minute
Transdermal patch 2.5 - 10mg 3 – 4 minutes
Oral 10 – 20mg, 2 – 3 times daily 30-60 minutes
Isosorbide 20 - 30mg, 2 - 3 times daily, 30 - 60 minutes
Oral up to 120mg in divided doses
mononitrate
* The dose of IV nitrates should be titrated every 5 - 10 minutes until symptoms and/or
ischaemia is relieved and the desired haemodynamic response is obtained
4.3.3.7 Antithrombotics
The antithrombotics that have been studied in STEMI are:

• Unfractionated heparin
• Low molecular weight heparin
• Synthetic pentasaccharide – fondaparinux
Heparin is indicated in patients with :

I,C - post infarct angina
I,C - atrial fibrillation

I,C - mural thrombus

I,C - extensive anterior infarction

I,A - post fibrin-specific fibrinolytic agent 31,32,33

IIa,B - post non fibrin-specific fibrinolytic agent 31

A) Unfractionated heparin (UFH)
Unfractionated heparin is administered as a bolus of 60units/kg

(maximum 4000units) followed by an infusion rate of 12units/kg/hour
(maximum 1000units/hour) adjusting the dose to maintain the aPTT
(activated partial thromboplastin time) of 1.5 to 2.5 times control.
19
B) Low molecular weight heparin (LMWH)
I,A Low molecular weight heparin is given subcutaneously twice a day.

LMWH was associated with better clinical outcomes as compared to
UFH when given following fibrinolytic therapy in STEMI 56,57.
I,A This benefit was seen with both fibrin-specific58,59 and non-fibrin
specific 57,60 agents, but at an increased risk of bleeding. These studies
however, were done prior to the usage of clopidogrel in STEMI.
In patients >75 years of age and with renal impairment (serum

creatinine > 200umol/L in women and >250umol/L in men), UFH is
preferable to LMWH59.
Table 6: Recommended dosages of LMWH in STEMI
Heparin Dosage Duration of therapy

< 75 yr:
30mg IV bolus, sc 1.0mg/kg bd
Enoxaparin Until hospital discharge
≥ 75 yr:
No bolus, sc 0.75mg/kg bd
60U/kg bolus (max 4000 U)
UFH ≥ 48 hours
Infusion 12U/kg/h (max 1000 U/h)

Patients given aspirin, clopidogrel, fibrinolytic therapy and LMWH
have been found to have a higher rate of patency of the infarct related
artery without an increase in the risk of bleeding complications in one
substudy61.
We caution the use of all 4 agents (aspirin, clopidogrel, fibrinolytic

therapy and UFH/LMWH) together until the efficacy and safety of the
combination is established in future trials.
C) Synthetic pentasaccharide
I,B A trial on fondaparinux at a dose of 2.5mg/kg per day, given for 8 days,
or the duration of index hospitalization to patients who were given
fibrinolytic agents or who were not reperfused, was shown to reduce
death or reinfarction at 30 days when compared to UFH. The risk of
bleeding was not increased62.
4.3.3.8 Glycoprotein IIb/IIIa Receptor Inhibitors

I,A Glycoprotein IIb/IIIa receptor inhibitors are used mainly in the setting of
primary PCI. In primary PCI, the glycoprotein IIb/IIIa receptor inhibitor,
abciximab, has been shown to improve patient outcomes63,64.
4.3.3.9 Statins
I,A Recent data has shown that statins started within 24 hours of admission
or continued after admission leads to a reduction in major adverse
cardiac events65,66,67.
20
4.3.3.10 Aldosterone Antagonists

I,B Eplerenone, a selective aldosterone receptor antagonist, when added
to β-blockers and ACE-I, has been shown to reduce mortality and
hospitalizations when given to patients post myocardial infarction with
impaired LV function and mild HF68.

4.3.3.11 Others – Magnesium, Lignocaine, Glucose – Insulin
Potasium Infusions
III,A Magnesium52,69 and Lignocaine70 are not recommended for routine use
in patients with STEMI.
IIb,A Although earlier studies and meta-analysis seem to indicate that

Glucose-Insulin–Potassium infusions are beneficial, more recent
studies have not shown reduction in mortality or infarct size 71,72.
Recommendations:
• All patients should receive 100 - 300 mg aspirin and 300 mg

clopidogrel followed by a maintenance dose of 75-150 mg of
aspirin long term and 75 mg of clopidogrel daily for at least a
month.
• All patients should be on β blockers if there are no specific

contraindications.
• Other medications that have been shown to improve survival

if given early are ACE inhibitors (or ARB if ACE intolerant) and
statins.
21
4.4 Complications of STEMI

These are:
• arrhythmias
• left ventricular dysfunction and shock
• mechanical complications
• right ventricular infarction
• others e.g. pericarditis
4.4.1 Arrhythmias
These include:
A) Tachyarrhythmias
• Pulseless ventricular tachyarrythmias.
This includes pulseless ventricular tachycardia and ventricular
fibrillation. Defibrillate immediately. Early VF occurs within the first 48
hours and is due to electrical instability. Late VF is associated with
large infarcts and poor pump function and carries a poor prognosis
(refer to algorithm 1)
[Shockable waves refers to the presence of recognizable organized
or disorganized cardiac rhythms on continuous ECG monitoring while
non shockable waves refers to the absence of any heart rhythm on
ECG monitoring]
• Stable Ventricular Tachycardia (VT).

Ventricular tachycardia in the setting of STEMI may arise from either
ischaemia or from myocardial scar resulting from the infarct. Treatment
of ischaemia may result in the termination of the tachycardia. (refer to
algorithm 2).

• Ventricular Premature Contractions (VPC).
These are often benign and do not require treatment. Correct underlying
ischaemia, hypoxia and electrolyte disturbances.

• Accelerated Idioventricular Rhythm (AIVR).
These do not require any treatment. This is a sign suggestive of
successful reperfusion.

• Atrial fibrillation (AF).
This is more commonly seen in the elderly and is associated with large
infarcts and atrial infarcts. It denotes a poorer prognosis73 and carries
an increased risk of thromboembolism. (refer to algorithm 3)
B) Bradyarrhythmias
These are:
• Sinus bradycardia.
This does not require treatment unless associated with symptoms and/
or hypotension.
• Atrio-ventricular Block (AV Block).

