1. No category

MOH/P/PAK/127.07(GU)
CLINICAL PRACTICE GUIDELINES
MANAGEMENT OF
ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
2007 - ( 2nd edition )
MINISTRY OF HEALTH
MALAYSIA
NATIONAL HEART ASSOCIATION
MALAYSIA
ACADEMY OF MEDICINE
MALAYSIA
Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
This guideline is meant to be a guide for clinical practice, based on the
best available evidence at the time of development. Adherence to this
guideline may not necessarily guarantee the best outcome in every case.
Every health care provider is responsible for the management of his/her
unique patient based on the clinical picture presented by the patient and
the management options available locally.
This guideline was issued in 2007 and will be reviewed in 2010 or sooner if
new evidence becomes available
CPG Secretariat
c/o Health Technology Assessment Unit
Medical Development Division
Ministry of Health Malaysia
4th floor, Block E1, Parcel E
62590, Putrajaya.
Electronic version available on the following website:
http:// www.moh.gov.my
http://www.acadmed.org.my
This is an update to the Clinical Practice Guideline on ST Elevated
MI (published 2001). This CPG supersedes the previous CPG on ST
Elevated MI (2001)
Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
MESSAGE FROM THE DIRECTOR GENERAL OF HEALTH
In this new millennium, there has been an exponential increase of scientific
knowledge and publications. Indeed, one of the greatest challenges of
modern day medical practice is to keep pace with this information and
applying them into routine clinical practice.
The publication of the Malaysian CPG on STEMI by the National Heart
Association of Malaysia, Academy of Medicine and Ministry of Health
Malaysia is therefore very timely. Apart from the updates in the clinical
scientific knowledge, adaptations have been made for the local setting.
With this CPG, patients presenting to any of the health care institutions in
the country with STEMI will be assured of the latest standards of clinical
practice. However, for any CPG to be a success, it has to be utilized
optimally and updated from time to time.
I would like to commend to the expert panel for the time and effort taken
by them in updating this CPG and for health care practitioners to translate
knowledge in this CPG into routine clinical practice, for the benefit of our
fellow Malaysians.
Y.Bhg Tan Sri Datuk Dr Hj Mohd Ismail Merican
Director General of Health Malaysia
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Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
Clinical Practice Guidelines Development Expert Panel
Chairperson:
Dr Robaayah Zambahari
Institute Jantung Negara, KL
Senior Consultant Cardiologist
Expert Panel Members (in alphabetical order):
Dr. Azlan Hussin (Secretary)
Consultant Cardiologist and
Electrophysiologist
Institute Jantung Negara,KL
Dr Aris Chandran
Consultant Physician
Ipoh General Hospital,Perak
Dr. Choo Gim Hooi
Consultant Cardiologist
Selangor Medical Centre, Selangor
Dr. Jeyamalar Rajadurai
Consultant Cardiologist
Subang Jaya Medical Centre, Selangor
Dr Khoo Kah Lin
Consultant Cardiologist
Pantai Medical Centre, KL
Dr Omar Ismail
Consultant Cardiologist
Penang General Hospital, Penang
Dr Rosli Mohd Ali
Consultant Cardiologist
Institute Jantung Negara, KL
Dr Sim Kui Hian
Consultant Cardiologist
Sarawak General Hospital, Sarawak
Dr Wan Azman Wan Ahmad
Consultant Cardiologist
University Malaya Medical Centre, KL
Dr Zurkarnai Yusof
Consultant Cardiologist
Hospital Universiti Sains Malaysia,
Kelantan
External Reviewers (in alphabetical order):
Dr Chan Hien Chuan
Consultant Emergency Physician
Sarawak General Hospital, Sarawak
Dr K. Sree Raman
Senior Consultant Physician
Hospital Tunku Jaa’far,
Negeri Sembilan
Dr Tee Lian Kim
General Practitioner
Young and Newton Clinic, KL
Dr V. Paranthaman
Family Medicine Specialist
Klinik Kesihatan Jelapang, Perak
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Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
Rationale and Process of Development of this CPG
Rationale
Acute Myocardial Infarction is a major health problem, with relatively high
morbidity and mortality. Although mortality has been reduced, it is still
substantial. In the management of established acute myocardial infarction,
time is the essence.
The Clinical Practice Guidelines (CPG) in the Management of ST
Elevated Myocardial Infarction (STEMI) was developed to provide a
clear and concise approach to all clinicians on the current concepts in
the management of acute MI patients. In Malaysia, a significant number
of acute MI patients are managed by non-cardiologists. We feel that it is
important to summarise and adapt relevant clinical trial data and current
treatment strategies to our local practice.
The 1st CPG on STEMI was published in 2001. Since then, there have
been many new developments in the management of STEMI. Thus an
update on the latest and current guidelines in the 1st revision on the CPG
in STEMI would be most appropriate.
This CPG has been prepared by a panel of committee members appointed
by the National Heart Association of Malaysia (NHAM), Academy of
Medicine (AOM) and Ministry of Health (MOH). The committee members
comprise of cardiologists and general physicians from the government,
private sector and the Universities.
Objectives
These guidelines are intended to provide awareness and education in
• early recognition of STEMI
• evidence-based practice for the management of STEMI
• secondary prevention following STEMI
with the intention of reducing the morbidity and mortality associated with
STEMI
Process
Evidence was obtained by systematic review of current medical literature
on STEMI using search engines available online. The other international
guidelines on STEMI were also taken into consideration. After many
in-depth discussions, the draft was completed by the members of the
Expert Panel and submitted to key health personnel in major hospitals of
the Ministry of Health, Malaysia, universities and private sector for review
and approval.
The level of recommendation and the grading of evidence used in this
CPG was adapted from the American Heart Association and the European
Society of Cardiology. The evidence supporting the recommendation was
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Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
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
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Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
LEVELS OF EVIDENCE AND GRADES OF RECOMMENDATION
LEVELS OF EVIDENCE
I
Conditions for which there is evidence and/or general agreement
that a given procedure/therapy is beneficial, useful and/or
effective.
II
Conditions for which there is conflicting evidence and/or
divergence of opinion about the usefulness/efficacy of a
procedure/therapy.
II-a
Weight of evidence/opinion is in favor of its usefulness/efficacy.
II-b
Usefulness/efficacy is less well established by evidence/opinion
III
Conditions for which there is evidence and/or general agreement
that a procedure/therapy is not useful/effective and in some
cases may be harmful.
