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

MINISTRY OF HEALTH
MALAYSIA
ACADEMY OF MEDICINE
MALAYSIA
NATIONAL HEART ASSOCIATION
MALAYSIA
CLINICAL PRACTICE GUIDELINES
MANAGEMENT OF
ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
2007 - ( 2nd Edition )
MOH/P/PAK/127.07(GU)
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 foor, 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)
i
MESSAGE FROM THE DIRECTOR GENERAL OF HEALTH
In this new millennium, there has been an exponential increase of scientifc
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
scientifc 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 beneft of our
fellow Malaysians.
Y.Bhg Tan Sri Datuk Dr Hj Mohd Ismail Merican
Director General of Health Malaysia
ii
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 Jaafar,
Negeri Sembilan
Dr Tee Lian Kim General Practitioner
Young and Newton Clinic, KL
Dr V. Paranthaman Family Medicine Specialist
Klinik Kesihatan Jelapang, Perak
iii
ii
iii
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 signifcant 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
iv
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
v
iv
v
(Adapted from the American Heart Association and the European Society of Cardiology)
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 benefcial, useful and/or
effective.
II Conditions for which there is conficting evidence and/or
divergence of opinion about the usefulness/effcacy of a
procedure/therapy.
II-a Weight of evidence/opinion is in favor of its usefulness/effcacy.
II-b Usefulness/effcacy 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
vi
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 Diffcult 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 fbrinolytic 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 -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
vii
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 -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
1
CliniCal PraCtiCe Guidelines on
ManaGeMent OF aCute st seGMent eleVatiOn
MYOCardial inFarCtiOn (steMi)
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 2000s
2
.

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 signifcant 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 benefts.
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 PathogenesisofSTEMI
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, fssuring 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 vasculitis
3
.
2
Figure1: Adapted with modifcation 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 ClinicalDiagnosisofSTEMI
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.
3
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
2.2.2Electrocardiographicchanges
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 ECGs 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.
Table1:ECGpatternsofvariousSTEMIlocations
2.2.3SerumCardiacBiomarkers
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
include
4
:-
Cardiac troponins (cTnT and cTnI)
Location Leads ECGfndings
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
4
(Reproduced with permission from Clinical Implications of the new defnition of myocardial infarction.
John K French, Harvey D White; Heart 2004;90:99106)
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 specifc 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 specifc 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 suffcient to indicate myocardial
necrosis
5
. They are useful in detecting myocardial infarction in patients
presenting with atypical histories and non diagnostic ECGs. 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 specifc for AMI with frequent false
positive elevations.
Figure 2: TimeCourseofElevationofSerumCardiacBiomarkersafterSTEMI
5
Table2:PropertiesofSerumCardiacBiomarkers
2.2.4 OtherDiagnosticModalities.
Imaging techniques such as chest radiography, echocardiography
6
, multi-
slice computed tomography (MSCT)
7
and radionuclide techniques
8
are
useful investigations in the patient presenting with acute chest pain. They
help to:
Rule out or confrm 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
diffcult diagnostic situations.
2.2.5 DiffcultDiagnosis
Sometimes the diagnosis of myocardial infarction is diffcult. 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 ECGs. Thus it is important to maintain good clinical
records that can be rapidly retrieved.
(Reproduced with permission from Clinical Implications of the new defnition of myocardial infarction.
John K French, Harvey D White; Heart 2004;90:99106)
* Hours after symptom onset.
CK, creatine kinase; LDH, lactate dehydrogenase
Protein Firstdetection* Durationofdetection Sensitivity Specifcity
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 ++ +
6
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 benefts
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.
7
3. PRE-HOSPITALMANAGEMENT
Immediate measures to be taken in suspected cases of STEMI
3.1 Forthegeneralpublic:
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 ForPatientswithknownCHD:
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 Forthegeneralpractitioner/familyphysician:
Ask patient to chew and swallow one 300mg tablet of aspirin
9
.