First degree and second degree type 1 (Mobitz 1) do not need
treatment. Patients with second degree type 2 (Mobitz 2) and complete
AV block may not require treatment if haemodynamically stable.
22
In patients who are haemodynamically unstable, arrangement must

be made for urgent temporary pacing. Atropine may be given in the
interim.(maximum 3 mg) (refer to algorithm 4)
In patients with anterior infarcts, second degree and complete AV block

carry a worse prognosis. They may require urgent temporary pacing
(refer to algorithm 4).
• Asystole/Pulseless Electrical Activity
Asystole/ Pulseless electrical activity can be differentiated from

pulseless ventricular tachyarrythmias by the presence of shockable
waves on ECG monitoring. (refer to Algorithm 1)

4.4.2 Left Ventricular Dysfunction and Shock
4.4.2.1 Presentation:
The clinical manifestation of left ventricular dysfunction varies

from asymptomatic to cardiogenic shock. An important prognostic
indicator is LV function which can be assessed objectively using
echocardiography.
A useful clinical classification is the Killip’s Classification74,75 (table 7)
Table 7: Clinical and Haemodynamic Subsets in AMI

KILLIP CLINICAL FEATURES APPROXIMATE 30 day - MORTALITY
CLASS75 PROPORTION OF (%)74
PATIENTS WITH
AMI (%)74
I No signs of LV failure 71 7
II S3 gallop, bibasal crackles 23 20
III Acute pulmonary oedema 3.7 39
IV Cardiogenic shock 2.4 70

4.4.2.2 Differential diagnoses of LV dysfunction and shock:
Differential diagnoses are:

• Pump failure due to extensive myocardial infarction
• Mechanical complications
• Right ventricular infarction
• Hypovolemia
• Arrhythmias
• Drugs
• Aortic root dissection.
23
4.4.2.3 Investigations:
Investigations that may be helpful in making the diagnosis and in the

management includes:
• Chest radiograph
• ECG
• Echocardiography
• Arterial blood gases
• Pulmonary artery catheter
4.4.2.4 Management:
A) Heart Failure
Acute management includes the following:
• Oxygen therapy
• Diuretics
• Intravenous nitroglycerine
• Intravenous morphine
• Inotropes if hypotensive.
Refer to the Malaysian Clinical Practice Guidelines on Heart Failure

2007 on the management of Acute Cardiogenic Pulmonary Edema.
B) Cardiogenic shock
Cardiogenic shock is defined as a systolic BP of < 90 mmHg associated

with signs of tissue hypoperfusion, and central filling pressure (PCWP)
is >20mmHg or cardiac index is <1.8L/min/m2. This condition is
associated with a very high mortality rate.
Emergency PCI may be life-saving and should be considered early.

Intra-aortic balloon pump may be useful.
When cardiogenic shock is due to a mechanical defect, urgent surgical

repair is indicated. Pre-operative coronary angiography and subsequent
coronary artery bypass graft (CABG) surgery in these patients remain
an issue of debate. The decision must be individualized.
4.4.3 Mechanical complications
These include the following:
• free wall rupture

• ventricular septal rupture
• papillary muscle rupture
The diagnosis should be suspected in patients with sudden clinical

deterioration and suggested by the presence of new murmurs
or diminished heart sounds. The diagnosis can be confirmed
by echocardiography. In these patients early surgery should be
considered.
24
4.4.4 Right Ventricular Infarction (RVI)

Patients with RVI may have varying clinical presentation, from
asymptomatic to cardiogenic shock76. Haemodynamically significant
RVI complicates approximately 5-10% of all STEMI. It occurs in 30
– 50% of patients with infero-posterior STEMI and is associated with
a significantly higher mortality. RVI can also occur in patients with
extensive anterior STEMI.

Clinical Diagnosis
The presence of RVI should be sought in all patients with inferior
STEMI. The clinical triad of hypotension, clear lung fields and elevated
jugular venous pressure in the setting of inferior STEMI is suggestive
of RVI.
ST elevation in the right precordial leads (V4R) is the most specific77
finding in diagnosing RVI. However, this ECG finding may be transient,
often resolving within 8-10 hours.
Management
Treatment strategies depend on the severity of peripheral hypoperfusion
and the degree of co-existing LV dysfunction. Drugs that reduce the
preload, such as nitrates and diuretics should be avoided.
Management includes:
• Optimization of intravenous fluid (saline or colloids)
• Inotropes
Failure to respond to these measures usually indicates concomitant

LV dysfunction. These patients require more aggressive management
with afterload reducing agents such as nitroprusside and intra-aortic
balloon pump.
4.4.5 Others
4.4.5.1 Chest pain post STEMI

Chest pain post STEMI may be due to reinfarction, ischaemia or
pericarditis. Non-cardiac causes must also be considered.

A) Reinfarction
Reinfarction occurs in about 3-4% of patients who had undergone
fibrinolytic therapy and received aspirin78. Reinfarction may be
diagnosed by:
• recurrence of ischaemic type chest pain

• recurrence of ST segment elevation of at least 0.1mV in at least
contiguous leads and/or
• re-elevation of serum cardiac biomarkers especially CK
Death, severe heart failure and arrhythmias are more common in these
patients. They should be considered for rescue PCI.
B) Post-infarct angina
Early recurrent angina, especially after successful reperfusion may

occur in up to 20% of patients79. The ECG in these patients may show
25
ST segment changes or pseudo-normalisation of inverted T-waves.

These patients should be sent for early coronary angiography with a
view to revascularization.
C) Pericarditis
Pericarditis secondary to STEMI may produce pain as early as the

first day and as late as 6 weeks80. The pain classically becomes worse
on deep inspiration and may be relieved when the patient sits up and
leans forward. A pericardial rub may be detected.
Dressler’s syndrome (post MI syndrome) usually occurs 2-10 weeks

after STEMI. This is immunologically mediated81. It is treated with
aspirin 600mg 3-4 times a day. Steroids and NSAIDS are best avoided
in the first 4 weeks of STEMI 82.
4.4.5.2 LV Thrombus and Arterial Embolism

LV mural thrombus has been identified in about 20-40% of patients with
STEMI. The majority of these occur following anterior or large infarcts.
Anticoagulation therapy for a minimum of 3-6 months is advocated in
these patients83.
4.4.5.3 Deep Venous Thrombosis (DVT)

In high risk patients (prolonged bed rest, heart failure, unable to
mobilize), prophylactic anti-coagulation therapy (subcutaneous heparin
5000 units bd, LMWH – e.g. enoxaparin 40mg od) may be considered
until the patient is ambulant.
4.5 Urgent/Emergent CABG surgery:

Urgent/emergent CABG surgery should be considered in the following
situations:
• At the time of surgical repair of post-infarction ventricular septal
defect (VSD) or mitral valve regurgitation (see section 4.4.3).
• Patients with failed reperfusion whose coronary anatomy and
clinical profile are suitable.
These patients should be supported with intra-aortic balloon pump.

In general, CABG surgery in this group of patients carries a very high
in-hospital mortality rate.
26
5. RISK STRATIFICATION POST-STEMI
Risk stratification serves to prognosticate and identify appropriate

treatment strategies. Risk stratification starts from admission and is a
continuing process.
Poor prognostic indicators include:
• older persons ( > 65 years)
• female gender
• previous MI
• anterior MI
• inferior MI with RV involvement
• diabetes mellitus
• ECG changes in multiple leads
• persistent or recurrent ischaemia as manifested by post-infarction
angina or ST segment depression at rest
• hypotension
• heart failure
• atrial fibrillation and late (after 48 hours) ventricular arrhythmias
• presumably new LBBB
The above high risk patients should be considered for early coronary
angiography. All other patients should be risk stratified early. This
helps:
• to identify patients who are likely to reinfarct or develop other
complications such as heart failure.
• in the rehabilitation of patients. Low risk patients may be allowed
to return to their former activities early.
Risk stratification may be done by assessing:
• Left ventricular function
–clinical, chest X-ray, echocardiogram, radionuclide studies or
cardiac MRI
• Presence of myocardial ischaemia -
oclinical (recurrent angina)
o exercise stress testing in asymptomatic patients.
- This may be done from day 5 post-STEMI (sub-maximal stress
test with a target heart rate of 70% of maximum predicted heart
rate) up to 6 weeks post-STEMI (maximal with a target heart rate
of 90% of maximum predicted heart rate for age or symptom
limited).
- If the pre-discharge sub-maximal stress test is negative, the
patient should be subjected to a maximal or symptom limited
stress test within 6 weeks after discharge.
- For those who cannot exercise, consider dobutamine stress
echocardiogram, radionuclide perfusion studies or cardiac MRI.
• Presence of malignant ventricular arrhythmias
The presence of angina, an abnormal stress test or late ventricular
arrhythmias necessitates early coronary angiography with a view to
revascularization.
In patients with poor LV function, myocardial viability studies
(dobutamine stress echocardiogram, radionuclide perfusion studies or
cardiac magnetic resonance imaging) would help to differentiate
27
scarred from viable ischaemic myocardium. The latter patients would

