ST-elevation

myocardial infarction

The right clinical information, right where it's needed

Last updated: Nov 13, 2017

 Table of Contents
Summary 3

Basics 4
Definition 4
Epidemiology 4
Aetiology 4
Pathophysiology 4
Classification 5

Prevention 6
Primary prevention 6
Screening 6
Secondary prevention 6

Diagnosis 7
Case history 7
Step-by-step diagnostic approach 7
Risk factors 8
History & examination factors 10
Diagnostic tests 11
Differential diagnosis 13
Diagnostic criteria 17

Treatment 19
Step-by-step treatment approach 19
Treatment details overview 24
Treatment options 30
Emerging 62

Follow up 63
Recommendations 63
Complications 63
Prognosis 67

Guidelines 68
Diagnostic guidelines 68
Treatment guidelines 69

Evidence scores 72

References 74

Images 82

Disclaimer 91
 Summary

◊ Presents with central chest pain that is classically heavy in nature, like a sensation of pressure or
squeezing. Examination is variable, and findings range from normal to a critically unwell patient in
cardiogenic shock.

◊ ST-elevation MI (STEMI) is suspected when a patient presents with persistent ST-segment elevation
in 2 or more anatomically contiguous ECG leads in the context of a consistent clinical history.

◊ CK-MB and cardiac-specific troponins confirm diagnosis. Treatment should, however, be started
immediately in patients with a typical history and ECG changes, without waiting for laboratory results.

◊ Immediate and prompt revascularisation can prevent or decrease myocardial damage and decrease
morbidity and mortality.

◊ About a quarter of patients in the US who have an acute MI will die of it, half within 1 hour of the
onset of symptoms.

◊ Survivors of acute MI should be closely followed up for adequate modification of risk factors and
development of complications.
 ST-elevation myocardial infarction Basics

Definition
MI is myocardial cell death that occurs because of a prolonged mismatch between perfusion and demand.
This is usually caused by occlusion in the coronary arteries. ST-elevation MI (STEMI) is suspected when a
BASICS

patient presents with persistent ST-segment elevation in 2 or more anatomically contiguous ECG leads in the
context of a consistent clinical history.

Epidemiology
Coronary heart disease (CHD) is the leading cause of death worldwide.[4] In the UK, 1 in 6 men and 1 in 10
women will die from CHD.[5] In the UK, around 640,000 men and 275,000 women will have a MI at some
point in their lives, with a total of 175,000 occurring annually.[5]

The overall prevalence of MI in the US is around 2.8% in adults aged 20 years or over.[2] The estimated
incidence is 550,000 new and 200,000 recurrent MIs annually.[2] According to American Heart Association
estimates, every 42 seconds an American will have an MI.[2] In 2013, 116,793 deaths in the US were
due to MI, and of these around 57% were in males and 43% were in females.[2] The risk of CHD as a
whole has been decreasing in developed countries and increasing in developing countries, probably as a
result of changing lifestyles, urbanisation, and increasing life expectancy. The risk is also seen to change
with migration (e.g., people living in Japan have a low risk, but on migrating to the US the risk increases
eventually to that of someone born in the US).

MI affects both men and women, but tends to occur at a younger age in men. The incidence in women
increases after the menopause. The average age of a person having a first MI is 65.1 years for men and 72
years for women.[2] About 90% of patients with CHD report at least one of the major risk factors, including
cigarette smoking, dyslipidaemia, hypertension, diabetes, and abdominal obesity.[6]

The percentage of patients with acute coronary syndrome (ACS) who have STEMI is around 38% in the US,
and around 47% in Europe.[2] About 15% of patients in the US who have an acute MI will die of it, half within
1 hour of the onset of symptoms.[2]

Aetiology
MI is usually a consequence of CAD. Atherosclerosis with plaque fissuring or rupture and thrombus formation
is the underlying aetiology for STEMI in most patients. A small proportion of patients present with STEMI
caused by coronary spasm reducing myocardial perfusion, or following chest trauma or spontaneous
coronary or aortic dissection.

Pathophysiology
Atherosclerotic plaques form gradually over years.[7] They begin with the accumulation of LDL cholesterol
and saturated fat in the intima (the inner layer) of blood vessels. This is followed by the adhesion of
leukocytes to endothelium, then diapedesis and entry into the intima, where they accumulate lipids and
become foam cells. Foam cells are a rich source of proinflammatory mediators. The lesion up to this point is
referred to as a fatty streak, and may be reversible to a certain extent.

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ST-elevation myocardial infarction Basics
Subsequent evolution involves migration of smooth muscle cells from the media, and their proliferation and
deposition of extracellular matrix, including proteoglycans, interstitial collagen, and elastin fibres.[7] Some of
the smooth muscle cells in advanced plaques exhibit apoptosis. Plaques often develop areas of calcification
as they evolve. The plaque initially evolves with the artery remodelling outwards, followed by encroachment

BASICS
on the arterial lumen. Eventually the stenosis can limit flow under conditions of increased demand, causing
angina.