Give sublingual GTN.
If the ECG shows ischemic changes, give 300mg of clopidogrel if
available.
10,11
Wherever possible, set up intravenous access.
Pain relief with intravenous opiates (IV morphine 3-5mg slowly).
Avoid intramuscular injections since this could result in
intramuscular hematomas if fbrinolytic agents are subsequently
administered.
Call an ambulance or ask the patients 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 ForAlliedHealthCarePersonnel:
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.
I,A
I,A
I,C
I,C
I,C
I,C
I,C
8
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 fbrinolysis 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.
9
4. IN-HOSPITALMANAGEMENT
Early management of STEMI is directed at:
Pain relief
Establishing early reperfusion
Treatment of complications - arrhythmias
4.1 InitialRecognitionandManagement
When the patient with suspected STEMI reaches the emergency
department, evaluation and initial management should take
place promptly (FAST TRACK - RED ZONE) because the
benefts of reperfusion therapy is greater the earlier it is initiated
12
.
A quick targeted history should be taken and vital signs noted. The
diagnosis should be confrmed with an ECG, which should be done
as soon as possible, preferably within 10 minutes of the patients
arrival in the emergency department. It is important to relieve pain
and quickly assess the patients suitability for reperfusion by either
fbrinolytic therapy or primary PCI.
The following should be done immediately and concomitantly in the
emergency department (see fow chart 1, page 44):-
Assessment and stabilization of the patients haemodynamics.
Sublingual GTN if chest pain persists (unless systolic blood
pressure (SBP) < 90 mmHg).
Continuous ECG monitoring.
300mg of aspirin chewed and swallowed if not given earlier
9
.
Clopidogrel at a dose of 300mg should be given if not given
earlier
10,11.
Oxygen by nasal prongs / facemask.
Venous access established and blood taken for cardiac
biomarkers, full blood count, renal profle, glucose and lipid profle.
Preferably 2 intravenous lines should be set up.
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.
Intramuscular injections should be avoided.
Assessment for reperfusion strategy.
I,A
I,C
I,C
I,C
I,C
I,A
I,A
I,C
I,C
I,C
I,C
I,C
10
4.2 ReperfusionStrategies
Early and prompt reperfusion is crucial as TIMELOST is
equivalent to MYOCARDIUMLOST
12,13,14.
Despite overwhelming data showing that prompt reperfusion therapy
improves survival
12,13
it is still widely underutilized and delayed.
Most studies indicate that primary PCI is superior to fbrinolytic
therapy as a reperfusion strategy
15,16.
However in patients who present within 3 hours of symptom onset
and are at low risk, both treatment strategies appear to have similar
benefts
17,18.
In the majority of our hospitals, fbrinolytic 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 frst medical contact
Time delay to PCI (time from hospital arrival to balloon dilatation
door to balloon time)
Time to hospital fbrinolysis (time from hospital arrival to
administration of fbrinolytic therapy door to needle time)
Contraindications to fbrinolytic therapy
High risk patients
The best reperfusion strategy will depend upon:
A)Timefromonsetofsymptoms
Earlypresentation(within3hours)
If both treatment options are readily available, they have been
shown to be equally effective
17,18
except for the following situations
where primary PCI is the preferred strategy:
- fbrinolytic therapy is contraindicated
- in high-risk patients
- PCI time delay [(door-to-balloon time) (door-to-needle time)] is
less than 60 minutes
19
Latepresentation(3to12hours)
Primary PCI is preferred
15,16
. The door to balloon time should be
within 90 min if the patient presents at a PCI capable facility
19
.
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 fbrinolytic therapy should be given.
Verylatepresentation(>12hours)
Both primary PCI and fbrinolytic therapy are not routinely
recommended in patients who are asymptomatic and
haemodynamically stable
12.
A
A
A
A
I,A
IIa,B
I,A
III,A
11
However, reperfusion therapy would still be benefcial in patients
with persistent ischaemic symptoms, haemodynamic or electrical
instability. In this subgroup, primary PCI is the preferred strategy.
B)Contraindicationstofbrinolytictherapy
See section 4.2.1.2
C)Highriskpatients
These include patients with:
Large infarcts
Anterior infarcts
Cardiogenic shock
Elderly patients
Post revascularization (post CABG and post PCI)
Post infarct angina
Primary PCI is the preferred strategy in these patients
21,22,23
.
The goals of time to reperfusion therapy should be within:
30 minutes door to needle time
12,13
90 minutes door to balloon time
19
4.2.1FibrinolyticTherapy
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 benefcial and has been shown to be
able to abort the infarction and reduce mortality by up to 50%
12,17
.
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.
Pre-hospital fbrinolytic therapy has been shown to achieve faster
reperfusion
17,24
.
Patients presenting with a low blood pressure (SBP < 90mm Hg)
should receive inotropic support prior to fbrinolytic therapy.
4.2.1.1Indications
Fibrinolytic therapy should only be given to patients with STEMI. It
has no role and may even be detrimental in patients with NSTEMI
12,25.
4.2.1.2Contraindications
Absolutecontraindications
Risk of Intracranial haemorrhage
Any history of intracranial haemorrhage
Ischaemic stroke within 3 months
I,A
I,A
I,B
I,A
I,A
I,A
I,C
I,A
12
Known structural cerebral vascular lesion (e.g. arteriovenous
malformation)
Known intracranial neoplasm
Risk of bleeding
Active bleeding or bleeding diathesis (excluding menses)
Signifcant head trauma within 3 months
Suspected aortic dissection
Relativecontraindications
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 frst usage) to
streptokinase (if planning to use same agent)