benefit from revascularization.
Patients with palpitations, near faints and syncope require

comprehensive evaluation. This includes:
• serum electrolytes
• resting ECG
• 24 hour ambulatory ECG recording
• evaluation of LV function
• assessment for reversible myocardial ischaemia
• coronary angiography
In these patients, reversible causes such as electrolyte disturbances

and ischaemia should be corrected.
The following medications have been shown to reduce the incidence

of sudden death :
I,A
- β-blockers84,85
I,A
- ACEI86.
I,B
- Aldosterone antagonist, eplerenone68.
IIb,B
- Statins87,88.
The following patients should be considered for an ICD :

I,A
• Secondary prevention in patients with resuscitated sudden
I,B cardiac death 89,90
• Primary prevention in patients with LV dysfunction (EF < 30%).
The ICD should be implanted 30 days post STEMI and 3 months
post revascularisation91,92,93.
6. DURATION OF HOSPITALIZATION
The duration of hospital stay following STEMI will depend on the extent
of myocardial damage, the patient and the presence of co-morbidity.
Asymptomatic patients with uncomplicated STEMI may be discharged

after 3-5 days94 particularly if patient has been successfully
reperfused. Patients with significant left ventricular dysfunction or
other complications may require a longer hospital stay.
28
7. SECONDARY PREVENTION
Patients who survive the initial course of STEMI are at increased risk
of morbidity and mortality because of reinfarction and the development
of other complications. Thus, it is very important that efforts be made
to reduce this risk.
These measures include:
7.1 Cessation of smoking

I,C Smoking cessation reduced CHD mortality by 36% as compared
to those who continue smoking . This lifestyle change confers a
95
risk reduction which is at least as great as other pharmacological

interventions.
Trials of nicotine replacement therapy using either transdermal nicotine

patch or nicotine chewing gum have proven to greatly increase
abstention rates after cessation. Such pharmacological programmes,
as well as physician-guided counseling, are cost-effective and should
be encouraged96.

7.2 Diet
I,B Dietary intervention has been shown to reduce cardiac event rates
post STEMI97:
Recommendations include:
• Total calorie intake should be tailored to the desirable body weight

• Wherever possible, substitute saturated and trans fat with
polyunsaturated fat.
Use more high fibre food and whole grains instead of rapidly
digested carbohydrates.
• Take more fruits, nuts and vegetables.
I,B • Increased intake of omega 3 – fatty acids (1g daily) is
beneficial 98,99. Eat fish at least twice a week.
7.3 Regular Exercise

I,C Recommended exercises include brisk walking, jogging, cycling,
swimming or other aerobic activity for at least 30 to 60 minutes on most
days of the week. It should be supplemented with an increase in daily
life-style activities such as walking up stairs whenever possible100.
7.4 Control of Hypertension

I,A After STEMI, prognosis is affected by both the pre existing and
the subsequent blood pressure. The higher the pre existing blood
pressure, the higher the fatality rate101. The target blood pressure
should be < 130/80mmHg. Drugs of choice include β- blockers, ACEIs
and Valsartan52 (if ACEI intolerant).
7.5 Good Glycemic control

I,B Good control of the blood glucose is important. Target fasting blood
102
glucose should be <6.0mmol/l and HBA1C < 6.5%
29
7.6 Antiplatelet Agents
I,A • Aspirin - Aspirin should be prescribed at 75-150mg daily as a

maintenance dose unless contraindicated 9,103.
In patients who cannot tolerate aspirin, alternatives include:

I,A • Clopidogrel , 75mg daily 10,11

II-b,C • Ticlopidine , 250mg bd
I,A Dual anti-platelet therapies should be given for at least one month post
fibrinolytic therapy for secondary prevention 10,11.
Following primary PCI a longer period of dual antiplatelet therapy is
necessary particularly if drug-eluting stents are used.
7.7 β- blockers
I,A
In general, β- blockers should be continued indefinitely in all patients if
there are no contraindications 32,43.
7.8 ACE Inhibitors and ARB
I,A ACEI should be continued indefinitely in all patients if there are no

contraindications45.
I,B In ACEI intolerant patients, the ARB valsartan may be used 52.
7.9 Lipid-lowering therapy
I,A Statins should be started soon after admission and continued

indefinitely. Target LDL cholesterol should be < 2.0mmol/L 104,105,106.
I,B Recent studies indicate that lowering LDL cholesterol even further
(< 1.8mmol/L) confers greater benefits 67,107,108.
7.10 Oral Anticoagulant (warfarin)
I,C Long term therapy should be considered for patients with persistent
atrial fibrillation.
I,C Warfarin should be given for 3-6 months in patients with LV thrombus.
7.11 Others
III,A - Hormone replacement therapy is not beneficial for secondary

prevention 109,110.
III,B - Postmenopausal women who were taking hormone replacement

therapy at the time of STEMI should discontinue it.
III,A - Vitamin E and anti-oxidants have no clinical benefit 111,112.
III,C - Garlic, lecithin, Vitamin A and C are not beneficial.
30
8. SPECIAL GROUPS
8.1 STEMI in the elderly

Patients above the age of 75 years have a much higher in-hospital
as well as one year mortality113. This may be due to their atypical
and delayed presentations, co-morbidities and under utilization of
aggressive therapeutic strategies.
Atypical features include silent ischaemia, dyspnoea, syncope and

acute confusion. Specific cardiac biomarkers such as CK-MB and
troponins should be measured.
Management
I,A A) Primary PCI
This is the preferred reperfusion strategy if facilities are available 23,114.
B) Fibrinolytic
I,A There is an increased risk of intracranial haemorrhage in the elderly
with the use of fibrin specific fibrinolytic agents as reperfusion strategy.
Therefore streptokinase is the preferred agent 26,27. Despite this, the
absolute benefits of fibrinolytic therapy in this age group are almost
twice that of younger patients with substantial decrease in mortality.
C) Concomitant Therapy
These patients have similar or greater benefits with the use of aspirin,
β- blockers, ACEI and statins as younger patients.
D) Risk Stratification
This has to be individualized taking into consideration the biological
age rather than the chronological age of the patient. The presence
of on-going ischaemia, symptomatic malignant arrhythmias and
a depressed LV function are bad prognostic indicators and would
generally necessitate a more aggressive approach. Both PCI and
CABG surgery, when indicated, can be carried out in the elderly with
acceptable morbidity and mortality by experienced operators. The
risks are however higher than in younger patients.
8.2 STEMI in Diabetics