STEMI typically occurs after abrupt and catastrophic disruption of a cholesterol-laden plaque. This results
in exposure of substances that promote platelet activation and aggregation, thrombin generation, and
thrombus formation, causing interruption of blood flow. If the occlusion is severe and persistent, myocardial
cell necrosis follows.

On interruption of blood flow in the coronary artery, the zone of myocardium supplied by that vessel
immediately loses its ability to shorten and perform contractile work. Early hyperkinesis of the non-infarcted
zones occurs, probably as a result of acute compensatory mechanisms including increased sympathetic
activity and Frank-Starling mechanism. As necrotic myocytes slip past each other, the infarction zone thins
and elongates, especially in anterior infarction, leading to infarction expansion.

If a sufficient quantity of myocardium undergoes ischaemic injury, left ventricular (LV) pump function
becomes depressed; cardiac output, stroke volume, blood pressure, and compliance are reduced; and end
systolic volume increases. Clinical heart failure occurs if 25% of myocardium has abnormal contraction, and
cardiogenic shock occurs on loss of >40% of LV myocardium. Decreased compliance and increased LV end
diastolic pressure give rise to diastolic dysfunction.

Classification
Acute coronary syndrome (ACS)
Classically ACS has been divided into 3 clinical categories according to the presence or absence of ST-
segment elevation on presenting ECG and on elevations of myocardial biomarkers such as troponin or CK.[1]
[2]

1. ST-elevation MI (STEMI): ECG shows persistent ST-segment elevation in 2 or more anatomically

contiguous leads.

2. Non-ST elevation MI (NSTEMI): ECG does not show ST-segment elevation, but cardiac biomarkers are
elevated. The ECG may show non-specific ischaemic changes such as ST-segment depression or T-wave
inversion.

3. Unstable angina pectoris: non-specific ischaemic ECG changes, but cardiac biomarkers are normal.

To reflect the pathophysiological continuum between NSTEMI and unstable angina, the American Heart
Association/American College of Cardiology (AHA/ACC) guidelines have grouped these conditions under the
single term 'non-ST-elevation acute coronary syndromes' (NSTE-ACS).[3]

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 ST-elevation myocardial infarction Prevention

Primary prevention
Patients at high risk (≥2 major risk factors) of CAD should aggressively modify risk factors. Major risk factors
include cigarette smoking, hypertension (BP ≥140/90 mmHg or on anti-hypertensive medication), diabetes
mellitus, chronic renal insufficiency, elevated LDL (>3.367 mmol/L [>130 mg/dL]), low HDL (<1.03 mmol/L
[<40 mg/dL]), family history of premature CAD, and age (men aged ≥45 years; women aged ≥55 years).[16]

The US Preventive Services Task Force (USPSTF) has recommended the use of low-dose aspirin for
primary prevention of CVD in adults aged 50 to 59 years with a 10% or greater 10-year CVD risk who are not
at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take daily low-
dose aspirin for at least 10 years.[17] The USPSTF has also recommended that the decision to give low-
dose aspirin should be individualised in adults aged 60 to 69 years with a 10% or greater 10-year CVD risk.
There were no recommendations from the USPSTF for other age groups due to insufficient evidence.

Screening
The US Preventive Services Task Force strongly recommends that screening for lipid disorders should start
at age 35 years in men, and 45 years in women at increased risk for coronary heart disease (i.e., those who
PREVENTION

have 1 or more risk factors [diabetes, hypertension, smoking, obesity, and family history]).[25]

Patients should be evaluated for major cardiovascular risk factors including hypertension, diabetes,
dyslipidaemia, smoking, and renal disease periodically every 3 to 5 years. Aggressive risk factor modification
improves the prognosis and decreases the incidence of myocardial infarction and death.[11]

Secondary prevention
SBP should be maintained at <140 mmHg and DBP <80 mmHg, LDL cholesterol <1.81 millimol/L (70 mg/
dL), and HbA1c <53 mmol/mol (<7%). For those with coronary heart disease, HbA1c may be maintained at
<64 mmol/mol (<8%).[10] Smoking cessation should be actively encouraged.[86] [87]

The ACC/AHA guidelines recommend that, where available, cardiac rehabilitation/secondary prevention
programmes are provided for patients with STEMI, particularly those with multiple modifiable risk factors and/
or those moderate- to high-risk patients in whom supervised exercise training is warranted.[86] [87]

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ST-elevation myocardial infarction Diagnosis

Case history
Case history #1
A middle-aged man with a medical history of hypertension, diabetes, dyslipidaemia, smoking, and family
history of premature CAD presents with retrosternal crushing chest pain (10/10 in intensity), radiating
down the left arm and left side of the neck. He feels nauseated and light-headed and is short of breath.
Examination reveals a hypotensive, diaphoretic man in considerable discomfort with diffuse bilateral rales
on chest auscultation. ECG reveals convex ST-segment elevation in leads V1 to V6.