* The blood pressure should be reduced prior to institution of fbrinolytic
therapy.
4.2.1.3ChoiceofFibrinolyticAgent
Presently the agents available in Malaysia are:
Streptokinase
This is the most widely used agent. It is not fbrin specifc and is
less effcacious than fbrin selective agents
26,27
. Despite
having a lower risk of intracranial haemorrhage, the reduction in
mortality is less than with fbrin specifc agents
26,28
.
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 frst administration
29
.
PCI or fbrin specifc 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.
I,A
I,B
13
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 hypotension
30
.
Alteplase
This agent is fbrin specifc and achieves better reperfusion at 90
min as compared to streptokinase
26,31
.
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
Secondgenerationfbrinspecifcagents:Tenecteplase,Reteplase
Tenecteplase has been recently introduced in Malaysia. These
second generation fbrin specifc agents are as effcacious 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
4.2.1.4IndicatorsofSuccessfulReperfusion
There is no sensitive bedside clinical method to reliably detect
successful reperfusion
35
. 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
fbrinolytic 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 fbrinolytic therapy or primary PCI
35
.
I,A
I,A
B
14
4.2.1.5FailedFibrinolysis
Failure of fbrinolytic 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.
The treatment of choice for these patients is rescue PCI
36
.
They should not be given a second dose of a fbrinolytic agent. This is
because there has been no difference in event free survival
demonstrated if these patients are given a repeat dose of a
fbrinolytic agent or if they are treated conservatively
36
.
4.2.2.PercutaneousCoronaryIntervention(PCI)
4.2.2.1PrimaryPCI
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 suffcient number of primary
PCI procedures.
4.2.2.2FacilitatedPCI
Current evidence indicates that strategies combining fbrinolytic
therapy is associated with higher reperfusion rates and TIMI fow.
However, it is associated with higher mortality and bleeding rates. It is
therefore not recommended
37,38
.
4.2.2.3RescuePCI
Rescue PCI may be considered in patients who have failed
fbrinolytic therapy or have recurrent chest pain and/or ischaemic
complications. Those who may beneft 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.
4.2.2.4DelayedPCI(>72hoursafterfbrinolytictherapy)
Routine angiography and PCI in asymptomatic and stable patients
post fbrinolytic therapy is controversial
39,40
.
I,B
I,A
IIa,A
15
Recommendations:
Patients presenting to the hospital need to be rapidly evaluated
for prompt reperfusion therapy.
Reperfusion therapy with either primary PCI or fbrinolytic 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 fbrinolysis is rescue PCI.
16
4.3CARDIACCAREUNITMANAGEMENT
4.3.1GeneralMeasures
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.
4.3.2Monitoring
The general condition of the patient, vital signs, pulse oximetry and
the ECG should be continuously monitored following STEMI, looking
for complications.
4.3.3ConcomitantTherapy

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

A)Aspirin
Aspirin is indicated in all patients at diagnosis and should be
continued indefnitely unless contraindicated. The initial dose of 100-
300mg should be followed by a maintenance dose of 75 - 150mg
daily
9
.
B)Clopidogrel
Clopidogrel, when given together with aspirin and fbrinolytic 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 fbrinolytic
therapy. Following PCI, a longer period of dual antiplatelet therapy
(up to 12 months) is necessary particularly when drug-eluting stents
are used.
I,C
I,A
I,A
17
4.3.3.3-blockers