Diabetic patients have higher in-hospital mortality (about 1.5 to 2
times) than non-diabetics following an STEMI115. The prognosis is
worse in diabetic women. There is a higher frequency of atypical and
silent presentations in these patients.
Management
Diabetic patients should be treated in a similar manner as non-
diabetics.
8.3 STEMI in Women

The perception that women are “protected” against ischaemic heart
disease leads to under recognition of this condition. Atypical and
delayed presentation, late diagnosis, older age at presentation and high
prevalence of co-morbidities result in a higher mortality in women.
31
Women are thus high risk patients and should be treated aggressively.
9. CARDIAC REHABILITATION IN STEMI
All patients’ post STEMI (including those post PCI or CABG surgery)
should undergo comprehensive cardiac rehabilitation. This programme
aims at improving the long-term prognosis and optimizing the physical,
psychological and social well-being of the patient. It comprises prescribed
exercise training and education, counseling, risk factor modification and
behavioral interventions.
Cardiac rehabilitation should start in the cardiac care unit, continue to

out-patient settings and extend to community care. It is a proven effective
intervention and every effort must be made to ensure minimal dropouts so
as to maximize beneficial effects of the programme.
10. FUTURE DEVELOPMENTS
There is ongoing research in various aspects of myocardial preservation in

the acute phase of STEMI utilizing stem cells, myocytes, growth factors and
other agents.
11. CHECK LISTS FOR FOLLOW-UP VISIT
The following should be assessed at each follow-up visit:
• Delineate the presence or absence of cardiac symptoms and

determine the functional class of the patients.
• Evaluate patients’ psychosocial (anxiety & depression) status and
the social integration and support network.
• Review pre discharge risk assessment and planned workup
- Evaluation for further cardiac ischaemia
- LV function
• Re-evaluate the list of all current medications and optimize their
doses.
• Actively review the following issues with the patient and family
members
- Principles of secondary prevention
- CPR training
- A plan for appropriate recognition and response to a potential
acute cardiac event
• Treat to target.
- Blood pressure: <130/80 mmHg
- Lipids: LDLC < 2.6mmol/L
- Diabetic control: Fasting blood glucose < 6.0mmol/L
HbA1C < 6.5%
- Achieve and maintain ideal body weight and waist
circumference
32
10. SUMMARY
• CHD is an important cause of death in Malaysia.
• The diagnosis of STEMI depends on the presence of ischaemic
type chest pain and ST elevation in the resting ECG or new onset
LBBB.
• TIME LOST IS MYOCARDIUM LOST, thus early diagnosis and
treatment is important.
• Early management of STEMI involves pain relief, stabilization of
haemodynamics and assessment for reperfusion.
• The occluded infarct-related artery should be opened as soon
as possible either by primary PCI or fibrinolytic therapy. Failed
fibrinolysis necessitates rescue PCI.
• Concomitant pharmacotherapy includes aspirin, clopidogrel, β-
blockers, ACEI/ARB and statins.
• Complications of STEMI include arrhythmias, LV dysfunction and
shock.
• Urgent/emergent CABG surgery should be considered in patients
with mechanical complications or failed reperfusion.
• High-risk patients should have early coronary angiography with
view to revascularization. The others should be risk stratified
according to the presence or absence of ischaemia, arrhythmias
and LV function.
• Secondary prevention is important and includes the use of aspirin,
β- blockers, ACEI/ARB and statins.
• All patients should be encouraged to undergo cardiac
rehabilitation.
33
34
Continue page 36
35
Continue from page 35
(Reproduced with
permission from 2005
American Heart
Association Guidelines
for Cardiopulmonary
Resuscitation and
Emergency
Cardiovascular Care,
Circulation. 2005;112
: IV-58 – IV-66.)
36
37
38
39
40
41
REFERENCES:
1. Number of discharges and deaths due to circulatory system by age

group and sex. Information and Documentation System Unit. Annual Report.
Ministry of Health Malaysia 2004
2. Hasai D, Begar S, Wallentin L et al. A prospective survey of the

characteristics, treatment and outcomes of patients with acute coronary
syndromes in Europe and the Mediterranean basin. The Euro Heart Survey
of Acute Coronary syndromes ( Euro Heart Survey ACS) Eur Heart J 2002;
15 : 1190-201.
3. Fallon JT. Pathology of myocardial infarction and reperfusion. In

Fuster V, Ross R and Topol EJ. (eds). Atherosclerosis and Coronary Artery
Disease. Philadelphia. Lippincott-Raven. 1996; 791-96.
4. Jaffe AS. Biochemical detection of acute myocardial infarction. In Acute

Myocardial Infarction, second ed. (eds) Gersh, Bernard J, Rahimtoola,
Shahbudin H. Chapman and Hall 1997; 136 -163
5. Stubbs P, Collinson P, Moseky D, et al. Prognostic significance of

admission Troponin T concentration in patients with myocardial infarction.
Circulation 1996; 94 : 1291-97
6. Quinones MA, Echocardiography in acute myocardial infarction. Cardio

Clin 1984; 2 : 123-34.

7. Mollet NR, Cademartiri F, van Mieghem CAG et al. High resolution
spiral computed tomography coronary angiography in patients referred for
diagnostic conventional coronary angiogram. Circulation 2005; 112 ; 2318-
23.
8. Guidelines for clinical use of cardiac imaging. Report of the American

College of Cardiology/American Heart Association Task Force on
Assessment of Diagnostic and Therapeutic Cardiovascular Procedures
(Committee on Radionucleide Imaging), developed in collaboration with the
American College of Nuclear Cardiology. J Am Coll Cardiol 1995; 25 : 521-
47.
9. The Second International Study of Infarct Survival Collaborative Group.

(ISIS-2). Randomised trial of intravenous streptokinase, oral aspirin, both
or neither among 17,187 cases of suspected acute myocardial infarction.
Lancet 1988; 2 : 349-60.
10. Sabatine MS, Cannon CP, Gibson CM et al for the CLARITY-TIMI 28

Investigators. Addition of clopidogrel to aspirin and fibrinolytic therapy for
myocardial infarction with ST-segment elevation. N Engl J Med 2005; 352 :
1179 –89.
11. COMMIT collaborative group. Addition of clopidogrel to aspirin in

45 852 patients with acute myocardial infarction: randomised, placebo-
controlled trial. Lancet 2005; 366 : 1607–21.
42
12. Fibrinolytic Therapy Trialist’ (FTT) Collaborative Group. Indications for

fibrinolytic therapy in suspected acute myocardial infarction: collaborative
overview of early mortality and major morbidiy results of all randomized
trials of more than 1000 patients. Lancet 1994; 343 : 311-22
13. De Luca G, Suryapranata H, Ottervanger JP et al. Time delay to

treatment and mortality in primary angioplasty for acute myocardial infarction;
every minute of delay counts. J Am Coll Cardiol 2003; 42 :991-7
14. Boersma E, Mercado N, Poldermans D et al. Acute myocardial

infarction. Lancet 2003; 361 : 847-58.
15. Keeley EC, Boura JS, Grines CL. Primary angioplasty versus
intravenous thrombolytic therapy for acute myocardial infarction: a
quantitative review of 23 randomised trials. Lancet 2003; 361 : 13-20
16. Aversano T, Aversano LT, Passamani E et al for the Atlantic