GRADES OF RECOMMENDATION
A
Data derived from multiple randomized clinical trails or meta
analyses
B
Data derived from a single randomized clinical trial or large
non randomized studies
C
Only consensus of opinions of experts, case studies or standard
of care
(Adapted from the American Heart Association and the European Society of Cardiology)
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Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
TABLE OF CONTENTS
Message from the Director General of Health
Members of the Expert Panel
Rationale and Process of Development of this CPG
Table of Contents
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1. INTRODUCTION
2. TERMINOLOGY
2.1 Pathogenesis of STEMI
2.2 Clinical Diagnosis of STEMI
2.2.1 History
2.2.2 Electrocardiographic changes
2.2.3 Serum Cardiac Biomarkers
2.2.4 Other Diagnostic Modalitites
2.2.5 Difficult Diagnostics
3. PRE-HOSPITAL MANAGEMENT
3.1 For the general public
3.2 For Patients with known CHD
3.3 For the general practitioner/ family physician
3.4 For Allied Health Care Personnel
4. IN-HOSPITAL MANAGEMENT
4.1 Initial Recognition and Management
4.2 Reperfusion Strategies
4.2.1 Fibrinolytic Therapy
4.2.1.1 Indications
4.2.1.2 Contraindications
4.2.1.3 Choice of Fibrinolytic Agent
4.2.1.4 Indicators of Successful Reperfusion
4.2.1.5 Failed Fibrinolysis
4.2.2 Percutaneous Coronary Intervention (PCI)
4.2.2.1 Primary PCI
4.2.2.2 Facilitated PCI
4.2.2.3 Rescue PCI
4.2.2.4 Delayed PCI (>72 hours after fibrinolytic therapy)
4.3 Cardiac Care Unit Management
4.3.1 General Measures
4.3.2 Monitoring
4.3.3 Concomitant Therapy
4.3.3.1 Oxygen
4.3.3.2 Antiplatelet Agents
4.3.3.3 β-Blockers
4.3.3.4 Angiotensin Converting Enzyme Inhibitors (ACEI) and
Angiotensin Receptor Blockeres (ARB)
4.3.3.5 Nitrates
4.3.3.6 Calcium Channel Blockers
4.3.3.7 Antithrombotics
4.3.3.8 Glycoprotein IIb/IIIa Receptor Inhibitors
4.3.3.9 Statins
4.3.3.10 Aldosterone Antagonists
4.3.3.11 Others – Magnesium, Lignocaine, Glucose-Insulin-Potassium Infusions
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Clinical Practice Guidelines on
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MYOCARDIAL INFARCTION (STEMI)
4.4 Complications of STEMI
4.4.1 Arrhythmias
4.4.2 Left Ventricular Dysfunction and Shock
4.4.2.1 Presentation
4.4.2.2 Differential diagnoses of LV dysfunction and shock
4.4.2.3 Investigations
4.4.2.4 Management
4.4.3 Mechanical complications
4.4.4 Right Ventricular Infarction (RVI)
4.4.5 Others
4.4.5.1 Chest pain post STEMI
4.4.5.2 LV Thrombus and Arterial Embolism
4.4.5.3 Deep Venous Thrombosis (DVT)
4.5 Urgent/ Emergent CABG surgery
5. RISK STRATIFICATION POST-STEMI
6. DURATION OF HOSPITALIZATION
7. SECONDARY PREVENTION
7.1 Cessation of Smoking
7.2 Diet
7.3 Regular Exercise
7.4 Control of Hypertension
7.5 Good Glycemic control
7.6 Antiplatelet Agents
7.7 β-Blockers
7.8 ACE Inhibitors and ARB
7.9 Lipid-lowering therapy
7.10 Oral Anticoagulant (warfarin)
7.11 Others
8. SPECIAL GROUPS
8.1 STEMI in elderly
8.2 STEMI in diabetics
8.3 STEMI in women
9. CARDIAC REHABILITATION IN STEMI
10. FUTURE DEVELOPMENTS
11. CHECK LISTS FOR FOLLOW-UP VISIT
12. SUMMARY
Flow Chart 1: Management of Patients Presenting with STEMI
Algorithm 1: Pulseless Arrhythmias
Algorithm 2: Stable Ventricular Tachycardia
Algorithm 3: Atrial Fibrillation
Algorithm 4: Bradyarrythmias
Appendix 1: Grades of recommendation and level of evidence for
acute therapy of STEMI
Appendix 2: Grade of recommendation and level of evidence for
secondary prevention post STEMI
Appendix 3: Pharmacokinetics of Phosphodiesterase 5 inhibitors
References
Acknowledgments
Disclosure Statement
Sources of funding
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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 20002005. Following an acute myocardial infarction (AMI) the mortality rate was
about 20% in 2004.1 This high rate could have been due to late
presentation and diagnosis, leading to delayed treatment. Occasionally the
diagnosis could have been missed. In developed countries the mortality
rate following an AMI had decreased to less than 9% by the early 2000’s2.
Much progress has been made in the management of AMI, especially
in the last two decades with the discovery that early reperfusion therapy
results in myocardial salvage and a significant reduction in morbidity and
mortality. The majority of deaths occur soon after the onset of symptoms,
the “pre-hospital phase”. To reduce these deaths, the public needs to be
educated of the symptoms of an infarct and on the need to seek
medical attention immediately. Healthcare personnel should be sensitized
and trained to deal with these patients urgently and appropriately.
Emergency Departments in hospitals need to develop critical pathways
and management strategies to maximize treatment benefits.
Guidelines help in the management of patients. All the recommendations
stated in this guideline may not be available to all eligible patients. Patient
care should be individualized and sound clinical judgement plays an
important role in decision making.
2. TERMINOLOGY Acute coronary syndrome is a clinical spectrum of ischemic heart disease
ranging from unstable angina, non-ST-elevation myocardial infarction
(NSTEMI) to ST-elevation myocardial infarction (STEMI) depending upon
the degree and acuteness of coronary occlusion.(see Figure 1)
STEMI: Myocardial infarction due to acute total occlusion of the
coronary artery
NSTEMI: Myocardial infarction due to acute sub-total occlusion of the
coronary artery
2.1 Pathogenesis of STEMI
STEMI is necrosis of heart muscle due to inadequate blood supply following
an acute total coronary occlusion. This occlusion is usually due to
atherosclerotic plaque rupture, fissuring or ulceration with superimposed
thrombosis and coronary vasospasm. Rarely, it may result from nonatherosclerotic arterial disease such as coronary vasospasm alone,
coronary embolism or vasculitis3.
Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
Figure 1: Adapted with modification from Antman EM, Anbe DT, Armstrong PW et al. “ACC/AHA
Guidelines for the management of patients with ST Elevation Myocardial Infarction” at www.acc.org
2.2
Clinical Diagnosis of STEMI
It is diagnosed by:
i. Clinical history of ischaemic type chest pain
ii. ECG changes – The following are integral to the diagnosis of
STEMI:
New onset ST-segment elevation of:
- ≥ 0.1 mV in 2 contiguous limb leads, or V4 to V6 and/or
- ≥ 0.2 mV in 2 contiguous precordial leads V1 to V3
Presumed new left-bundle branch block
iii. Evidence of myocardial injury or necrosis as indicated by
elevated serum cardiac biomarkers
2.2.1 History
A good history is vital in raising the clinical suspicion and making a
diagnosis of STEMI. Chest pain of STEMI is typically retrosternal, severe,
crushing, squeezing or pressing in nature, lasting more than 30 minutes,
associated with profuse sweating, nausea, vomiting and shortness of
breath. It is sometimes described as chest tightness only. The pain may
radiate to the jaw or down the left upper limb. It may occur at rest or with
activity. Occasionally the pain may be burning in nature and of lesser
severity. It may be in the epigastric region and be misinterpreted as
indigestion or heart burn. Rarely may it be localized to the back in the
interscapular region only resulting in a misdiagnosis.
Other atypical presentations include unexplained nausea and vomiting,
weakness, dizziness, lightheadedness and syncope, which may occur in
the presence or absence of chest pain.
Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
Diabetics, the elderly and females may not present with typical chest
pains. Common presenting symptoms in these patients are dyspnoea and
atypical chest pains.
Other important points to note in the history are the presence of:
- previous history of ischemic heart disease, percutaneous coronary
intervention (PCI) or coronary artery bypass surgery (CABG)
- risk factors for atherosclerosis
- symptoms suggestive of previous transient ischemic attack or other
forms of cerebrovascular disease
- symptoms suggestive of peripheral vascular disease
2.2.2 Electrocardiographic changes
The diagnosis of STEMI depends upon the presence of characteristic ECG
changes. These evolving ECG changes are hyperacute changes of a tall
peaked T-wave, ST segment elevation followed by the development of
Q-wave, return of the ST segment to isoelectric and T-wave inversion. The
cut off points for new or presumed new ST segment elevation are ≥ 0.2mV
in leads V1, V2, or V3 and ≥ 0.1mV in other leads. This should be present
in 2 or more contiguous leads. The presence of new onset or presumably
new left bundle branch block (LBBB) in a patient with typical type chest
pain indicates an infarct.
However in some cases especially when the patient presents early, the
ECG may be normal or equivocal. In patients with ongoing chest pain and
in whom the clinical index of suspicion of STEMI is high, 12 lead ECG
tracings repeated at close intervals of at least 15 minutes might show
evolving changes. Comparison with previous ECG’s may also be helpful in
such situations.
In patients with an inferior infarct, one should look for associated
posterior, lateral and RV infarct. The latter requires right sided chest leads
for diagnosis.
For localization of infarct see Table 1.
Table 1: ECG patterns of various STEMI locations
Location
Anteroseptal
Extensive anterior
Posterior
Posterior
Anterolateral
Inferior
Right Ventricular
Leads
ECG findings
V1 – V3
ST elevation, Q wave
V1 – V6
ST elevation, Q wave
V7 – V8
T elevation, Q wave
V1 – V2
ST depression, Tall R wave
I, AVL, V5 – V6
ST elevation, Q wave
II, III, AVF
ST elevation, Q wave
V4R, V5R
ST elevation, Q wave
2.2.3 Serum Cardiac Biomarkers
A rise and fall in the levels of serum cardiac biomarkers support the
diagnosis of STEMI. One should not, however, wait for the results of these
biomarkers before initiating reperfusion therapy. These cardiac biomarkers
include4 :
•
Cardiac troponins (cTnT and cTnI)
Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
•
•
•
•
Creatine kinase-Myocardial Band (CK-MB)
Creatine kinase (CK)
Myoglobin
Fatty Acid Binding Proteins
For the relative timing, rate of rise, peak value, duration of elevation and
properties of these cardiac biomarkers following STEMI, see Figure 2 and
Table 2.