Current recommendations are to use oral -blockers early in all
patients without specifc contraindications
42,43
.
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 - 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
Table3:Recommendeddosagesof-blockersinSTEMI
4.3.3.4AngiotensinConvertingEnzymeInhibitors(ACEI)and
AngiotensinReceptorBlockers(ARB)
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 benefts of ACEI are greatest in patients with:
Heart failure
45,46
Anterior infarcts
45,47
Asymptomatic left ventricular dysfunction ( LV ejection
fraction < 40% on echocardiography)
48,49
In patients who cannot tolerate ACEI, the ARB, valsartan, has been
shown to have a similar survival beneft
50
.
Contraindications to ACEI and ARB therapy:
1) Systolic BP < 100mmHg
2) Established contraindications e.g. bilateral renal artery
stenosis, worsening renal function.
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
I,A
I,B
I,A
I,A
I,A
I,A
I,B
18
Table4:RecommendeddosagesofACEIandARBinSTEMI
4.3.3.5Nitrates
The routine use of nitrates has not been shown to have a survival
beneft
51,52
.
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 frst 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)
4.3.3.6CalciumChannelBlockers
There is no data to support the routine use of calcium channel
blockers post STEMI
53,54
.
However they may be used as adjunctive therapy in patients with
hypertension and/or on-going ischaemia despite -blockers and
nitrates.
In patients who cannot tolerate -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.
II-a,B
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
III,A
I,C
III,A
19
Table5:RecommendeddosesofNitratesinSTEMI
4.3.3.7Antithrombotics
The antithrombotics that have been studied in STEMI are:
Unfractionated heparin
Low molecular weight heparin
Synthetic pentasaccharide fondaparinux

Heparin is indicated in patients with :
- post infarct angina
- atrial fbrillation

- mural thrombus

- extensive anterior infarction

- post fbrin-specifc fbrinolytic agent
31,32,33
- post non fbrin-specifc fbrinolytic agent
31

A)Unfractionatedheparin(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.
Compound Route Dosage Time of Onset
Intravenous 5 - 200g/min* 1 minute
Sublingual 0.3 - 0.6mg, can repeat up to
3 times at 5 minute intervals
2 minute
GTN Spray 0.4 - 0.8mg per metered dose,
no more than 3 sprays
at 5 minute intervals
2 minute
Transdermal patch 0.2 - 0.8mg over 12 hours on,
then 12 hours off
1 - 2 hours
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

Oral
20 - 30mg, 2 - 3 times daily,
up to 120mg in divided doses
30 - 60 minutes
I,C
I,C
I,C
I,C
I,A
IIa,B
* 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
Nitroglycerine,
Glyceryl
trinitrate
Isosorbide
mononitrate
Isosorbide
dinitrate
20
B)Lowmolecularweightheparin(LMWH)
Low molecular weight heparin is given subcutaneously twice a day.
LMWH was associated with better clinical outcomes as compared to
UFH when given following fbrinolytic therapy in STEMI
56,57
.
This beneft was seen with both fbrin-specifc
58,59
and non-fbrin
specifc
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 LMWH
59
.
Table 6: RecommendeddosagesofLMWHinSTEMI

Patients given aspirin, clopidogrel, fbrinolytic 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
substudy
61
.
We caution the use of all 4 agents (aspirin, clopidogrel, fbrinolytic
therapy and UFH/LMWH) together until the effcacy and safety of the
combination is established in future trials.
C)Syntheticpentasaccharide
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
fbrinolytic 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 increased
62
.
4.3.3.8GlycoproteinIIb/IIIaReceptorInhibitors
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 outcomes
63,64
.
4.3.3.9Statins
Recent data has shown that statins started within 24 hours of admission
or continued after admission leads to a reduction in major adverse
cardiac events
65,66,67
.
Heparin Dosage Duration of therapy

Enoxaparin
< 75 yr:
30mg IV bolus, sc 1.0mg/kg bd
Until hospital discharge
75 yr:
No bolus, sc 0.75mg/kg bd

UFH
60U/kg bolus (max 4000 U)
48 hours
Infusion 12U/kg/h (max 1000 U/h)
I,A
I,A
I,B
I,A
I,A
21
4.3.3.10AldosteroneAntagonists
Eplerenone, a selective aldosterone receptor antagonist, when added

to -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 HF
68
.