Cardiovascular Patient Outcomes Research Team (C-PORT). Thrombolytic
therapy vs primary percutaneous coronary intervention for myocardial
infarction in patients presenting to hospitals without onsite cardiac surgery:
a randomized controlled trial. JAMA 2002; 287 : 1943-51
17. Bonne Foy E, Lapostolle F, Leizorovicz A et al for the Comparison of

Angioplasty and Pre hospital Thrombolysis in Acute Myocardial Infarction
study group- Primary angioplasty versus prehospital fibrinolysis in acute
myocardial infarction: a randomized study. Lancet 2002; 360 : 825-9
18. Widimsky P, Budensinsky T, Vorac D et al. Long distance transport

for primary angioplasty vs immediate thrombolysis in acute myocardial
infarction: final results of the randomized national multicentre trial: PRAGUE
2. Eur Heart J 2003; 24 : 94-104
19. Nalamothu BK, Bates ER. Percutaneous coronary intervention

versus fibrinolytic therapy in acute myocardial infarction: Is timing (almost)
everything. Am J of Cardiol 2003; 92 : 824-6
20. Andersen HR, Nielsen TT, Rasmussen K, et al for the DANAMI-2

Investigators. A comparison of coronary angioplasty with fibrinolytic therapy
in acute myocardial infarction. N Engl J Med 2003; 349 : 733-42.
21. Hochman JS, Sleeper LA, Weebb JG et al. for the Should We
Emergently revascularise Occluded Coronaries for Cardiogenic Shock. Early
revascularization in acute myocardial infarction complicated by cardiogenic
shock. N Engl J Med 1999; 341 : 625-34.
22. Wu AH, Parsons L, Every NR et al. for the Second National Registry
of Myocardial Infarction. Hospital outcomes in patients presenting with
congestive heart failure complicating acute myocardial infarction: a report
from the Second National registry of Myocardial Infarction (NRMI-2) J Am
Coll Cardiol 2002; 40 : 1389-94.
43
23. Zahn R, Schiele R, Schneider S et al. Primary angioplasty versus

intravenous thrombolysis in acute myocardial infarction: Results from the
pooled data of the maximal individual therapy in acute myocardial infarction
registry and the myocardial infarction registry. J Am Coll Cardiol 2001; 37 :
1827-35.
24. Weaver DW, Cerqueira M, Hallstrom AP et al Prehospital initiated vs

hospital initiated thrombolytic therapy. The Myocardial Infarction Triage and
Intervention Trial. JAMA 1993; 270 : 1211-6.
25. Effects of tissue plasminogen activator and a comparison of early

invasive and conservative strategies in unstable angina and non Q wave
myocardial infarction: results of the TIMI 111 B Trial. Thrombolysis in
MyocardiaI Ischemia. Circulation 1994; 89 : 1545-56.
26. The GUSTO Investigators. An international randomized trial comparing

four thrombolytic strategies for acute myocardial infarction. N Engl J Med
1993; 329 ; 673-82.
27. ISIS-3 Collobartive Group. ISIS-3: A randomized comparison of

streptokinase vs tissue plasminagen activator vs anistreplase and of aspirin
plus heparin vs aspirin alone among 41,299 cases of suspected acute
myocardial infarction. Lancet 1992; 39 : 753-70.
28. Armstrong PW, Collen D. Fibrinolysis for acute myocardial infarction:

current status and new horizons for pharmacological reperfusion, part 1.
Circulation 2001; 103 : 2862-6.
29. Elliot JM, Cross DB, Cederholm-Williams SA, White HD. Neutralizing
antibodies to streptokinase 4 yaers after intravenous thrombolytic therapy.
Am J Cardiol 1993; 71 : 640-3.
30. Tatu- Chitoiu G, Teodorescu C, Dan M et al . Efficacy and safety of a

new streptokinase regimen with enoxaparin in acute myocardial infarction. J
Thrombosis and Thrombolysis 2003; 15 : 171-9
31. The GUSTO Angiographic Investigators. The effect of tissue

plasminogen activator, streptokinase or both on coronary artery- patency,
ventricular function and survival after myocardial infarction. N Engl J Med
1993; 329 : 1615-22.
32. Collins R, Peto, Baigent C, Sleight P. Aspirin, heparin and fibrinolytic

therapy in suspected AMI. New Engl J Med 1997, 336 : 847-60
33. Mahaffey KW, Granger CB, Collins R et al. Overview of randomized

trials of intravenous heparin in patients with acute myocardial infarction
treated with thrombolytic therapy. Am J Cardiol 1996; 77: 551-6.
34. Single bolus tenecteplase compared with front loaded alteplase in

acute myocardial infarction: the ASSENT-2 double blind randomized trial.
Assessment of the Safety and Efficacy of a New Thrombolytic Investigators.
Lancet 1999; 354 : 716-22.
44
35. Shah PK, Cercek B, Lew A, et al. Angiographic validation of bedside

markers of reperfusion. J Am Coll Cardiol 1993; 21 : 51-61.
36. Gershlick AH, Stephens– Lloyd A, Hughes S et al for the REACT Trial
Investigators. Rescue Angioplasty after failed thrombolytic therapy for acute
myocardial infarction. N Engl J Med 2005; 353 : 2758-68.
37. The ASSENT 4 Investigators. Assessment of the safety and efficacy

of a new treatment strategy with percutaneous coronary intervention in
patients with ST-segment elevation acute myocardial infarction (ASSENT 4
PCI) : randomized trial. Lancet 2006; 367 : 569-78.
38. Borden WB, Faxon DP. Facilitated Percutaneous Coronary Intervention.

J Am Coll Cardiol 2006; 48 : 1120-8.
39. Collet J-P, Montalescot G, May ML, et al. Percutaneous coronary

intervention after fibrinolysis. A multiple meta-analyses approach according
to the type of strategy. J Am Coll Cardiol 2006; 48 ; 1326-35.
40. Hochman JS, Lamas GA, Buller CE et al. Coronary Intervention for
persistent occlusion after myocardial infarction. N Engl J Med 2006; 355 :
2395-407.
41. Taggart P, Sutton P, John R et al. Monophasic action potential

recordings during acute changes in ventricular loading induced by the
Valsalva manoeuvre. Br Heart J 1992; 67 : 221-9.
42. Gottlieb SS, McCarter RJ, Vogel RA et al. Effect of beta-blockade on

mortality among high risk and low risk patients after myocardial infarction. N
Engl J Med 1998; 339 : 489-97.
43. Yusuf S, Peto R, Lewis J et al. Beta blockade during and after
myocardial infarction: An overview of the randomized trials. Prog Cardiovasc
Dis 1985; 27 : 335-43.
44. The CAPRICORN Investigators. Effect of carvedilol on outcome

after myocardial infarction in patients with left ventricular dysfunction: the
CAPRICORN randomized trial. Lancet 2001; 357 : 1385-90.
45. ACE –Inhibitor MI Collaborative group. Evidence for early beneficial

effect of ACE inhibitors started within the first day in patients with AMI:
Results of systematic overview among 100000 patients. Circulation 1996;
94: 1-90.
46. The Acute Infarction Ramipril Efficacy (AIRE) Study Investigators.