Cardiac troponins and CK-MB are the most specific cardiac biomarkers.
It takes about 3-8 hours after STEMI for them to rise. Thus, too early a
measurement may result in a misleadingly low level.
For the diagnosis of STEMI, the value of CK-MB should be twice the upper
limit of normal. Persistently elevated values of CK-MB are almost never
due to myocardial necrosis. CK-MB rises early and falls early. Hence, CKMB measurements are useful for the diagnosis of reinfarction. CK is not
as sensitive or as specific as CK-MB. Nevertheless, it is also useful for the
diagnosis of STEMI and reinfarction.
A single measurement of a raised Troponin T or I (99th percentile of the
values for a reference control group) is sufficient to indicate myocardial
necrosis5. They are useful in detecting myocardial infarction in patients
presenting with atypical histories and non diagnostic ECG’s. Elevated
troponin levels are more important for the diagnosis of NSTEMI than
STEMI. Troponins may remain elevated for up to 14 days. Therefore it is
not useful for the diagnosis of reinfarction.
It is recommended that measurement of cardiac biomarkers be done at
periodic intervals, at hospital admission and again at 12-24 hours. This
would help to establish or exclude the diagnosis and may be useful for an
estimation of infarct size.
AST and LDH levels are not sensitive or specific for AMI with frequent false
positive elevations.
Figure 2: Time Course of Elevation of Serum Cardiac Biomarkers after STEMI
(Reproduced with permission from “Clinical Implications of the new definition of myocardial infarction”.
John K French, Harvey D White; Heart 2004;90:99–106)
Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
Table 2: Properties of Serum Cardiac Biomarkers
Protein
Fatty acid binding protein
Myoglobin
CK-MB
Troponin I
Troponin T
CK
Aspartate Transaminase
LDH
First detection* Duration of detection Sensitivity Specificity
1.5 – 2 hours
8 – 12 hours
+++
++
1.5 – 2 hours
8 – 12 hours
+++
+
2 – 3 hours
1 – 2 days
+++
+++
3 – 4 hours
7 – 10 days
++++
++++
3 – 4 hours
7 – 14 days
++++
++++
4 – 6 hours
2 – 3 days
++
++
6 – 10 hours
3 – 5 days
++
+
6 –10 hours
5 – 7 days
++
+
* Hours after symptom onset.
CK, creatine kinase; LDH, lactate dehydrogenase
(Reproduced with permission from “Clinical Implications of the new definition of myocardial infarction”.
John K French, Harvey D White; Heart 2004;90:99–106)
2.2.4 Other Diagnostic Modalities.
Imaging techniques such as chest radiography, echocardiography6, multislice computed tomography (MSCT)7 and radionuclide techniques8 are
useful investigations in the patient presenting with acute chest pain. They
help to:
• Rule out or confirm the presence of acute infarction or ischaemia.
• Identify non-ischaemic conditions causing chest pain such as valvular
heart disease, pulmonary embolism, aortic dissection and
pneumothorax.
• Identify mechanical complications of acute infarction.
• Provide prognostic information.
Echocardiography is a particularly useful bedside imaging technique in
difficult diagnostic situations.
2.2.5 Difficult Diagnosis
Sometimes the diagnosis of myocardial infarction is difficult. About 2-8%
of patients presenting with chest pains to the emergency department have
been misdiagnosed and sent home. The morbidity and mortality in these
patients is high. To reduce this misdiagnosis, we suggest the following
measures be taken in all patients presenting with chest pains:
• They should be given priority in the emergency department and attended
to urgently.
• Myocardial ischemia or infarction should be excluded in all these
patients.
• Clinical suspicion should be high in all patients with predisposing risk
factors for atherosclerosis.
• A careful history will often help in making the diagnosis.
• An ECG should be done as soon as possible in all patients with chest
pains especially when the clinical suspicion of AMI is high. The threshold
for doing an ECG in a patient presenting with chest pain should be low.
• Where the initial ECG is non diagnostic, it should be repeated and
compared with old ECG’s. Thus it is important to maintain good clinical
records that can be rapidly retrieved.
Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
• Cardiac biomarkers especially the troponins, are helpful in ruling in or
ruling out a myocardial infarction.
• Where the diagnosis is unclear but the clinical suspicion is high, these
patients should be observed in the emergency department for a few
hours and the resting ECG and cardiac biomarkers repeated to look for
serial changes. If these remain stable, then the patient may be sent home
but asked to return for an early review in the outpatient clinic.
In addition, the hospital needs to:
• educate all medical staff on the importance of early detection and
treatment of AMI because this results in myocardial salvage and
improved patient outcomes.
• have regular refresher courses on ECG interpretation.
• implement critical pathways for patients presenting with chest pains to the
emergency department.
Recommendations:
•
The public and allied health care personnel should be
educated on the importance of early diagnosis and the benefits
of early reperfusion therapy.
•
STEMI is diagnosed by the clinical history of chest pain, ECG
changes of ST elevation/ LBBB and elevated serum cardiac
biomarkers.
•
Atypical presentations can occur in the elderly, women and in
diabetic patients.
•
If the initial ECG is non-diagnostic, it may need to be repeated
at frequent intervals to detect evolving changes of STEMI.
•
Too early a measurement can sometimes result in a
misleadingly low level of serum cardiac biomarkers.
Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
3. PRE-HOSPITAL MANAGEMENT
Immediate measures to be taken in suspected cases of STEMI
3.1 For the general public:
• Seek immediate medical attention at the nearest hospital.
• Call for an ambulance (dial 991 or hospital direct line if known) or
get someone to take you immediately to the nearest hospital.
• Do not drive yourself.
• If not on regular aspirin and with no history of allergy, chew and
swallow one 300mg tablet of aspirin immediately.
3.2 For Patients with known CHD:
• If the pain is suggestive of STEMI (see section 2.2.1), take one
dose of sublingual GTN and be rapidly transported to the hospital.
• If the pain is not severe, take one tablet of GTN and repeat every
5 minutes for a maximum of 3 doses. If the pain still persists after
15 minutes, go to the hospital.
3.3 For the general practitioner / family physician:
I, A • Ask patient to chew and swallow one 300mg tablet of aspirin9.
I, C • Give sublingual GTN.
I, A • If the ECG shows ischemic changes, give 300mg of clopidogrel if
available.10,11
I, C • Wherever possible, set up intravenous access.
I, C • Pain relief with intravenous opiates (IV morphine 3-5mg slowly).
I, C • Avoid intramuscular injections since this could result in
intramuscular hematomas if fibrinolytic agents are subsequently
administered.
I, C • Call an ambulance or ask the patient’s relative or friend to send
the patient immediately to the nearest hospital.
• Wherever possible, contact the doctor at the hospital so that the
patient can be treated promptly on arrival.
3.4 For Allied Health Care Personnel:
Immediate measures to be taken when there is an ambulance call:
• Note nature of complaint.
• Obtain name of caller, address and telephone number.
• If possible, request that a relative or friend wait at a strategic place
to help locate the patient.
• Dispatch an adequately equipped ambulance with trained
paramedics immediately.
• Patient should be given oxygen and aspirin (if he has not taken)
and transported to hospital.
Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
• Upon reaching the hospital, the patient should be taken directly to
the Emergency Department.
An ECG should be done as soon as possible. In hospitals where
networking facilities are available, allied health care personnel in the
ambulance should relay/transmit the ECG to the call centre for review by
the Specialist, for consideration of pre-hospital fibrinolysis or primary PCI.
Allied Health care personnel should be trained:
• to identify patients at high risk of developing CHD.
• to identify patients presenting with AMI.
• on the importance of early referral and treatment.
• in basic and advanced cardiopulmonary resuscitation (CPR).
Recommendations:
• Patients with suspected STEMI should be given sublingual GTN,
aspirin and clopidogrel.
• These patients should be rapidly transported to the hospital.
Clinical Practice Guidelines on
MANAGEMENT OF ACUTE ST SEGMENT ELEVATION
MYOCARDIAL INFARCTION (STEMI)
4. IN-HOSPITAL MANAGEMENT
Early management of STEMI is directed at:
• Pain relief
• Establishing early reperfusion
• Treatment of complications - arrhythmias
4.1 Initial Recognition and Management
I, A
When the patient with suspected STEMI reaches the emergency
department, evaluation and initial management should take
place promptly (FAST TRACK - RED ZONE) because the
benefits of reperfusion therapy is greater the earlier it is initiated 12.