Case history #2
A 70-year-old woman is 2 days post-operative for knee replacement surgery. Her past medical history
includes type 2 diabetes and a 40-pack-a-year history of smoking. She reports feeling suddenly unwell
with dizziness, nausea, and vomiting. She denies any chest pain. On examination she is hypotensive and
diaphoretic. ECG shows convex ST-segment elevation in leads II, III, and aVF with reciprocal ST segment
depression and T-wave inversion in leads I and aVL.

Other presentations
Patients with STEMI may also be asymptomatic or present with atypical chest pain or epigastric pain.

Step-by-step diagnostic approach

All patients presenting to hospital with chest pain should be urgently evaluated and cardiac and non-cardiac
causes differentiated. History, examination, and initiation of therapy need to be done simultaneously.

History

DIAGNOSIS
A description of the chest pain (i.e., onset, nature, location, radiation, intensity, duration, associated
features) and an enquiry about any associated symptoms or major risk factors for CAD (e.g.,
hypertension, diabetes, dyslipidaemia, obesity, chronic renal insufficiency, smoking) are essential. Other
risk factors for MI include male gender, advanced age, and cocaine use in younger people.

Classically the pain is described as diffuse, severe, 'heavy' or 'crushing', located centrally in the chest,
with radiation to the left arm or jaw and occurring at rest. However, it may be atypical by location (i.e.,
epigastric, jaw, arm, neck pain) or by nature (i.e., burning, throbbing, uneasiness).

Associated features include nausea, vomiting, dyspnoea, palpitations, weakness, dizziness, and light-
headedness. Some patients can present with only these symptoms without chest pain.

Physical examination
The clinical picture of acute MI is variable, and no signs are specific to this condition. On general
inspection, patients are typically distressed, diaphoretic, tachycardic, and appear pale or grey. Rales
on lung examination suggest heart failure. An audible S3 or S4 on cardiac examination indicates poor
cardiac muscle compliance of the infarcted muscle.

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 ST-elevation myocardial infarction Diagnosis
Alternatively, the patient may be in cardiogenic shock with a decreasing level of consciousness, profound
hypotension, acute SOB, and imminent cardiac arrest.

Investigations
ECG should be ordered as early as possible (i.e., within 10 minutes of presentation).[18] If presentation
is outside hospital, a pre-hospital ECG should be obtained as early as possible and sent to the receiving
hospital.[18] Serial ECGs should be checked in patients with a normal initial ECG if there is a high clinical
suspicion for myocardial ischaemia. If the ECG shows ST-segment elevation, the patient should be
urgently assessed for reperfusion therapy.[11] ST depression in two or more leads V1-V4 should be
strongly considered as a posterior STEMI.
[Fig-1]

[Fig-2]

[Fig-3]

[Fig-4]

[Fig-5]

[Fig-6]

[Fig-7]

Cardiac biomarkers (i.e., CK, CK-MB, troponin) are ordered on presentation for any patient with chest
pain and risk factors. A basic metabolic panel should also be done, and serum glucose and lipids
should be measured. Cholesterol levels may be lowered by high catecholamine levels produced by the
myocardial infarction in its early phases, and serum lipids should therefore be repeated in 30 to 60 days.
Copeptin, which is a surrogate for arginine vasopressin, has emerged as a potential biomarker in the
diagnosis of acute MI and the assessment of prognosis.

CXR (with a portable machine) is done to exclude other diagnoses, such as aortic dissection, and to look
DIAGNOSIS

for evidence of heart failure.

The definitive diagnostic test for STEMI is coronary angiography. Angiography can lead to immediate
treatment as the vessel can often be opened and stented at the same procedure. If angiography is not
immediately available, a further history should be taken to exclude contra-indications to thrombolysis.

Echocardiogram is indicated for all patients with acute MI after reperfusion therapy, to assess LV function.

Risk factors
Strong
smoking
• Single most important modifiable risk factor.
• People who smoke 20 or more cigarettes a day have a 2- to 3-fold increased risk of dying from
coronary heart disease compared with non-smokers. Even mild and passive smoking is associated
with increased risk.[8]

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ST-elevation myocardial infarction Diagnosis
hypertension
• Only 2 out of 3 patients with hypertension are diagnosed and only 1 in 3 are adequately controlled on
treatment.
• Systolic blood pressure (SBP) and diastolic blood pressure (DBP) both contribute to development of
CAD.
• Even high-normal blood pressure (SBP 130 to 139 mmHg and DBP 85 to 89 mmHg, or both)
increases risk 2-fold compared with normal levels.[8]

diabetes
• Patients with diabetes have impaired endothelial and smooth muscle function with increased leukocyte
adhesion, promoting atherosclerosis.
• They have a 4-fold increased risk of cardiovascular disease compared with people who do not have
diabetes.[9]
• A HbA1c of <53 mmol/mol (<7%) is the goal of treatment for patients with diabetes.[8] [10] However,
for patients with coronary heart disease, this goal may be less stringent (i.e., <64 mmol/mol
[<8%]).[10]

obesity
• Increased risk in patients with a BMI >25.[8]

metabolic syndrome
• May be present in men with a waist circumference >100 cm (>39 in) and women with a waist
circumference >90 cm (>35 in).[11]
• Characterised by glucose intolerance, hyperinsulinaemia, elevated triglycerides, low HDL cholesterol,
and central obesity and is a marker for increased risk of CAD, even in patients without diabetes.[8] [12]

dyslipidaemia
• Elevated LDL cholesterol, elevated triglycerides, decreased HDL, and elevated ratio of LDL to HDL are
all independently associated with increased risk of atherosclerosis.