4.3.3.11 Others Magnesium, Lignocaine, Glucose Insulin
PotasiumInfusions
Magnesium
52,69
and Lignocaine
70
are not recommended for routine use
in patients with STEMI.
Although earlier studies and meta-analysis seem to indicate that
Glucose-InsulinPotassium infusions are benefcial, 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 blockers if there are no specifc
contraindications.
Other medications that have been shown to improve survival
if given early are ACE inhibitors (or ARB if ACE intolerant) and
statins.
I,B
III,A
IIb,A
22
4.4ComplicationsofSTEMI
These are:
arrhythmias
left ventricular dysfunction and shock
mechanical complications
right ventricular infarction
others e.g. pericarditis
4.4.1Arrhythmias
These include:
A)Tachyarrhythmias
Pulselessventriculartachyarrythmias.
This includes pulseless ventricular tachycardia and ventricular
fbrillation. Defbrillate immediately. Early VF occurs within the frst 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]
StableVentricularTachycardia(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).

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

AcceleratedIdioventricularRhythm(AIVR).
These do not require any treatment. This is a sign suggestive of
successful reperfusion.

Atrialfbrillation(AF).
This is more commonly seen in the elderly and is associated with large
infarcts and atrial infarcts. It denotes a poorer prognosis
73
and carries
an increased risk of thromboembolism. (refer to algorithm 3)
B)Bradyarrhythmias
These are:
Sinusbradycardia.
This does not require treatment unless associated with symptoms and/
or hypotension.
Atrio-ventricularBlock(AVBlock).
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.
23
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/PulselessElectricalActivity
Asystole/ Pulseless electrical activity can be differentiated from
pulseless ventricular tachyarrythmias by the presence of shockable
waves on ECG monitoring. (refer to Algorithm 1)
4.4.2LeftVentricularDysfunctionandShock
4.4.2.1Presentation:
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 classifcation is the Killips Classifcation
74,75
(table 7)
Table7:ClinicalandHaemodynamicSubsetsinAMI
4.4.2.2DifferentialdiagnosesofLVdysfunctionandshock:
Differential diagnoses are:
Pump failure due to extensive myocardial infarction
Mechanical complications
Right ventricular infarction
Hypovolemia
Arrhythmias
Drugs
Aortic root dissection.
APPROXIMATE
PROPORTIONOF
PATIENTSWITH
AMI(%)
74
71
23
3.7
2.4
CLINICALFEATURES
No signs of LV failure
S3 gallop, bibasal crackles
Acute pulmonary oedema
Cardiogenic shock
KILLIP
CLASS
75
I
II
III
IV
30day-MORTALITY
(%)
74
7
20
39
70
24
4.4.2.3Investigations:
Investigations that may be helpful in making the diagnosis and in the
management includes:
Chest radiograph
ECG
Echocardiography
Arterial blood gases
Pulmonary artery catheter
4.4.2.4Management:
A)HeartFailure
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)Cardiogenicshock
Cardiogenic shock is defned as a systolic BP of < 90 mmHg associated
with signs of tissue hypoperfusion, and central flling pressure (PCWP)
is >20mmHg or cardiac index is <1.8L/min/m
2
. 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.
4.4.3Mechanicalcomplications
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 confrmed
by echocardiography. In these patients early surgery should be
considered.
25
4.4.4RightVentricularInfarction(RVI)
Patients with RVI may have varying clinical presentation, from
asymptomatic to cardiogenic shock
76
. Haemodynamically signifcant
RVI complicates approximately 5-10% of all STEMI. It occurs in 30
50% of patients with infero-posterior STEMI and is associated with
a signifcantly higher mortality. RVI can also occur in patients with
extensive anterior STEMI.
ClinicalDiagnosis
The presence of RVI should be sought in all patients with inferior
STEMI. The clinical triad of hypotension, clear lung felds 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 specifc
77