I, C
A quick targeted history should be taken and vital signs noted. The
diagnosis should be confirmed with an ECG, which should be done
as soon as possible, preferably within 10 minutes of the patient’s
arrival in the emergency department. It is important to relieve pain
and quickly assess the patient’s suitability for reperfusion by either
fibrinolytic therapy or primary PCI.
The following should be done immediately and concomitantly in the
emergency department (see flow chart 1, page 44):-
I, C • Assessment and stabilization of the patient’s haemodynamics.
I, C • Sublingual GTN if chest pain persists (unless systolic blood
pressure (SBP) < 90 mmHg).
I, C • Continuous ECG monitoring.
I, A • 300mg of aspirin chewed and swallowed if not given earlier 9.
I, A • Clopidogrel at a dose of 300mg should be given if not given
earlier 10,11.
I, C • Oxygen by nasal prongs / facemask.
I, C • Venous access established and blood taken for cardiac
biomarkers, full blood count, renal profile, glucose and lipid profile.
Preferably 2 intravenous lines should be set up.
I, C •
Pain relief - morphine should be administered intravenously at
2-5mg every 5-15 minutes until pain is relieved. Watch for
evidence of toxicity – hypotension and respiratory depression.
Anti-emetics ( IV metoclopromide 10mg or promethazine 25mg )
should be given.
I, C • Intramuscular injections should be avoided.
I, C • Assessment for reperfusion strategy.
Clinical Practice Guidelines on
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MYOCARDIAL INFARCTION (STEMI)
4.2 Reperfusion Strategies
A
Early and prompt reperfusion is crucial as TIME LOST is
equivalent to MYOCARDIUM LOST 12,13,14.
A
A
A
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 fibrinolytic
therapy as a reperfusion strategy15,16.
However in patients who present within 3 hours of symptom onset
and are at low risk, both treatment strategies appear to have similar
benefits17,18.
In the majority of our hospitals, fibrinolytic therapy is more readily
available and constitutes the main reperfusion strategy. If both
choices are available, the following factors help guide the choice of
reperfusion strategies:
•
•
•
•
•
Time from symptom onset to first medical contact
Time delay to PCI (time from hospital arrival to balloon dilatation –
door to balloon time)
Time to hospital fibrinolysis (time from hospital arrival to
administration of fibrinolytic therapy – door to needle time)
Contraindications to fibrinolytic therapy
High risk patients
The best reperfusion strategy will depend upon:
A)Time from onset of symptoms
• Early presentation (within 3 hours)
If both treatment options are readily available, they have been
I,A
shown to be equally effective17,18 except for the following situations
where primary PCI is the preferred strategy:
- fibrinolytic therapy is contraindicated
- in high-risk patients
- PCI time delay [(door-to-balloon time) – (door-to-needle time)] is
less than 60 minutes19
• Late presentation (3 to 12 hours)
I,A
IIa,B
Primary PCI is preferred 15,16. The door to balloon time should be
within 90 min if the patient presents at a PCI capable facility19.
If transferred from a center with no PCI facilities, it should be less
than 2 hours. (including transfer delay)20
If the time delay to primary PCI is longer than as mentioned,
then fibrinolytic therapy should be given.
• Very late presentation (> 12 hours)
Both primary PCI and fibrinolytic therapy are not routinely
III, A
recommended in patients who are asymptomatic and
haemodynamically stable 12.
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However, reperfusion therapy would still be beneficial in patients
with persistent ischaemic symptoms, haemodynamic or electrical
instability. In this subgroup, primary PCI is the preferred strategy.
B)Contraindications to fibrinolytic therapy
See section 4.2.1.2
C)High risk patients
These include patients with:
• Large infarcts
• Anterior infarcts
• Cardiogenic shock
• Elderly patients
• Post revascularization (post CABG and post PCI)
• Post infarct angina
I,A Primary PCI is the preferred strategy in these patients 21,22,23.
I,A The goals of time to reperfusion therapy should be within:
• 30 minutes door to needle time12,13
I,B
• 90 minutes door to balloon time 19
4.2.1 Fibrinolytic Therapy
I,A
Fibrinolytic therapy has been shown to reduce mortality when given
within the appropriate time frame. When given within 1 hour from time
of onset of symptoms, it is most beneficial and has been shown to be
able to abort the infarction and reduce mortality by up to 50%12,17.
I,A
The door-to-needle time should be within 30 mins. Strategies should
be put in place to achieve this target. Fibrinolytic therapy should be
made available in all hospitals and there should be protocols to
initiate it in the emergency department.
I,A Pre-hospital fibrinolytic therapy has been shown to achieve faster
reperfusion17,24.
I,C Patients presenting with a low blood pressure (SBP < 90mm Hg)
should receive inotropic support prior to fibrinolytic therapy.
4.2.1.1 Indications
I,A Fibrinolytic therapy should only be given to patients with STEMI. It
has no role and may even be detrimental in patients with NSTEMI12,25.
4.2.1.2 Contraindications
Absolute contraindications
Risk of Intracranial haemorrhage
Any history of intracranial haemorrhage
Ischaemic stroke within 3 months
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Known structural cerebral vascular lesion (e.g. arteriovenous
malformation)
Known intracranial neoplasm
Risk of bleeding
Active bleeding or bleeding diathesis (excluding menses)
Significant head trauma within 3 months
Suspected aortic dissection
Relative contraindications
Risk of intracranial haemorrhage
Severe uncontrolled hypertension on presentation (BP > 180/110
mm Hg)*
Ischaemic stroke more than 3 months ago
History of chronic, severe uncontrolled hypertension
Risk of Bleeding
Current use of anticoagulation in therapeutic doses (INR > 2)
Recent major surgery < 3 weeks
Traumatic or prolonged CPR >10 minutes
Recent internal bleeding (e.g. gastrointestinal or urinary tract
haemorrhage) within 4 weeks
Non-compressible vascular puncture
Active peptic ulcer
Others
Pregnancy
Prior exposure (>5 days and within 12 months of first usage) to
streptokinase (if planning to use same agent)
* The blood pressure should be reduced prior to institution of fibrinolytic
therapy.
4.2.1.3 Choice of Fibrinolytic Agent
Presently the agents available in Malaysia are:
I, A
Streptokinase
This is the most widely used agent. It is not fibrin specific and is less efficacious than fibrin selective agents 26,27. Despite
having a lower risk of intracranial haemorrhage, the reduction in
mortality is less than with fibrin specific agents26,28.
I, B
Streptokinase is antigenic and promotes the production of
antibodies. Thus the utilization of this agent for re-infarction is
less effective if given again 5 days after the first administration 29.
PCI or fibrin specific agents should then be considered.
Regimen:
- 1.5 mega units in 100 ml normal saline or 5% dextrose over 1 hour.
Other regimens are:
- 1.5 mega units over 20 minutes, or
- 0.75 mega unit bolus and then repeated at the same dose after an
interval of 50 minutes if there is no clinical reperfusion.
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The last 2 regimens achieve a higher coronary artery patency rate
and are associated with lower in-hospital mortality. However they are
associated with a higher incidence of hypotension30.
Alteplase
I,A
I,A
This agent is fibrin specific 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
Second generation fibrin specific agents: Tenecteplase, Reteplase
B
Tenecteplase has been recently introduced in Malaysia. These
second generation fibrin specific agents are as efficacious as
alteplase 34. Tenecteplase has been shown to have a slightly lower
bleeding risk as compared to alteplase 34. The mainadvantage of
using these agents is that they are easier to administer. They are
given as single or double bolus injections and also do not induce
antibody production.
Regimen: Tenecteplase (TNK-tPA) single i.v. bolus
30mg if < 60kg
35mg if 60 to < 70kg
40mg if 70 to < 80kg
45mg if 80 to < 90kg
50mg if >90kg
Heparin needs to be given for 48 hours
4.2.1.4 Indicators of Successful Reperfusion
There is no sensitive bedside clinical method to reliably detect
successful reperfusion35. Some useful guides are:
• resolution of chest pain (may be confounded by the use of narcotic
analgesics).
• early return of ST segment elevation to isoelectric line or a decrease
in the height of the ST elevation by 50% in the lead that records the
highest ST elevation therapy within 60-90mins of initiation of
fibrinolytic therapy.
• early peaking of CK and CK-MB levels.
• restoration and/or maintenance of haemodynamic and/or electrical
stability
The occurrence of ‘reperfusion arrhythmias’ is not a reliable indicator of
successful reperfusion. An exception is accelerated idioventricular rhythm
and sudden sinus bradycardia which have been correlated with a patent
infarct related coronary artery after fibrinolytic therapy or primary PCI35.