DIAGNOSIS
• Early studies on cholesterol showed that a reduction in serum cholesterol by diet and medications
reduces non-fatal MI by 25% and fatal MI by 14%.[11]
• Current guidelines recommend high-dose statin therapy in patients with known CAD or CAD
equivalent, irrespective of LDL levels.[13] Other lipid-lowering treatments can be considered in patients
who are contraindicated or intolerant of statins.

renal insufficiency
• Renal dysfunction is a marker of vascular damage.[14]
• Excess cardiovascular disease in patients with chronic kidney disease is caused, at least in part, by
higher prevalence of traditional risk factors in this group.[8]

established CAD
• 18% of coronary events are in patients with preceding long-standing angina pectoris.[8]

FHx of premature CAD

• Onset affecting first-degree male family member aged <55 years or female family member <65
years.[8]

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 ST-elevation myocardial infarction Diagnosis
cocaine use
• Regular use of cocaine predisposes young people (aged 18-45 years) to MI.
• The risk is increased by 24 times over baseline 1 hour following cocaine use, and chronic exposure
appears to accelerate atherosclerosis.[15]

male gender
• Men have an increased risk of acute MI compared with pre-menopausal women of the same age. The
incidence is similar in post-menopausal women and men of the same age.

advanced age
• Older patients are at an increased risk of acute MI. Average annual rates of first major cardiovascular
events rise from 7 per 1000 men at ages 35 to 44 years to 68 per 1000 at ages 85 to 94 years. For
women, comparable rates occur 10 years later in life.[8]

History & examination factors

Key diagnostic factors
chest pain (common)
• Classically presents with diffuse, severe chest pain that can occur at rest or with exertion, is heavy in
nature, located centrally with radiation to the left arm or jaw, and lasts for at least 20 minutes.

dyspnoea (common)
• Common feature associated with MI due to pulmonary congestion from diastolic dysfunction.

pallor (common)
• Common feature associated with MI due to high sympathetic output.

diaphoresis (common)
DIAGNOSIS

• Common feature associated with MI due to high sympathetic output.

cardiogenic shock (uncommon)

• Associated with reduced consciousness, profound hypotension, acute SOB, and imminent cardiac
arrest.

Other diagnostic factors

nausea and/or vomiting (common)
• Common feature associated with MI. Non-specific for MI, but commonly associated with inferior-wall
MI due to increased vagal tone, and can be the only indicator of inferior-wall MI.

dizziness or light-headedness (common)

• Common feature associated with MI due to hypotension or bradycardia.

weakness (common)
• Common feature associated with MI due to hypotension or bradycardia.

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ST-elevation myocardial infarction Diagnosis
distressed (common)
• Common feature associated with MI.
• Patients often report a sense of doom or death.

tachycardia (common)
• Common feature associated with MI, especially anterior-wall MI, due to high sympathetic output.

additional heart sounds (common)

• An audible S3 or S4 on cardiac examination indicates poor cardiac muscle compliance of the infarcted
muscle.

atypical location or nature of pain (uncommon)

• Pain may be atypical by location (i.e., epigastric, jaw, arm, neck pain) or by nature (i.e., burning,
throbbing, uneasiness).

reduced consciousness (uncommon)

• Associated with severe shock or bradycardia and hypotension.

hypotension (uncommon)
• Associated with shock or with inferior-wall MI. Associated right-ventricular infarction should be
considered if patients are hypotensive.

abnormal breath sounds (uncommon)

• Rales on lung examination suggest heart failure.

Diagnostic tests
1st test to order

DIAGNOSIS
Test Result
serum lipids normal or elevated
• Cholesterol levels may be lowered by high catecholamine levels
produced by the myocardial infarction in its early phases, and serum
lipids should therefore be repeated in 30 to 60 days.
glucose normal or elevated
• Determines if any treatment for glucose abnormalities is necessary.
• Hyperglycaemia is common in the setting of acute MI, with or without
a history of diabetes.[19] Follow-up is needed to determine if a
diagnosis of diabetes exists after an acute MI episode.
electrolytes, urea, and creatinine may be abnormal
• Determines if any disturbances that may need management are
present.