Effect of ramipril on mortality and morbidity of survivors of acute myocardial
infarction with clinical evidence of heart failure. Lancet 1993: 342 : 821-8.
47. Ambrosioni E, Borghi C, Magnani B et bal. The effect of the angiotensin-

converting enzyme inhibiter zofenopril on mortality and morbidity after
anterior myocardial infarct. The SMILE Study Investigators. N Engl J Med
1995; 32: 80-5.
45
48. Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopril on mortality
and morbidity in patients with left ventricular dysfunction after myocardial
infarction. Results of the Survival and Ventricular enlargement (SAVE) N
Engl J Med 1992; 327: 369-77.
49. The Trandopril Cardiac Evaluation (TRACE) Study Group. A clinical

trial of the angiotensin converting enzyme inhibiter trandopril in patients with
left ventricular dysfunction after myocardial infarction. N Engl J Med 1995;
333 : 1670-76.
50. Pfeffer MA, McMurray JJ, Velazquez EJ et al for the Valsartan in Acute
Myocardial Infarction Trial Investigators. Valsartan, captopril or both in
myocardial infarction complicated by heart failure, left-ventricular dysfunction
or both. N Engl J Med 2003; 349 : 1893-906.
51. Gruppo Italiano per lo Studio della Supravvivenza nell’Infarto

Miocardico. GISSI-3: Effects of lisinopril and transdermal glyceryl trinitrate
singly or together on 6 - week mortality and ventricular function after
myocardial infarction. Lancet 1994; 343 : 1115-22.
52. ISIS- 4 Collaborative Group. ISIS - 4. A randomised factorial trial

assessing oral captopril , oral mononitrate and intravenous magnesium
sulphate in 58 050 patients with suspected acute myocardial infarction.
Lancet 1994; 345 : 669-85.
53. Held PH, Yusuf S. Calcium antagonists in the treatment of ischaemic

heart disease: Myocardial infarction. Coronary Artery Disease 1994; 5 : 21-
6.
54. Goldbourt U, Behar S, Reicher –Reiss H et al. Early administration of

nifedipine in suspected acute myocardial infarction. Arch Intern Med 1993;
153 : 345-53.
55. Yusuf S, Held P, Furberg C. Update of effects of calcium antagonist in

MI or angina in light of DAVIT-II and other recent studies. Am J Cardiol 1991;
67 : 1295-7
56. Antman EM, Morrow DA, McCabe CH et al. Enoxaparin versus

unfractionated heparin with fibrinolysis for ST-Elevation myocardial
Infarction. N Engl J Med 2006; 354 : 1477-88.
57. The CREATE Trial Group Investigators. Effects of reviparin, a low-

molecular-weight heparin, on mortality, reinfarction, and strokes in patients
with acute myocardial infarction presenting with ST-segment elevation.
JAMA, 2005; 293 : 427-36
58. Eikelboom JW, Quinlan DJ, Mehta SR et al. Unfractionated and low
molecular weight heparin as adjuncts to thrombolysis in aspirin treated
patients with ST Elevation Acute Myocardial Infarction: A meta – analysis of
randomized trials. Circulation 2005; 112 : 3855-67.
46
59. Wallentin L, Goldstein P, Armstrong PW et al. Efficacy and Safety of

tenecteplase in combination with low molecular weight heparin enoxaparin
or unfractionated heparin in the prehospital setting : the Assessment of the
Safety and Efficacy of a New Thrombolytic Regimen ( ASSENT) -3 PLUS
randomized trial in acute myocardial infarction. Circulation; 108 : 135-42.
60. Simoons M, Krzeminska-Pakula M, Alonso A, et al for the AMI-SK

Investigators. Improved reperfusion and clinical outcome with enoxaparin
as an adjunct to streptokinase thrombolysis in acute myocardial infarction.
The AMI-SK study. Eur Heart J 2002; 23 : 1282 -90
61. Sabatine MS, Morrow D, Montalescot G et al. Angiographic and

clinical outcomes in patients receiving low-molecular weight heparin versus
unfractionated heparin in ST-elevation myocardial infarction treated with
fibrinolytics in the CLARITY-TIMI 28 trial. Circulation 2005; 112 : 3846-54
62. The OASIS -6 Trial Group. Effects of fondaparinux on mortality

and reinfarction in patients with acute ST-segment elevation myocardial
infarction. The OASIS-6 randomized trial. JAMA 2006; 295: 1519-30
63. Montalescot G, Barragan P, Wittenberg O, et al, for the Abcimixab before

Direct Angioplasty and Stenting in Myocardial Infarction regarding Acute and
Long term follow up (ADMIRAL) Investigators. Platelet glycoprotein IIb/IIIa
inhibition with coronary stenting for acute myocardial infarction. N Engl J
Med 2001; 344 : 1895-1903
64. Stones GW, Grines CL, Cox DA et al. For the Controlled Abciximab and
Device Investigation to Lower Late Angioplasty Complications ( CADILLAC)
Investigators. Comparison of angioplasty with stenting, with or without
abciximab, in acute myocardial infarction. N Engl J Med 2002; 346 : 957-
66.
65. Schwartz GG, Olsson AG, Ezekowitz MD et al for the Myocardial

Ischemia Reduction with aggressive Cholesterol Lowering (MIRACL) Study
Investigators. Effects of atorvastatin on early recurrent ischemic events in
acute coronary syndromes: The MIRACL Study: a randomised controlled
trial. JAMA 2001; 285 : 1711-8
66. Fonarow GC, Wright S, Spencer FA at al. Effect of statin use within the
first 24 hours of admission for AMI on early morbidity and mortality. Am J
Cardiol 2005; 96 : 611-6
67. Cannon CP, Braunwald E, McCabe CH et al. Comparison of intensive

and moderate lipid lowering with statins after acute coronary syndromes. N
Engl J Med 2004; 350 : 1562-4.
68. Pitt B, Remme W, Zannad F et al. Eplerenone, a selective aldosterone

blocker, in patients with left ventricular dysfunction after myocardial infarction.
N Engl J Med 2003; 348 : 1309-21.
47
69. ISIS- 4 Collaborative Group. ISIS - 4. A randomised factorial trial

assessing oral captopril , oral mononitrate and intravenous magnesium
sulphate in 58 050 patients with suspected acute myocardial infarction.
Lancet 1994; 345 : 669-85.
70. MacMahon S, Collins R, Peto R, et al. Effects of prophylactic lidocaine

in suspected acute myocardial infarction: An overview of results from
randomized clinical trials. JAMA 1988; 260 : 1910-6.
71. The CREATE – ECLA Trial Study Group Investigators. Effect of glucose
– insulin –potassium infusion on mortality in patients with acute ST segment
elevation myocardial infarction: The CREATE –ECLA randomized controlled
trial. JAMA 2005; 293 ; 437-6.
72. Timmer JR, Svilaas T, Ottervanger JP et al. Glucose-insulin-potassium

infusion in patients with acute myocardial infraction without signs of heart
failure. J Am Coll Cardiol 2006; 47 : 1730-1.
73. Sugiura T, Iwasaka T, Ogawa A, et al. Atrial fibrillation in acute

myocardial infarction. J Am Coll Cardiol 1985; 56 : 27-9.
74. Effectiveness of intravenous thrombolytic treatment in acute myocardial

infarction. Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto
Miocardico (GISSI). Lancet 1986; 8478 : 397-402
75. Killip T 3rd, Kimball JT. Treatment of myocardial infarction in a coronary

care unit. A two year experience with 250 patients. Am J Cardiol 1967; 20:
457-64
76. Kinch JW, Ryan TJ. Right ventricular infarction. N Eng J Med 1994;
330 : 1211-7.
77. Morgera T, Alberti E, Silvestri F, et al. Right precordial ST and