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4.2.1.5 Failed Fibrinolysis
Failure of fibrinolytic agents to open up the occluded infarct related
artery is manifested as continuing chest pain, persistent ST segment
elevation and hemodynamic instability. These patients are more likely
to develop complications such as heart failure and arrhythmias.
I,B
The treatment of choice for these patients is rescue PCI36.
They should not be given a second dose of a fibrinolytic agent. This is
because there has been no difference in event free survival
demonstrated if these patients are given a repeat dose of a
fibrinolytic agent or if they are treated conservatively36.
4.2.2. Percutaneous Coronary Intervention (PCI)
4.2.2.1 Primary PCI
I,A
Primary PCI is the reperfusion strategy of choice as indicated earlier
(section 4.2)15,16 It should be performed promptly by experienced
operators and in centers performing a sufficient number of primary
PCI procedures.
4.2.2.2 Facilitated PCI
IIa,A
Current evidence indicates that strategies combining fibrinolytic
therapy is associated with higher reperfusion rates and TIMI flow.
However, it is associated with higher mortality and bleeding rates. It is
therefore not recommended37,38 .
4.2.2.3 Rescue PCI
Rescue PCI may be considered in patients who have failed
fibrinolytic therapy or have recurrent chest pain and/or ischaemic
complications. Those who may benefit are patients with:
• ongoing chest pains
• haemodynamic and electrical instability
• cardiogenic shock in patient < 75 years old, within 36 hours of
STEMI and <18 hours of shock whose coronary anatomy is
suitable for revascularization
• heart failure and onset of chest pain within 12 hours
• cardiogenic shock – In these high risk patients, those who are <75
years of age and who present within 36 hours of STEMI and <18
hours of shock may be considered for rescue PCI if their coronary
anatomy is suitable for revascularization
This strategy is associated with high mortality and morbidity rates. As
such, patients should be individually evaluated.
4.2.2.4 Delayed PCI (> 72 hours after fibrinolytic therapy)
Routine angiography and PCI in asymptomatic and stable patients
post fibrinolytic therapy is controversial 39,40.
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Recommendations:
• Patients presenting to the hospital need to be rapidly evaluated
for prompt reperfusion therapy.
• Reperfusion therapy with either primary PCI or fibrinolytic therapy
reduces mortality and is useful in patients presenting within 12
hours from onset of symptoms.
• We should aim to achieve a door-to-needle time of less than 30
min and a door-to-balloon time of less than 90 min.
• Fibrinolytic therapy if given within 3 hours of onset of symptom
gives equivalent results as primary PCI.
• The preferred strategy is primary PCI if the time of onset of
symptoms is between 3-12 hours.
• The treatment of choice for failed fibrinolysis is rescue PCI.
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4.3 CARDIAC CARE UNIT MANAGEMENT
4.3.1 General Measures
A period of at least 12 hours of complete bed rest is recommended
following admission to CCU. Patients with uncomplicated infarcts are
encouraged to ambulate early. Those with haemodynamic instability
will need a longer period of monitoring.
Sedatives may be useful.
Use of bedside commodes and assisted bedside washing should be
safe in most patients.
The Valsalva maneuver has been shown to precipitate dangerous
haemodynamic and electrocardiographic changes particularly in the
young 41 and thus prevention of constipation with stool softeners is
encouraged.
4.3.2 Monitoring
The general condition of the patient, vital signs, pulse oximetry and
the ECG should be continuously monitored following STEMI, looking
for complications.
4.3.3 Concomitant Therapy
4.3.3.1 Oxygen
I,C
Oxygen is indicated in the presence of hypoxemia. In uncomplicated
cases, its use should probably be limited to the first 24 hours.
Oxygen, via nasal prongs, at 2 - 4 litres/min is usually adequate. One
should aim to maintain the oxygen saturation above 95%.
4.3.3.2 Antiplatelet Agents
I,A
Aspirin is indicated in all patients at diagnosis and should be
continued indefinitely unless contraindicated. The initial dose of 100300mg should be followed by a maintenance dose of 75 - 150mg daily9.
A) Aspirin B) Clopidogrel I,A
Clopidogrel, when given together with aspirin and fibrinolytic therapy
in STEMI, has been shown to reduce the odds of an occluded infarct
related artery, death or reinfarction without increasing the risk of
bleeding or cerebrovascular accidents. 10,11 A loading dose of 300 mg
should be given followed by a maintenance dose of 75 mg daily.
We recommend treatment for at least 1 month after fibrinolytic
therapy. Following PCI, a longer period of dual antiplatelet therapy
(up to 12 months) is necessary particularly when drug-eluting stents
are used.
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4.3.3.3 β-blockers
I,A Current recommendations are to use oral β-blockers early in all
patients without specific contraindications 42,43.
I,B In patients with asymptomatic LV dysfunction (LV ejection fraction
on echocardiogram < 40%) and not in overt heart failure, carvedilol
has been shown to reduce the frequency of death and recurrent
AMI44. When indicated, it should be started in patients who are
hemodynamically stable after 48 hours.
Contraindications to β - blockers:
1) Bradycardia < 60/minute
2) SBP < 100mmHg
3) Pulmonary congestion with crepitations beyond the lung
bases
4) Signs of peripheral hypoperfusion
5) Second or third degree atrio-ventricular (AV) block
6) Asthma or chronic obstructive airway disease ( COAD)
7) Severe peripheral vascular disease
Table 3: Recommended dosages of β -blockers in STEMI
Type
Initiation dose
Target dose
Metoprolol
Atenolol
Propranolol
Carvedilol
25mg bd
25mg od
5mg tds
3.125mg bd
100mg bd
100mg od
80mg tds
25mg bd
4.3.3.4 Angiotensin Converting Enzyme Inhibitors (ACEI) and
Angiotensin Receptor Blockers (ARB)
I,A
Early use of ACEI (within 24 hours) following STEMI has been shown
to improve survival 45. ACEI should be started when the blood
pressure is stable and systolic blood pressure (SBP) remains above
100mmHg.
The benefits of ACEI are greatest in patients with:
• Heart failure45,46
I,A
I,A
•
•
I,A
Anterior infarcts45,47
Asymptomatic left ventricular dysfunction ( LV ejection
fraction < 40% on echocardiography)48,49
I,B In patients who cannot tolerate ACEI, the ARB, valsartan, has been
shown to have a similar survival benefit 50.
Contraindications to ACEI and ARB therapy:
1) Systolic BP < 100mmHg
2) Established contraindications e.g. bilateral renal artery
stenosis, worsening renal function.
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Table 4: Recommended dosages of ACEI and ARB in STEMI
Type
Initiation dose
Target dose
Captopril
Ramipril
Enalapril
Lisinopril
Perindopril
Valsartan
6.25mg bd –tds
2.5mg bd
2.5 - 5mg od
5mg od
2mg od
80mg od
25 - 50mg tds
10mg od
10mg od
10mg od
4mg od
160mg bd
4.3.3.5 Nitrates
III,A The routine use of nitrates has not been shown to have a survival
benefit51,52.
I,C Nitrates can be considered in patients with:
• Continuing chest pain and / or ischemia
• Heart failure
• Hypertension
In the acute stage, IV nitrates are recommended because of their
rapid onset of action, ease of titration and potential for prompt
termination in the event of side effects. After the first 48 hours, oral
or topical nitrates may be continued in patients with persisting
ischemia and/or heart failure.
Contraindications to nitrate therapy:
1) Hypotension (SBP< 90mmHg)
2) RV infarction
3) History of phospho-diesterase 5 inhibitors ingestion
depending upon the half-life of the agent. (Appendix 3)
4.3.3.6 Calcium Channel Blockers
III,A
There is no data to support the routine use of calcium channel
blockers post STEMI53,54.
However they may be used as adjunctive therapy in patients with hypertension and/or on-going ischaemia despite β-blockers and
nitrates.
In patients who cannot tolerate β-blockers, verapamil or diltiazem
II-a,B
55
may be used for secondary prevention .
Calcium channel blockers should be avoided in patients with LV
dysfunction, pulmonary congestion, bradycardia and AV block.