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 ST-elevation myocardial infarction Diagnosis

Test Result
ECG ST-segment elevation of
at least 1 mm in 2 or more
• Ordered as early as possible (i.e., within 10 minutes of presentation)
contiguous leads
for any patient with a history of chest pain and suspected STEMI.[18]
If presentation is outside hospital, a pre-hospital ECG should be
obtained and sent to the receiving hospital.[18]
[Fig-3]

[Fig-4]

[Fig-5]

[Fig-6]

[Fig-7]
• If the ECG shows ST-segment elevation, the patient should be
urgently assessed for reperfusion therapy.[11] ST depression in two
or more leads V1-V4 should be strongly considered as a posterior
STEMI and treated as above.
[Fig-1]

[Fig-2]
• Leads are left in place to help with comparison for subsequent ECGs.
Serial ECGs should be obtained every 5 to 10 minutes in patients
with high clinical suspicion and initial normal ECG.[11]
• In patients with inferior STEMI, right-sided ECG leads should be
obtained to screen for ST elevation, as right ventricular infarction is
present in 40% of inferior infarcts.[20]
cardiac biomarkers elevated CK, CK-MB, and
troponin
• Cardiac biomarkers are ordered on presentation for any patient with
chest pain and risk factors.
• CK is not specific for myocardial damage and can be released with
any muscle damage.
DIAGNOSIS

• The isoenzyme CK-MB is more cardiac-specific but can also be

released from skeletal muscle.
• Troponins are highly specific for myocardial damage and will be
elevated around 4 to 6 hours after injury. They remain elevated for
around 10 days, which can make it difficult to determine the time of
myocardial injury.[21] Patients with elevated troponin levels have a
worse prognosis than those with normal troponin levels.[22]
CXR normal
• Patients with STEMI should have a portable CXR, but this should not
delay implementation of reperfusion therapy.[11]
• Used to exclude possible alternative diagnosis of cause of chest pain
and to assess current cardiac functioning.
• Widened mediastinum suggests aortic dissection.
• Pulmonary oedema indicates impaired cardiac function.
coronary angiogram presence of thrombus
with occlusion of the
• Diagnostic modality of choice to confirm acute MI in patients with
artery
STEMI.
• Coronary angiography carried out as early as possible, with target
first medical contact-to-device time <90 minutes in patients with
STEMI to facilitate early reperfusion and save myocardium.

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ST-elevation myocardial infarction Diagnosis

Other tests to consider

Test Result
echocardiogram hypokinesis, dyskinesis,
or akinesis
• Indicated for all patients with acute MI after reperfusion therapy, to
assess LV function.
• Useful for further risk stratification in patients with an atypical
presentation.
• Echocardiography is carried out in patients with acute
decompensation after acute MI, to evaluate for complications such as
mitral regurgitation, ventricular septal rupture, or ventricular free wall
rupture.

Emerging tests

Test Result
copeptin elevated
• Copeptin is a surrogate for arginine vasopressin and has emerged
as a potential biomarker in the diagnosis of acute MI and the
assessment of prognosis.[23] Although troponin appears to
have better diagnostic accuracy than copeptin for acute MI, the
combination of copeptin and troponin has been shown to significantly
improve the sensitivity and negative predictive value compared with
troponin alone.

Differential diagnosis

Condition Differentiating signs / Differentiating tests

symptoms

DIAGNOSIS
Unstable angina • Clinical presentation may not • ECG may show non-specific
differentiate. ST-segment and T-wave
changes.
• Cardiac biomarkers are
normal.

Non-ST-elevation • Clinical presentation may not • ECG may show non-specific

myocardial infarction differentiate. ST-segment and T-wave
changes, but does not show
ST-segment elevation.
• Cardiac biomarkers are
elevated in both non-ST-
elevation MI and STEMI.

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 ST-elevation myocardial infarction Diagnosis

Condition Differentiating signs / Differentiating tests

symptoms
Aortic dissection • Patients typically present • CXR may show a widened
with tearing chest pain, mediastinum.
notably between the • ECG may be unremarkable,
shoulder blades. show sinus tachycardia, or
• They can be in show ST-segment changes
considerable distress and if the dissection extends
haemodynamically unstable. proximally and involves the
• Peripheral pulses may be coronary ostium.
unequal or absent distally. • A CT of chest and abdomen
with IV contrast showing the
presence of a dissection flap
and a true lumen and false
lumen is diagnostic for aortic
dissection.
• A trans-oesophageal
echocardiogram may also
show the dissection flap with
the true and false lumens.
DIAGNOSIS

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ST-elevation myocardial infarction Diagnosis