fnding in diagnosing RVI. However, this ECG fnding 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 fuid (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.
4.4.5Others
4.4.5.1ChestpainpostSTEMI
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
fbrinolytic therapy and received aspirin
78
. 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-infarctangina
Early recurrent angina, especially after successful reperfusion may
occur in up to 20% of patients
79
. The ECG in these patients may show
26
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
frst day and as late as 6 weeks
80
. 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.
Dresslers syndrome (post MI syndrome) usually occurs 2-10 weeks
after STEMI. This is immunologically mediated
81
. It is treated with
aspirin 600mg 3-4 times a day. Steroids and NSAIDS are best avoided
in the frst 4 weeks of STEMI
82
.
4.4.5.2LVThrombusandArterialEmbolism
LV mural thrombus has been identifed 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 patients
83
.
4.4.5.3DeepVenousThrombosis(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.
4.5Urgent/EmergentCABGsurgery:
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 profle 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.
27
5.RISKSTRATIFICATIONPOST-STEMI
Risk stratifcation serves to prognosticate and identify appropriate
treatment strategies. Risk stratifcation 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 fbrillation 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 stratifed 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 stratifcation 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
28
scarred from viable ischaemic myocardium. The latter patients would
beneft 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 :
- -blockers
84,85
- ACEI
86
.
- Aldosterone antagonist, eplerenone
68
.
- Statins
87,88
.

The following patients should be considered for an ICD :
Secondary prevention in patients with resuscitated sudden
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 revascularisation
91,92,93
.
6. DURATIONOFHOSPITALIZATION
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 days
94
particularly if patient has been successfully
reperfused. Patients with signifcant left ventricular dysfunction or
other complications may require a longer hospital stay.
I,A
I,A
I,B
IIb,B
I,A
I,B
29
7. SECONDARYPREVENTION
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:
7.1Cessationofsmoking
Smoking cessation reduced CHD mortality by 36% as compared
to those who continue smoking
95
. This lifestyle change confers a
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 encouraged
96
.

7.2Diet
Dietary intervention has been shown to reduce cardiac event rates
post STEMI
97
:
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 fbre food and whole grains instead of rapidly
digested carbohydrates.
Take more fruits, nuts and vegetables.
Increased intake of omega 3 fatty acids (1g daily) is
benefcial
98,99
. Eat fsh at least twice a week.
7.3RegularExercise
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 possible
100
.
7.4ControlofHypertension
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 rate
101
. The target blood pressure
should be < 130/80mmHg. Drugs of choice include - blockers, ACEIs
and Valsartan
52
(if ACEI intolerant).
7.5GoodGlycemiccontrol
Good control of the blood glucose is important
102
. Target fasting blood
glucose should be <6.0mmol/l and HBA1C < 6.5%
I,C
I,B
I,B
I,C
I,A
I,B
30
7.6 AntiplateletAgents
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:
Clopidogrel , 75mg daily
10,11
Ticlopidine , 250mg bd

Dual anti-platelet therapies should be given for at least one month post
fbrinolytic 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 -blockers
In general, - blockers should be continued indefnitely in all patients if
there are no contraindications
32,43
.
7.8 ACEInhibitorsandARB
ACEI should be continued indefnitely in all patients if there are no
contraindications
45
.
In ACEI intolerant patients, the ARB valsartan may be used
52
.
7.9Lipid-loweringtherapy
Statins should be started soon after admission and continued
indefnitely. Target LDL cholesterol should be < 2.0mmol/L
104,105,106
.
Recent studies indicate that lowering LDL cholesterol even further
(< 1.8mmol/L) confers greater benefts
67,107,108
.
7.10OralAnticoagulant(warfarin)
Long term therapy should be considered for patients with persistent
atrial fbrillation.
Warfarin should be given for 3-6 months in patients with LV thrombus.
7.11Others
- Hormone replacement therapy is not benefcial for secondary
prevention
109,110
.
- Postmenopausal women who were taking hormone replacement
therapy at the time of STEMI should discontinue it.
- Vitamin E and anti-oxidants have no clinical beneft
111,112
.
- Garlic, lecithin, Vitamin A and C are not benefcial.
I,A
I,A
II-b,C
I,A
I,A
I,A
I,B
I,A
I,B
I,C
I,C
III,A
III,B
III,A
III,C
31
8. SPECIALGROUPS
8.1 STEMIintheelderly
Patients above the age of 75 years have a much higher in-hospital
as well as one year mortality
113
. 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. Specifc cardiac biomarkers such as CK-MB and
troponins should be measured.