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Table 5: Recommended doses of Nitrates in STEMI
Compound
Route
Dosage
Time of Onset
Intravenous
5 - 200µg/min*
1 minute
Nitroglycerine,
Sublingual
0.3 - 0.6mg, can repeat up to
2 minute
Glyceryl
3 times at 5 minute intervals
trinitrate
GTN Spray
0.4 - 0.8mg per metered dose,
no more than 3 sprays
2 minute
at 5 minute intervals
Transdermal patch 0.2 - 0.8mg over 12 hours on,
1 - 2 hours
then 12 hours off
Isosorbide
Intravenous
1.25 - 5mg / hour
1 minute
dinitrate
Transdermal patch
2.5 - 10mg
3 – 4 minutes
Oral
10 – 20mg, 2 – 3 times daily 30-60 minutes
20 - 30mg, 2 - 3 times daily, 30 - 60 minutes
Isosorbide
Oral
up to 120mg in divided doses
mononitrate
* The dose of IV nitrates should be titrated every 5 - 10 minutes until symptoms and/or
ischaemia is relieved and the desired haemodynamic response is obtained
4.3.3.7 Antithrombotics
The antithrombotics that have been studied in STEMI are:
•
Unfractionated heparin
•
Low molecular weight heparin
•
Synthetic pentasaccharide – fondaparinux
Heparin is indicated in patients with :
I,C
-
post infarct angina
I,C
I,C
I,C
I,A
-
atrial fibrillation
-
mural thrombus
-
extensive anterior infarction
-
post fibrin-specific fibrinolytic agent 31,32,33
- post non fibrin-specific fibrinolytic agent 31
IIa,B
A) Unfractionated heparin (UFH)
Unfractionated heparin is administered as a bolus of 60units/kg
(maximum 4000units) followed by an infusion rate of 12units/kg/hour
(maximum 1000units/hour) adjusting the dose to maintain the aPTT
(activated partial thromboplastin time) of 1.5 to 2.5 times control.
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B) Low molecular weight heparin (LMWH)
I,A Low molecular weight heparin is given subcutaneously twice a day.
LMWH was associated with better clinical outcomes as compared to
UFH when given following fibrinolytic therapy in STEMI 56,57.
I,A This benefit was seen with both fibrin-specific58,59 and non-fibrin
specific 57,60 agents, but at an increased risk of bleeding. These studies
however, were done prior to the usage of clopidogrel in STEMI.
In patients >75 years of age and with renal impairment (serum
creatinine > 200umol/L in women and >250umol/L in men), UFH is
preferable to LMWH59.
Table 6: Recommended dosages of LMWH in STEMI
Heparin
Dosage
Duration of therapy
< 75 yr:
30mg IV bolus, sc 1.0mg/kg bd
Enoxaparin
Until hospital discharge
≥ 75 yr:
No bolus, sc 0.75mg/kg bd
60U/kg bolus (max 4000 U)
UFH
≥ 48 hours
Infusion 12U/kg/h (max 1000 U/h)
Patients given aspirin, clopidogrel, fibrinolytic therapy and LMWH
have been found to have a higher rate of patency of the infarct related
artery without an increase in the risk of bleeding complications in one
substudy61.
We caution the use of all 4 agents (aspirin, clopidogrel, fibrinolytic
therapy and UFH/LMWH) together until the efficacy and safety of the
combination is established in future trials.
C) Synthetic pentasaccharide
I,B A trial on fondaparinux at a dose of 2.5mg/kg per day, given for 8 days,
or the duration of index hospitalization to patients who were given
fibrinolytic agents or who were not reperfused, was shown to reduce
death or reinfarction at 30 days when compared to UFH. The risk of
bleeding was not increased62.
4.3.3.8 Glycoprotein IIb/IIIa Receptor Inhibitors
I,A Glycoprotein IIb/IIIa receptor inhibitors are used mainly in the setting of
primary PCI. In primary PCI, the glycoprotein IIb/IIIa receptor inhibitor,
abciximab, has been shown to improve patient outcomes63,64.
4.3.3.9 Statins
I,A Recent data has shown that statins started within 24 hours of admission
or continued after admission leads to a reduction in major adverse
cardiac events65,66,67.
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4.3.3.10 Aldosterone Antagonists
I,B Eplerenone, a selective aldosterone receptor antagonist, when added
to β-blockers and ACE-I, has been shown to reduce mortality and
hospitalizations when given to patients post myocardial infarction with
impaired LV function and mild HF68.
4.3.3.11 Others – Magnesium, Lignocaine, Glucose – Insulin
Potasium Infusions
III,A Magnesium52,69 and Lignocaine70 are not recommended for routine use
in patients with STEMI.
IIb,A Although earlier studies and meta-analysis seem to indicate that
Glucose-Insulin–Potassium infusions are beneficial, more recent
studies have not shown reduction in mortality or infarct size 71,72.
Recommendations:
• All patients should receive 100 - 300 mg aspirin and 300 mg
clopidogrel followed by a maintenance dose of 75-150 mg of
aspirin long term and 75 mg of clopidogrel daily for at least a
month.
• All patients should be on β blockers if there are no specific
contraindications.
• Other medications that have been shown to improve survival
if given early are ACE inhibitors (or ARB if ACE intolerant) and
statins.
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4.4 Complications of STEMI
These are:
•arrhythmias
•left ventricular dysfunction and shock
•mechanical complications
•right ventricular infarction
•others e.g. pericarditis
4.4.1 Arrhythmias
These include:
A) Tachyarrhythmias
•Pulseless ventricular tachyarrythmias.
This includes pulseless ventricular tachycardia and ventricular
fibrillation. Defibrillate immediately. Early VF occurs within the first 48
hours and is due to electrical instability. Late VF is associated with
large infarcts and poor pump function and carries a poor prognosis
(refer to algorithm 1)
[Shockable waves refers to the presence of recognizable organized
or disorganized cardiac rhythms on continuous ECG monitoring while
non shockable waves refers to the absence of any heart rhythm on
ECG monitoring]
•Stable Ventricular Tachycardia (VT).
Ventricular tachycardia in the setting of STEMI may arise from either
ischaemia or from myocardial scar resulting from the infarct. Treatment
of ischaemia may result in the termination of the tachycardia. (refer to
algorithm 2).
•Ventricular Premature Contractions (VPC).
These are often benign and do not require treatment. Correct underlying
ischaemia, hypoxia and electrolyte disturbances.
•Accelerated Idioventricular Rhythm (AIVR).
These do not require any treatment. This is a sign suggestive of
successful reperfusion.
•Atrial fibrillation (AF).
This is more commonly seen in the elderly and is associated with large
infarcts and atrial infarcts. It denotes a poorer prognosis73 and carries
an increased risk of thromboembolism. (refer to algorithm 3)
B) Bradyarrhythmias
These are:
•Sinus bradycardia.
This does not require treatment unless associated with symptoms and/
or hypotension.
•Atrio-ventricular Block (AV Block).
First degree and second degree type 1 (Mobitz 1) do not need
treatment. Patients with second degree type 2 (Mobitz 2) and complete
AV block may not require treatment if haemodynamically stable.
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In patients who are haemodynamically unstable, arrangement must
be made for urgent temporary pacing. Atropine may be given in the
interim.(maximum 3 mg) (refer to algorithm 4)
In patients with anterior infarcts, second degree and complete AV block
carry a worse prognosis. They may require urgent temporary pacing
(refer to algorithm 4).
• Asystole/Pulseless Electrical Activity
Asystole/ Pulseless electrical activity can be differentiated from
pulseless ventricular tachyarrythmias by the presence of shockable
waves on ECG monitoring. (refer to Algorithm 1)
4.4.2 Left Ventricular Dysfunction and Shock
4.4.2.1 Presentation:
The clinical manifestation of left ventricular dysfunction varies
from asymptomatic to cardiogenic shock. An important prognostic
indicator is LV function which can be assessed objectively using
echocardiography.
A useful clinical classification is the Killip’s Classification74,75 (table 7)
Table 7: Clinical and Haemodynamic Subsets in AMI
KILLIP
CLASS75
CLINICAL FEATURES
APPROXIMATE
30 day - MORTALITY
PROPORTION OF (%)74 PATIENTS WITH
AMI (%)74
I
No signs of LV failure
71
7
II
S3 gallop, bibasal crackles
23
20
III
Acute pulmonary oedema
3.7
39
IV
Cardiogenic shock
2.4
70
4.4.2.2 Differential diagnoses of LV dysfunction and shock:
Differential diagnoses are:
•Pump failure due to extensive myocardial infarction
•Mechanical complications
•Right ventricular infarction
•Hypovolemia
•Arrhythmias
•Drugs
•Aortic root dissection.
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4.4.2.3 Investigations:
Investigations that may be helpful in making the diagnosis and in the
management includes:
•Chest radiograph
•ECG
•Echocardiography
•Arterial blood gases
•Pulmonary artery catheter
4.4.2.4 Management:
A) Heart Failure
Acute management includes the following:
•Oxygen therapy
•Diuretics
•Intravenous nitroglycerine
•Intravenous morphine
•Inotropes if hypotensive.