Condition Differentiating signs / Differentiating tests

symptoms
Pulmonary embolism • Patients classically present • Patients are hypoxic with an
with acute onset of sharp increased arterial-alveolar
stabbing chest pain that gradient on the arterial blood
is pleuritic in nature and gas.
associated with SOB. • ECG may show sinus
• A background of increased tachycardia or right
clotting tendency, such ventricular strain with
as known inheritable prominent S wave in lead
thrombophilia or connective I, prominent Q in lead
tissue disease; known deep III, and flipped T in lead
venous thrombosis (DVT); or III (S1Q3T3), or can be
previous PE increases the unremarkable.
likelihood of the diagnosis. • D-dimer is useful for
• Other risk factors screening. A negative
include recent prolonged d-dimer excludes PE; if
immobilisation and limb positive, further work-up is
trauma. required to confirm PE.
• V/Q scan of the lungs will
show a mismatch between
ventilation and perfusion
images. A high-probability
scan confirms PE and a
normal scan excludes PE.
Indeterminate scans need
further work-up if indicated
by the clinical picture.
• Spiral CT scanning of the
chest with contrast will
show a filling defect in the
pulmonary artery if a blood
clot is present.
• By consensus, pulmonary
angiography is the best test

DIAGNOSIS
to show thrombus in the
pulmonary artery; however,
it is an invasive study and is
uncommonly used.

Pneumothorax • Patients present with sudden • CXR shows a visceral

onset of pleuritic chest pleural line.
discomfort and SOB.
• Tachycardia, hypotension,
and cyanosis suggest a
tension pneumothorax.
• Known underlying medical
conditions that predispose
to pneumothorax, such
as chronic obstructive
pulmonary disease,
connective tissue disease,
or recent chest trauma, may
support this diagnosis.

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 ST-elevation myocardial infarction Diagnosis

Condition Differentiating signs / Differentiating tests

symptoms
Pneumonia • Patients usually have • WBC count is usually
an insidious onset of elevated with neutrophilia.
fevers, cough (that may be • CXR shows increased
productive of sputum), and alveolar markings.
SOB. • Blood and sputum cultures
• Chest discomfort may be may be positive for an
pleuritic in nature. infective organism.
• Examination will usually
confirm pneumonic
consolidation with decreased
resonance, decreased air
entry, and rales over the
affected lung.

Pericarditis • Patients can present with • ECG may have diffuse ST-
chest pain of varying quality segment elevation that
that is typically better on is concave up ('saddle-
sitting up and leaning shaped') with PR segment
forwards and worse with depression.[24]
lying down. • Cardiac biomarkers
• There may be a history of can be elevated if
recent viral syndrome and inflammation extends into
a pericardial friction rub on the myocardium.
clinical examination. • Inflammatory markers such
as CRP and ESR may be
elevated.
• CXR demonstrating a
globular cardiac shadow is
suggestive.
• Echocardiogram may show
a pericardial effusion or may
be unremarkable.
DIAGNOSIS

Myocarditis • Patients often have a • ECG changes and cardiac

recent history of influenza- biomarkers can mimic MI.
like illness or underlying • Inflammatory markers (ESR
autoimmune condition such and CRP) and autoimmune
as SLE. assays may be elevated.
• They are likely to be young • Test of choice is cardiac
and often do not have risk magnetic resonance
factors for CAD. imaging, with delayed
• Myocarditis is more likely enhancement imaging
to present with symptoms showing an epicardial or
of cardiac failure than with mid-myocardial involvement.
chest pain.

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ST-elevation myocardial infarction Diagnosis

Condition Differentiating signs / Differentiating tests

symptoms
Gastro-oesophageal reflux • Patients present with burning • Diagnosis is usually clinical.
disease retrosternal discomfort that is • Cardiac biomarkers, ECG,
relieved by antacids. and CXR are normal.
• Discomfort/pain is usually • Oesophagogastroduodenoscopy
non-exertional. (OGD) is indicated for
patients with persistent or
atypical symptoms and may
show oesophagitis (erosions,
ulcerations, strictures) or
Barrett's oesophagus.

Oesophageal spasm • Patients present with • Cardiac biomarkers, ECG,

squeezing retrosternal and CXR are normal.
discomfort that may be • Oesophageal manometry or
relieved by glyceryl trinitrate barium swallow may show
(due to relaxation of the evidence of dysmotility.
spasm).
• Discomfort/pain is usually
non-exertional.

Costochondritis • Musculoskeletal chest wall • Cardiac biomarkers, ECG,

discomfort that is worse with and CXR are normal.
certain movement and deep
breaths.
• Focal tenderness over the
costochondral joints may be
present.

Anxiety or panic at tack • Normal examination; • Cardiac biomarkers, ECG,

however, evidence and CXR are all normal.
of hyperventilation is
sometimes present.

DIAGNOSIS
Diagnostic criteria
ST elevation on ECG[1]
New or presumed new ST-segment elevation at the J point in 2 or more contiguous leads with the cut-off
points of ≥0.2 mV in leads V1, V2, or V3 and ≥0.1 mV in other leads. Note: ST depressions in leads V1-V4
should be considered as a posterior STEMI.

Criteria for acute, evolving, or recent MI[1]

Either one of the following criteria:

1. Typical rise of biomarkers of myocardial necrosis (troponin or CK-MB) with at least one of the following:

• Ischaemic symptoms
• Development of pathological Q waves on ECG
• ECG changes indicative of ischaemia (ST-segment elevation or depression)

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 ST-elevation myocardial infarction Diagnosis
• Coronary artery intervention (e.g., coronary angiography).