QRS changes in the diagnosis of right ventricular infarction. Am Heart J
1984;108:13-18.
78. Ohman EM, Amstrong PW, Guerci AD, et al. For the GUSTO Trial
Investigators. Reinfarction after thrombolytic therapy: Experience from
GUSTO trial (abstract). Circulation 1993; 88 (suppl I)1-490.
79. Bosch X, Theroux P. Early Post infarction ischaemia: clinical,

angiographic and prognostic significence. Circulation 1987; 75 : 988-95
80. Tofler GH, Muller JE, Stone PH, Pericarditis in acute myocardial
infarction: Characterization and clinical significance. Am Heart J 1989; 117 :
86-92.
81. Khan AH: The post cardiac injury syndromes. Clin Cardiol 1992; 20 :
1594-8.
82. Reineck H, Wichter T, Weynand M. Left ventricular pseudoaneursym

in patients with Dressler’s syndrome after myocardial infarction. Heart 1998;
80 : 98
48
83. Vaitkus PT, Barnathan ES. Embolic potential, prevention and

management of mural thrombus complicating anterior myocardial infarction:
A meta - analysis. J Am Coll Cardiol 1993;22 : 1004-9.
84. Nutall SL, Toescu V, Kendall MJ . Beta blockers have a key role in
reducing morbidity and mortality after infarction. BMJ 2000; 320 : 581
85. Lopez-Sendon J, Swedberg K, ray J et al. Expert consensus document

on beta adrenergic receptor blockers. Eur Heart J 2004; 25 : 1341-62.
86. Domanski MJ, Exner DV, Borkowf CB et al. The effect of angiotensin-
converting-enzyme inhibitor on sudden cardiac death in patients following
myocardial infarction: a meta analysis of randomized clinical trails. J Am Coll
Cardiol 1999; 33 : 598-604.
87. Mitchell LB, Powell JL, Gillis AM et al. Are lipid lowering drugs also anti
arrhythmic drugs? An analysis of the Anti-arrhythmics versus implantable
defibrillators (AVID) Trial. J Am Coll Cardiol 2003; 42 : 81-7.
88. Chiu JH, Abdelhadi RH, Chung MK et al. The effect of statin therapy on
risk of ventricular arrhythmias among patients with coronary artery disease
and on implantable cardioverter defibrillators. Am J Cardiol 2005; 95 : 490-
1.
89. Moss AJ, Hall WJ, Cannom DS et al. For the Multicenter Automatic
Defibrillator Implantation Trial (MADIT) Investigators. Improved survival
with an implanted defibrillator in patients with coronary disease at high risk
for ventricular arrhythmia. N Engl J Med 1996; 335 : 1933-40.
90. The Antiarrhythmics vs Implantable Defibrillator (AVID) Investigators. A

comparison of antiarrhythmic drug therapy with implantable defibrillators in
patients resuscitated from near fatal ventricular arrhythmias. N Engl J Med
1997; 337 : 1576-83.
91. Gregoratos G, Abrams J, Epstein AE et al. ACC/AHA/NASPE 2002

guideline update for implantation of cardiac pacemaker and antiarrhythmia
devices: summary article: a report of the American College of Cardiology/
American Heart Association Task Force on Practice Guidelines (ACC/AHA/
NASPE Committee to update the1998 pacemaker guidelines) J Am Coll
Cardiol 2002; 40 : 1703-19.
92. Moss AJ, Zareba W, Hall WJ, et al, for the Multicenter Automatic
Defibrillator ImplantationTrial II Investigators. Prophylactic implantation of
a defibrillator in patients with myocardial infarction and reduced ejection
fraction. N Engl J Med 2002; 346 : 877-3.
93. Lee KL, Hafley G, Fisher JD, et al, for the Multicenter Unsustained
Tachycardia Trail Investigators. Effect of implantable defibrillators on
arrhythymic events and mortality in the multicenter unsustained tachycardia
trial. Circulation 2002; 106 : 233-8.
94. Wilkinson P, Stevenson R, Ranjayadalan et. al. Early discharge after

acute myocardial infarction : risk and benefits . Br Heart J 1995; 74 : 71-5
49
95. Critchley JA, Capewell S. Mortality risk reduction associated with

smoking cessation in patients with coronary heart disease : a systematic
review. JAMA 2003; 290 : 86- 97.
96. The Tobacco Use and Dependence Clinical Practice Guideline Panel,
staff and Consortium Representatives. A clinical practice guideline for
treating tobacco use and dependence. A US Public Health Service report.
JAMA 2000; 283 : 3244-54.
97. de Lorgeril M, Salen P, Martin JL et al. Mediterranean diet, traditional

risk factors, and the rate of cardiovascular complications after myocardial
infarction; final report of the Lyon Diet Heart Study Circulation 1999; 99 :
779-85.
98. Dietary supplementation with n-3 polyunsaturated fatty acids and

vitamin E after myocardial infarction: results of the GISSI – Prevenzione trial,
Gruppo Italiano per lo Studio della Suprovvivenza nell’ infarto miocardico.
Lancet 1999; 354 : 447-55.
99. Kris- Etherton PM, Harris WS. Aprel LJ: Fish consumption, fish oil,
omega-3-fatty acids and cardiovascular disease. Circulation 2002; 106 :
2747-57
100. SShephard RJ, Balady GJ. Exercise as cardiovascular therapy.

Circulation 1999; 99 : 963-72.
101. Haider AW, Chen L . Larson MG et al : Antecedent hypertension

confers increased risk for adverse outcomes after initial myocardial
infarction. Hypertension 1997; 30 : 1020-4
102. UK Prospective Diabetes Study Group. Intensive blood glucose control

with sulponylureas or insulin compared with conventional treatment and the
risk of complications in patients with Type 2 diabetes ( UKPDS 33). Lancet
1998; 352 : 854-65.
103. Antiplatelet Trialists’ Collaboration. In Collaborative overview of

randomized trails of anti platelet therapy. 1. Prevention of death, myocardial
infarction and stroke by prolonged antiplatelet therapy in various categories
of patients. Br Med J 1994; 308 : 81-106.
104. Heart Protection Study Group Collaborative Group. MRC/BHF Heart

Protection Study of cholesterol lowering with simvastatin in 20,536 high risk
individuals: a randomised placebo controlled trial Lancet 2002; 360 : 7-22.
105. Sacks FM, Tonkin AM, Shepherd J et al. Effect of pravastatin on

coronary disease events in subgroups defined by coronary risk factors: The
Prospective Pravastatin Pooling Project. Circulation 2000; 102 : 1893-900.
106. Niessen SE, Tuscu EM, Schoenhagen P et al, REVERSAL Investigators.