Refer to the Malaysian Clinical Practice Guidelines on Heart Failure
2007 on the management of Acute Cardiogenic Pulmonary Edema.
B) Cardiogenic shock
Cardiogenic shock is defined as a systolic BP of < 90 mmHg associated
with signs of tissue hypoperfusion, and central filling pressure (PCWP)
is >20mmHg or cardiac index is <1.8L/min/m2. This condition is
associated with a very high mortality rate.
Emergency PCI may be life-saving and should be considered early.
Intra-aortic balloon pump may be useful.
When cardiogenic shock is due to a mechanical defect, urgent surgical
repair is indicated. Pre-operative coronary angiography and subsequent
coronary artery bypass graft (CABG) surgery in these patients remain
an issue of debate. The decision must be individualized.
4.4.3 Mechanical complications
These include the following:
•free wall rupture
•ventricular septal rupture
•papillary muscle rupture
The diagnosis should be suspected in patients with sudden clinical
deterioration and suggested by the presence of new murmurs
or diminished heart sounds. The diagnosis can be confirmed
by echocardiography. In these patients early surgery should be
considered.
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4.4.4 Right Ventricular Infarction (RVI)
Patients with RVI may have varying clinical presentation, from
asymptomatic to cardiogenic shock76. Haemodynamically significant
RVI complicates approximately 5-10% of all STEMI. It occurs in 30
– 50% of patients with infero-posterior STEMI and is associated with
a significantly higher mortality. RVI can also occur in patients with
extensive anterior STEMI.
Clinical Diagnosis
The presence of RVI should be sought in all patients with inferior
STEMI. The clinical triad of hypotension, clear lung fields and elevated
jugular venous pressure in the setting of inferior STEMI is suggestive
of RVI.
ST elevation in the right precordial leads (V4R) is the most specific77
finding in diagnosing RVI. However, this ECG finding may be transient,
often resolving within 8-10 hours.
Management
Treatment strategies depend on the severity of peripheral hypoperfusion
and the degree of co-existing LV dysfunction. Drugs that reduce the
preload, such as nitrates and diuretics should be avoided.
Management includes:
• Optimization of intravenous fluid (saline or colloids)
• Inotropes
Failure to respond to these measures usually indicates concomitant
LV dysfunction. These patients require more aggressive management
with afterload reducing agents such as nitroprusside and intra-aortic
balloon pump.
4.4.5 Others
4.4.5.1 Chest pain post STEMI
Chest pain post STEMI may be due to reinfarction, ischaemia or
pericarditis. Non-cardiac causes must also be considered.
A) Reinfarction
Reinfarction occurs in about 3-4% of patients who had undergone
fibrinolytic therapy and received aspirin78. Reinfarction may be
diagnosed by:
•recurrence of ischaemic type chest pain
•recurrence of ST segment elevation of at least 0.1mV in at least
contiguous leads and/or
• re-elevation of serum cardiac biomarkers especially CK
Death, severe heart failure and arrhythmias are more common in these
patients. They should be considered for rescue PCI.
B) Post-infarct angina
Early recurrent angina, especially after successful reperfusion may
occur in up to 20% of patients79. The ECG in these patients may show
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ST segment changes or pseudo-normalisation of inverted T-waves.
These patients should be sent for early coronary angiography with a
view to revascularization.
C) Pericarditis
Pericarditis secondary to STEMI may produce pain as early as the
first day and as late as 6 weeks80. The pain classically becomes worse
on deep inspiration and may be relieved when the patient sits up and
leans forward. A pericardial rub may be detected.
Dressler’s syndrome (post MI syndrome) usually occurs 2-10 weeks
after STEMI. This is immunologically mediated81. It is treated with
aspirin 600mg 3-4 times a day. Steroids and NSAIDS are best avoided
in the first 4 weeks of STEMI 82.
4.4.5.2 LV Thrombus and Arterial Embolism
LV mural thrombus has been identified in about 20-40% of patients with
STEMI. The majority of these occur following anterior or large infarcts.
Anticoagulation therapy for a minimum of 3-6 months is advocated in
these patients83.
4.4.5.3 Deep Venous Thrombosis (DVT)
In high risk patients (prolonged bed rest, heart failure, unable to
mobilize), prophylactic anti-coagulation therapy (subcutaneous heparin
5000 units bd, LMWH – e.g. enoxaparin 40mg od) may be considered
until the patient is ambulant.
4.5 Urgent/Emergent CABG surgery:
Urgent/emergent CABG surgery should be considered in the following
situations:
•At the time of surgical repair of post-infarction ventricular septal
defect (VSD) or mitral valve regurgitation (see section 4.4.3).
•Patients with failed reperfusion whose coronary anatomy and
clinical profile are suitable.
These patients should be supported with intra-aortic balloon pump.
In general, CABG surgery in this group of patients carries a very high
in-hospital mortality rate.
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5. RISK STRATIFICATION POST-STEMI
Risk stratification serves to prognosticate and identify appropriate
treatment strategies. Risk stratification starts from admission and is a
continuing process.
Poor prognostic indicators include:
•older persons ( > 65 years)
•female gender
•previous MI
•anterior MI
•inferior MI with RV involvement
•diabetes mellitus
•ECG changes in multiple leads
•persistent or recurrent ischaemia as manifested by post-infarction
angina or ST segment depression at rest
•hypotension
•heart failure
•atrial fibrillation and late (after 48 hours) ventricular arrhythmias
•presumably new LBBB
The above high risk patients should be considered for early coronary
angiography. All other patients should be risk stratified early. This
helps:
•to identify patients who are likely to reinfarct or develop other
complications such as heart failure.
•in the rehabilitation of patients. Low risk patients may be allowed
to return to their former activities early.
Risk stratification may be done by assessing:
•Left ventricular function
–clinical, chest X-ray, echocardiogram, radionuclide studies or
cardiac MRI
• Presence of myocardial ischaemia oclinical (recurrent angina)
o exercise stress testing in asymptomatic patients.
- This may be done from day 5 post-STEMI (sub-maximal stress
test with a target heart rate of 70% of maximum predicted heart
rate) up to 6 weeks post-STEMI (maximal with a target heart rate
of 90% of maximum predicted heart rate for age or symptom
limited).
- If the pre-discharge sub-maximal stress test is negative, the
patient should be subjected to a maximal or symptom limited
stress test within 6 weeks after discharge.
- For those who cannot exercise, consider dobutamine stress
echocardiogram, radionuclide perfusion studies or cardiac MRI.
• Presence of malignant ventricular arrhythmias
The presence of angina, an abnormal stress test or late ventricular
arrhythmias necessitates early coronary angiography with a view to
revascularization.
In patients with poor LV function, myocardial viability studies
(dobutamine stress echocardiogram, radionuclide perfusion studies or
cardiac magnetic resonance imaging) would help to differentiate
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scarred from viable ischaemic myocardium. The latter patients would
benefit from revascularization.
Patients with palpitations, near faints and syncope
comprehensive evaluation. This includes:
•serum electrolytes
•resting ECG
•24 hour ambulatory ECG recording
•evaluation of LV function
•assessment for reversible myocardial ischaemia
•coronary angiography
require
In these patients, reversible causes such as electrolyte disturbances
and ischaemia should be corrected.
The following medications have been shown to reduce the incidence
of sudden death :
I,A
I,A
I,B
IIb,B
-β-blockers84,85
-ACEI86.
-Aldosterone antagonist, eplerenone68.
-Statins87,88.
The following patients should be considered for an ICD :
I,A
I,B
•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 revascularisation91,92,93.
6. DURATION OF HOSPITALIZATION
The duration of hospital stay following STEMI will depend on the extent
of myocardial damage, the patient and the presence of co-morbidity.
Asymptomatic patients with uncomplicated STEMI may be discharged
after 3-5 days94 particularly if patient has been successfully
reperfused. Patients with significant left ventricular dysfunction or
other complications may require a longer hospital stay.
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7. SECONDARY PREVENTION
Patients who survive the initial course of STEMI are at increased risk
of morbidity and mortality because of reinfarction and the development
of other complications. Thus, it is very important that efforts be made
to reduce this risk.
These measures include:
7.1Cessation of smoking
mortality by 36% as compared
I,C Smoking cessation reduced CHD
95
to those who continue smoking . 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 encouraged96.
7.2Diet
has been shown to reduce cardiac event rates
I,B Dietary intervention
post STEMI97:
Recommendations include:
• Total calorie intake should be tailored to the desirable body weight
• Wherever possible, substitute saturated and trans fat with
polyunsaturated fat.