Management
A)PrimaryPCI
This is the preferred reperfusion strategy if facilities are available
23,114
.
B)Fibrinolytic
There is an increased risk of intracranial haemorrhage in the elderly
with the use of fbrin specifc fbrinolytic agents as reperfusion strategy.
Therefore streptokinase is the preferred agent
26,27
. Despite this, the
absolute benefts of fbrinolytic therapy in this age group are almost
twice that of younger patients with substantial decrease in mortality.
C)ConcomitantTherapy
These patients have similar or greater benefts with the use of aspirin,
- blockers, ACEI and statins as younger patients.
D)RiskStratifcation
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 STEMIinDiabetics
Diabetic patients have higher in-hospital mortality (about 1.5 to 2
times) than non-diabetics following an STEMI
115
. 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 STEMIinWomen
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.

I,A
I,A
32
Women are thus high risk patients and should be treated aggressively.
9.CARDIACREHABILITATIONINSTEMI
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 modifcation 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 benefcial effects of the programme.
10.FUTUREDEVELOPMENTS
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.CHECKLISTSFORFOLLOW-UPVISIT

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
33
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 fbrinolytic therapy. Failed
fbrinolysis necessitates rescue PCI.
Concomitant pharmacotherapy includes aspirin, clopidogrel, -
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 stratifed
according to the presence or absence of ischaemia, arrhythmias
and LV function.
Secondary prevention is important and includes the use of aspirin,
- blockers, ACEI/ARB and statins.
All patients should be encouraged to undergo cardiac
rehabilitation.
34
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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 signifcance 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 fbrinolytic 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 : 160721.
43
12. Fibrinolytic Therapy Trialist (FTT) Collaborative Group. Indications for
fbrinolytic 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 fbrinolysis 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: fnal 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 fbrinolytic 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 fbrinolytic 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.
44
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 . Effcacy 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 fbrinolytic
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 Effcacy of a New Thrombolytic Investigators.
Lancet 1999; 354 : 716-22.
45
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 effcacy
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 fbrinolysis. 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 benefcial
effect of ACE inhibitors started within the frst day in patients with AMI:
Results of systematic overview among 100000 patients. Circulation 1996;
94: 1-90.
46. The Acute Infarction Ramipril Effcacy (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.
46
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 nellInfarto
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 fbrinolysis 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.
47
59. Wallentin L, Goldstein P, Armstrong PW et al. Effcacy 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 Effcacy 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
fbrinolytics 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
frst 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.
48
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 fbrillation 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 nellInfarto
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 signifcence. Circulation 1987; 75 : 988-95
80. Tofer GH, Muller JE, Stone PH, Pericarditis in acute myocardial
infarction: Characterization and clinical signifcance. 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 Dresslers syndrome after myocardial infarction. Heart 1998;
80 : 98
49
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
defbrillators (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 defbrillators. Am J Cardiol 2005; 95 : 490-
1.
89. Moss AJ, Hall WJ, Cannom DS et al. For the Multicenter Automatic
Defbrillator Implantation Trial (MADIT) Investigators. Improved survival
with an implanted defbrillator in patients with coronary disease at high risk
for ventricular arrhythmia. N Engl J Med 1996; 335 : 1933-40.
90. The Antiarrhythmics vs Implantable Defbrillator (AVID) Investigators. A
comparison of antiarrhythmic drug therapy with implantable defbrillators 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
Defbrillator ImplantationTrial II Investigators. Prophylactic implantation of
a defbrillator in patients with myocardial infarction and reduced ejection
fraction. N Engl J Med 2002; 346 : 877-3.
93. Lee KL, Hafey G, Fisher JD, et al, for the Multicenter Unsustained
Tachycardia Trail Investigators. Effect of implantable defbrillators 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 benefts . Br Heart J 1995; 74 : 71-5
50
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; fnal 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, fsh 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 defned 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.
51
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
Womens Health Initiative Investigators. Risks and benefts of estrogen plus
progestin in healthy postmenopausal women: principal results from the
Womens 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, vant 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. Infuence of diabetes mellitus
on clinical outcome in the thrombolytic era of acute myocardial infarction. J
Am Coll Cardiol 1997; 30 : 171-9.
52
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 Sanof-Aventis
DISCLOSURESTATEMENT
The panel members have no potential confict of interest to disclose.
SOURCESOFFUNDING
This CPG was made possible by an unrestricted educational grant from
Sanof-Aventis and Bristol-Myers Squibb.

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Eplerenone, a selective aldosterone receptor antagonist, when added

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