Effect of intensive compared with moderate lipid lowering therapy on
progression of coronary atherosclerosis: a randomised controlled trial.
JAMA 2004; 291 ; 1071-80.
50
107. Pedersen TR, Faergeman O, Kastelein JJ et al. Incremental decrease

in end points through aggressive lipid lowering ( IDEAL) Study Group. High
dose atorvastatin vs usual dose simvastatin for secondary prevention after
myocardial infarction: the IDEAL Study: a randomized controlled trial. JAMA
2005; 294 : 2437-45.
108. La Rosa JC, Grundy SM, Waters DD et al. Treating to New Targets
(TNT) Investigators. Intensive lipid lowering with atorvastatin in patients with
stable coronary disease. N Engl J Med 2005; 352 : 1425-35.
109. Hulley S, Grady D, Bush T, et al. Randomized trial of estrogen

plus progestin for secondary prevention of coronary heart disease in
postmenopausal women. Heart and Estrogen/Progestin Replacement Study
(HERS). JAMA 1998; 280 : 605-13.
110. Rossouw JE, Anderson GL, Prentice RL et al. WritingGroup for the
Women’s Health Initiative Investigators. Risks and benefits of estrogen plus
progestin in healthy postmenopausal women: principal results from the
Women’s Health Initiative randomized controlled trial. JAMA 2002; 288 :
321-33.
111. Lonn E, Bosch J, Yusuf S et al for the HOPE and HOPE-TOO Trial
Investigators. Heart Outcome Prevention Evaluation & Heart Outcome
Prevention Evaluation – The Ongoing Outcome Trial. Effects of long
term vitamin E supplementation on cardiovascular event and cancer : a
randomized controlled trail. JAMA 2005; 293 ; 1338-47.
112. Heart Protection Study Collaboration Group. MRC/BHF Heart

protection study of antioxidant vitamin supplementation in 20,536 high risk
individuals: a randomized placebo controlled trail. Lancet 2002; 360 ; 23-
33.
113. Solomon CG, Lee TH, Cook EF. Comparison of clinical presentation of
acute myocardial infarction in patients older than 65 years of age to younger
patients: The multicenter chest pain study experience. J Am Coll Cardiol
1989; 63 : 772-6.
114. de Boer MJ, Ottervanger JP, van’t Hof AW et al. Reperfusion therapy in
elderly patients with acute myocardial infarction : a randomized comparison
of primary angioplasty and thrombolytic therapy. J Am Coll Cardiol 2002; 39
: 1723-8.
115. Mak KH, Moliterno DJ, Granger CB, et al. Influence of diabetes mellitus
on clinical outcome in the thrombolytic era of acute myocardial infarction. J
Am Coll Cardiol 1997; 30 : 171-9.
51
ACKNOWLEDGEMENTS
The committee would like to thank the following for all their assistance:
• Technical Advisory Committee, Clinical Practice Guidelines,

Ministry of Health
• Panel of experts who reviewed the draft
• Secretariat from Sanofi-Aventis
DISCLOSURE STATEMENT
The panel members have no potential conflict of interest to disclose.
SOURCES OF FUNDING
This CPG was made possible by an unrestricted educational grant from

Sanofi-Aventis and Bristol-Myers Squibb.
52

CPG Management of Acute ST Segment Elevation Myocardial Infarction (2nd Edition)

Diunggah oleh

Informasi Dokumen

Deskripsi Asli:

Hak Cipta

Format Tersedia

Bagikan dokumen Ini

Bagikan atau Tanam Dokumen

Opsi Berbagi

Apakah menurut Anda dokumen ini bermanfaat?

Apakah konten ini tidak pantas?

Hak Cipta:

Format Tersedia

CPG Management of Acute ST Segment Elevation Myocardial Infarction (2nd Edition)

Diunggah oleh

Hak Cipta:

Format Tersedia

MOH/P/PAK/127.

CLINICAL PRACTICE GUIDELINES

MINISTRY OF HEALTH NATIONAL HEART ASSOCIATION ACADEMY OF MEDICINE

This guideline is meant to be a guide for clinical practice, based on the

Electronic version available on the following website:

This is an update to the Clinical Practice Guideline on ST Elevated

MESSAGE FROM THE DIRECTOR GENERAL OF HEALTH

In this new millennium, there has been an exponential increase of scientific

The publication of the Malaysian CPG on STEMI by the National Heart

Y.Bhg Tan Sri Datuk Dr Hj Mohd Ismail Merican

Clinical Practice Guidelines Development Expert Panel

Dr Robaayah Zambahari Senior Consultant Cardiologist

Expert Panel Members (in alphabetical order):

Dr. Azlan Hussin (Secretary) Consultant Cardiologist and

External Reviewers (in alphabetical order):

Rationale and Process of Development of this CPG

Acute Myocardial Infarction is a major health problem, with relatively high

The Clinical Practice Guidelines (CPG) in the Management of ST

This CPG has been prepared by a panel of committee members appointed

These guidelines are intended to provide awareness and education in

• early recognition of STEMI

Evidence was obtained by systematic review of current medical literature

The level of recommendation and the grading of evidence used in this

Clinical Questions Addressed

LEVELS OF EVIDENCE AND GRADES OF RECOMMENDATION

Message from the Director General of Health i

4.4 Complications of STEMI 22

Cardiovascular disease remains an important cause of death in Malaysia

Much progress has been made in the management of AMI, especially

Guidelines help in the management of patients. All the recommendations

Acute coronary syndrome is a clinical spectrum of ischemic heart disease

STEMI: Myocardial infarction due to acute total occlusion of the

2.1 Pathogenesis of STEMI

STEMI is necrosis of heart muscle due to inadequate blood supply following

2.2 Clinical Diagnosis of STEMI

A good history is vital in raising the clinical suspicion and making a

Other atypical presentations include unexplained nausea and vomiting,

2.2.3 Serum Cardiac Biomarkers

• Creatine kinase-Myocardial Band (CK-MB)

Table 2: Properties of Serum Cardiac Biomarkers

2.2.4 Other Diagnostic Modalities.

Echocardiography is a particularly useful bedside imaging technique in

2.2.5 Difficult Diagnosis

Sometimes the diagnosis of myocardial infarction is difficult. About 2-8%

• They should be given priority in the emergency department and attended

• Cardiac biomarkers especially the troponins, are helpful in ruling in or

In addition, the hospital needs to:

• educate all medical staff on the importance of early detection and

• The public and allied health care personnel should be

• STEMI is diagnosed by the clinical history of chest pain, ECG

• Atypical presentations can occur in the elderly, women and in

• If the initial ECG is non-diagnostic, it may need to be repeated

• Too early a measurement can sometimes result in a

Immediate measures to be taken in suspected cases of STEMI

3.1 For the general public:

3.2 For Patients with known CHD:

3.3 For the general practitioner / family physician:

I, C • Give sublingual GTN.

I, A • If the ECG shows ischemic changes, give 300mg of clopidogrel if

I, C • Wherever possible, set up intravenous access.

I, C • Pain relief with intravenous opiates (IV morphine 3-5mg slowly).

I, C • Avoid intramuscular injections since this could result in

I, C • Call an ambulance or ask the patient’s relative or friend to send