Use more high fibre food and whole grains instead of rapidly
digested carbohydrates.
• Take more fruits, nuts and vegetables.
I,B • Increased intake of omega 3 – fatty acids (1g daily) is
beneficial 98,99. Eat fish at least twice a week.
7.3Regular Exercise
I,C Recommended exercises include brisk walking, jogging, cycling,
swimming or other aerobic activity for at least 30 to 60 minutes on most
days of the week. It should be supplemented with an increase in daily
life-style activities such as walking up stairs whenever possible100.
7.4Control of Hypertension
I,A After STEMI, prognosis is affected by both the pre existing and
the subsequent blood pressure. The higher the pre existing blood
pressure, the higher the fatality rate101. The target blood pressure
should be < 130/80mmHg. Drugs of choice include β- blockers, ACEIs
and Valsartan52 (if ACEI intolerant).
7.5Good Glycemic control I,B Good control of the blood glucose is important
102
. Target fasting blood
glucose should be <6.0mmol/l and HBA1C < 6.5%
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7.6 Antiplatelet Agents
I,A
•Aspirin - Aspirin should be prescribed at 75-150mg daily as a
maintenance dose unless contraindicated 9,103.
I,A
In patients who cannot tolerate aspirin, alternatives include:
•Clopidogrel , 75mg daily 10,11
II-b,C
•Ticlopidine , 250mg bd
I,A
Dual anti-platelet therapies should be given for at least one month post
fibrinolytic therapy for secondary prevention 10,11.
Following primary PCI a longer period of dual antiplatelet therapy is
necessary particularly if drug-eluting stents are used.
7.7 β- blockers
I,A
In general, β- blockers should be continued indefinitely in all patients if
there are no contraindications 32,43.
7.8 ACE Inhibitors and ARB
ACEI should be continued indefinitely in all patients if there are no
contraindications45.
I,B In ACEI intolerant patients, the ARB valsartan may be used 52.
I,A
7.9Lipid-lowering therapy
Statins should be started soon after admission and continued
indefinitely. Target LDL cholesterol should be < 2.0mmol/L 104,105,106.
I,B Recent studies indicate that lowering LDL cholesterol even further
(< 1.8mmol/L) confers greater benefits 67,107,108.
I,A
7.10 Oral Anticoagulant (warfarin)
Long term therapy should be considered for patients with persistent
atrial fibrillation.
I,C Warfarin should be given for 3-6 months in patients with LV thrombus.
I,C
7.11Others
III,A
- Hormone replacement therapy is not beneficial for secondary
prevention 109,110.
III,B
III,A
- Postmenopausal women who were taking hormone replacement
therapy at the time of STEMI should discontinue it.
- Vitamin E and anti-oxidants have no clinical benefit 111,112.
III,C
- Garlic, lecithin, Vitamin A and C are not beneficial.
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8.
SPECIAL GROUPS
8.1 STEMI in the elderly
Patients above the age of 75 years have a much higher in-hospital
as well as one year mortality113. This may be due to their atypical
and delayed presentations, co-morbidities and under utilization of
aggressive therapeutic strategies.
Atypical features include silent ischaemia, dyspnoea, syncope and
acute confusion. Specific cardiac biomarkers such as CK-MB and
troponins should be measured.
Management
I,A A) Primary PCI
This is the preferred reperfusion strategy if facilities are available 23,114.
B) Fibrinolytic
I,A There is an increased risk of intracranial haemorrhage in the elderly
with the use of fibrin specific fibrinolytic agents as reperfusion strategy.
Therefore streptokinase is the preferred agent 26,27. Despite this, the
absolute benefits of fibrinolytic therapy in this age group are almost
twice that of younger patients with substantial decrease in mortality.
C) Concomitant Therapy
These patients have similar or greater benefits with the use of aspirin,
β- blockers, ACEI and statins as younger patients.
D) Risk Stratification
This has to be individualized taking into consideration the biological
age rather than the chronological age of the patient. The presence
of on-going ischaemia, symptomatic malignant arrhythmias and
a depressed LV function are bad prognostic indicators and would
generally necessitate a more aggressive approach. Both PCI and
CABG surgery, when indicated, can be carried out in the elderly with
acceptable morbidity and mortality by experienced operators. The
risks are however higher than in younger patients.
8.2 STEMI in Diabetics
Diabetic patients have higher in-hospital mortality (about 1.5 to 2
times) than non-diabetics following an STEMI115. The prognosis is
worse in diabetic women. There is a higher frequency of atypical and
silent presentations in these patients.
Management
Diabetic patients should be treated in a similar manner as nondiabetics.
8.3 STEMI in Women
The perception that women are “protected” against ischaemic heart
disease leads to under recognition of this condition. Atypical and
delayed presentation, late diagnosis, older age at presentation and high
prevalence of co-morbidities result in a higher mortality in women.
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Women are thus high risk patients and should be treated aggressively.
9. CARDIAC REHABILITATION IN STEMI
All patients’ post STEMI (including those post PCI or CABG surgery)
should undergo comprehensive cardiac rehabilitation. This programme
aims at improving the long-term prognosis and optimizing the physical,
psychological and social well-being of the patient. It comprises prescribed
exercise training and education, counseling, risk factor modification and
behavioral interventions.
Cardiac rehabilitation should start in the cardiac care unit, continue to
out-patient settings and extend to community care. It is a proven effective
intervention and every effort must be made to ensure minimal dropouts so
as to maximize beneficial effects of the programme.
10. FUTURE DEVELOPMENTS
There is ongoing research in various aspects of myocardial preservation in
the acute phase of STEMI utilizing stem cells, myocytes, growth factors and
other agents.
11. CHECK LISTS FOR FOLLOW-UP VISIT
The following should be assessed at each follow-up visit:
• Delineate the presence or absence of cardiac symptoms and
determine the functional class of the patients.
• Evaluate patients’ psychosocial (anxiety & depression) status and
the social integration and support network.
• Review pre discharge risk assessment and planned workup
- Evaluation for further cardiac ischaemia
- LV function
• Re-evaluate the list of all current medications and optimize their
doses.
• Actively review the following issues with the patient and family
members
- Principles of secondary prevention
- CPR training
- A plan for appropriate recognition and response to a potential
acute cardiac event
• Treat to target.
- Blood pressure: <130/80 mmHg
- Lipids: LDLC < 2.6mmol/L
- Diabetic control: Fasting blood glucose < 6.0mmol/L
HbA1C < 6.5%
- Achieve and maintain ideal body weight and waist
circumference
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10. SUMMARY
• CHD is an important cause of death in Malaysia.
• The diagnosis of STEMI depends on the presence of ischaemic
type chest pain and ST elevation in the resting ECG or new onset
LBBB.
• TIME LOST IS MYOCARDIUM LOST, thus early diagnosis and
treatment is important.
• Early management of STEMI involves pain relief, stabilization of
haemodynamics and assessment for reperfusion.
• The occluded infarct-related artery should be opened as soon
as possible either by primary PCI or fibrinolytic therapy. Failed
fibrinolysis necessitates rescue PCI.
• Concomitant pharmacotherapy includes aspirin, clopidogrel, βblockers, ACEI/ARB and statins.
• Complications of STEMI include arrhythmias, LV dysfunction and
shock.
• Urgent/emergent CABG surgery should be considered in patients
with mechanical complications or failed reperfusion.
• High-risk patients should have early coronary angiography with
view to revascularization. The others should be risk stratified
according to the presence or absence of ischaemia, arrhythmias
and LV function.
• Secondary prevention is important and includes the use of aspirin,
β- blockers, ACEI/ARB and statins.
• All patients should be encouraged to undergo cardiac
rehabilitation.
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34
Continue page 36
35
Continue from page 35
36
(Reproduced with
permission from 2005
American Heart
Association Guidelines
for Cardiopulmonary
Resuscitation and
Emergency
Cardiovascular Care,
Circulation. 2005;112
: IV-58 – IV-66.)
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MYOCARDIAL INFARCTION (STEMI)
ACKNOWLEDGEMENTS
The committee would like to thank the following for all their assistance:
• Technical Advisory Committee, Clinical Practice Guidelines,
Ministry of Health
• Panel of experts who reviewed the draft
• Secretariat from Sanofi-Aventis
DISCLOSURE STATEMENT
The panel members have no potential conflict of interest to disclose.
SOURCES OF FUNDING
This CPG was made possible by an unrestricted educational grant from
Sanofi-Aventis and Bristol-Myers Squibb.
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