2. Pathological findings of acute MI.

Criteria for established MI[1]

Any one of the following:

1. Development of pathological Q waves on serial ECGs. The patient may or may not remember previous
symptoms. Biochemical markers of myocardial necrosis may have normalised, depending on the length of
time that has passed since the infarct developed.

2. Pathological findings of a healed or healing MI.

3. Cardiac magnetic resonance imaging with the delayed enhancement imaging showing a classic sub-
endocardial or transmural infarct in a coronary artery distribution.
DIAGNOSIS

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ST-elevation myocardial infarction Treatment

Step-by-step treatment approach

The main goals of treatment are to limit myocardial damage by restoring myocardial blood flow as quickly as
possible and to decrease subsequent remodelling, which can have deleterious effects on ventricular function
and prognosis.[11] [21]

Immediate and prompt revascularisation with percutaneous coronary intervention (PCI) within 90 minutes
of first presentation, or thrombolysis within 12 hours of symptom onset, can prevent or decrease myocardial
damage and decrease morbidity and mortality by preventing acute complications. It is strongly recommended
that local communities or regional areas should develop a rapid response system for treatment of STEMI.

Initial management
Patient should be admitted to a unit with continuous cardiac monitoring and started on strict bed rest
for the first 12 to 24 hours. Supplemental oxygen is indicated only if oxygen saturation is less than
94%.[18] [26] Guidelines recommend that oxygen should not be routinely administered in normoxic
patients with suspected or confirmed acute coronary syndrome (ACS).[18] [26] Aspirin is given
immediately.1[A]Evidence

Adequate analgesia with morphine is essential to relieve pain and its related sympathetic activity, which
can further increase myocardial oxygen demand.

Glyceryl trinitrate should also be given immediately, if the patient is not hypotensive, as it reduces
myocardial oxygen demand and lessens ischaemia, and may rarely abort MI if there is coronary spasm.
However, it should not be given in doses that interfere with analgesic therapy. Sublingual dosing should
be given first to all patients, while intravenous therapy is reserved for patients with hypertension or heart
failure.

Haemodynamically unstable
Cardiogenic shock occurs in 5% of people surviving the first hour after an acute MI, with a mortality of
50% to 80% in the first 48 hours.[9]

Emergency revascularisation within 48 hours of MI reduces mortality at 12 months compared with medical
treatment alone.[9] 2[C]Evidence

If revascularisation fails, or there is persistent pain or haemodynamic instability, urgent coronary artery
bypass graft (CABG) is recommended.

Patients with low cardiac output states and cardiogenic shock may benefit from a dobutamine
infusion.3[C]Evidence Guidelines also recommend the use of an intra-aortic balloon pump (IABP) or a
ventricular mechanical circulatory support device if pharmacological measures do not quickly improve
shocked state.[11] However, results from observational studies appear to be conflicting for IABP in acute
MI, and in RCTs it has not been shown to reduce mortality after acute MI even in patients with cardiogenic
shock.[27]
TREATMENT

Antiplatelet and anticoagulant therapy

• Antiplatelet and anticoagulant agents (e.g., oral aspirin; P2Y12 inhibitors [clopidogrel, prasugrel,
ticagrelor, or cangrelor]; glycoprotein [GP] IIb/IIIa inhibitors; and intravenous heparin) are also
indicated for the treatment of STEMI as they limit secondary thrombosis, by inhibiting platelet

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BMJ Best Practice topics are regularly updated and the most recent version
19
of the topics can be found on [Link] . Use of this content is
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 ST-elevation myocardial infarction Treatment
activation and subsequent platelet aggregation. Cangrelor, an intravenous P2Y12 inhibitor,
can be used as an adjunct to PCI to reduce the risk of periprocedural MI, repeat coronary
revascularisation, and stent thrombosis in patients who have not previously been treated with a
P2Y12 inhibitor and are not being treated with a GPIIb/IIIa inhibitor. [28]
• Bivalirudin can be used as a single-agent alternative to a GPIIb/IIIa inhibitor and heparin.[29]
Bivalirudin has been shown to significantly reduce 30-day rates of major bleeding and other
adverse clinical events compared with a combination of a GPIIb/IIIa inhibitor plus heparin.[30] [31]
4[A]Evidence However, choice of anticoagulation is based on clinician preference.[32] [33] [34]
Supportive measures

• Adequate analgesia with morphine is essential to relieve pain and its related sympathetic activity,
which can further increase myocardial oxygen demand.
• Supplemental oxygen is indicated only if oxygen saturation is less than 94%.[18] [26] Guidelines
recommend that oxygen should not be routinely administered in normoxic patients with suspected
or confirmed ACS.[18] [26]
• Glycaemic control, including the use of insulin where appropriate, should also be maintained,
although rigid control has not been shown to be beneficial in critically ill patients.[10]

Electrically unstable
Emergency revascularisation is recommended in patients with a cardiac arrest who have been
resuscitated and are haemodynamically stable and show ECG evidence for a STEMI. Hypothermia is
recommended for cardiac arrest patients who have been resuscitated and remain comatose.

Haemodynamically stable: within 90 minutes of first medical

contact
Percutaneous coronary intervention (PCI)

• Primary PCI, with stent placement (using bare metal stents or drug-eluting stents), is the preferred
method of revascularisation, provided it can be performed in a timely manner with an experienced
team of operators. Primary PCI should be considered in patients presenting within 12 hours of
symptom onset or in patients presenting after 12 hours but with ongoing ischaemia.[11] [35] [36]
[37] 5[C]Evidence It involves immediate transfer to the catheterisation laboratory with the intention
of opening the artery with stent placement. Drug-eluting stents are preferred.[38] Third-generation
drug-eluting stents composed of biodegradable polymers are currently being investigated.[39] [40]
[Fig-8]

[Fig-9]

[Fig-10]
• Patients with acute MI frequently have multi-vessel PCI. In the past, guidelines recommended
against PCI of non-culprit vessels at the time of primary PCI, and they did not address staged PCI
of non-culprit vessels. However, based on current RCT evidence, guidelines now recommend that
TREATMENT

a strategy of multi-vessel PCI may be considered either at the time of primary PCI or as a staged
procedure in selected patients with STEMI and multi-vessel disease who are haemodynamically
stable.[41] [42] [43] [44] However, physicians should consider factors such as clinical data,
haemodynamic stability, lesion severity/complexity, and risk of contrast nephropathy to determine
the optimal PCI strategy.

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ST-elevation myocardial infarction Treatment
• Guidelines also recommend against routine manual aspiration thrombectomy before primary
PCI as the evidence does not suggest any benefit of this procedure over PCI alone.[41] [45]
Furthermore, studies have suggested that routine aspiration thrombectomy might increase the risk
of stroke.[46] [47]

• Many hospitals have 24-hour PCI capacity; however, in facilities without catheterisation
laboratories, routine transfer to a PCI facility should be considered for all patients within 30 minutes
of presentation, and ideally within 30 minutes of symptom onset.
• Radial approach is preferable to femoral approach as it results in better outcomes (e.g., reduction
in mortality, major adverse cardiovascular events, major bleeding, and bleeding complications)
particularly if the operator is experienced in radial access.[37] [48] [49]

• Early revascularisation prevents scar formation, decreases the occurrence of heart failure later on,
and decreases the incidence of future ventricular arrhythmias caused by scar formation.
Coronary artery bypass graft (CABG)

• Emergency revascularisation with CABG should be strongly considered in patients who fail PCI,
and should be performed within 12 hours of symptom onset, ideally within 6 hours.
Antiplatelet and anticoagulant therapy

• Antiplatelet and anticoagulant agents (e.g., oral aspirin; P2Y12 inhibitors [clopidogrel, prasugrel,
ticagrelor, or cangrelor]; GPIIb/IIIa inhibitors; and intravenous heparin) are also indicated for
the treatment of STEMI as they limit secondary thrombosis, by inhibiting platelet activation and
subsequent platelet aggregation. Cangrelor, an intravenous P2Y12 inhibitor, can be used as an
adjunct to PCI to reduce the risk of periprocedural MI, repeat coronary revascularisation, and stent
thrombosis in patients who have not previously been treated with a P2Y12 inhibitor and are not
being treated with a GPIIb/IIIa inhibitor.[28]

• Bivalirudin can be used as a single-agent alternative to a GPIIb/IIIa inhibitor and heparin.[29]

Bivalirudin has been shown to significantly reduce 30-day rates of major bleeding and other
adverse clinical events compared with a combination of a GPIIb/IIIa inhibitor plus heparin.[30] [31]
4[A]Evidence However, choice of anticoagulation is based on clinician preference.[32] [33] [34]
Supportive measures

• Oral beta-blockers should be started as soon as possible, as they decrease infarction size,
although care should be taken in patients with evidence of heart failure, hypotension, bradycardia,
or asthma.[50] 6[A]Evidence Intravenous beta-blockers are recommended only in patients who are
hypertensive or have ongoing ischaemia.[11] [51]

• Statin therapy should also be initiated in high doses for plaque stabilisation if there are no
contraindications and if tolerated, whatever the results of serum lipid measurements.[13] Adding
ezetimibe to a statin regimen may also be considered in patients requiring additional lowering of
LDL.[52]
• Evolocumab and alirocumab are proprotein convertase subtilisin/kexin type 9 (PCSK9) antibody
TREATMENT

inhibitors approved for use as adjunct therapy to diet and maximally tolerated statin therapy for
adult patients with heterozygous familial hypercholesterolaemia (HeFH), or clinical atherosclerotic
CVD, who require additional lowering of LDL.

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 ST-elevation myocardial infarction Treatment
• Non-statin lipid-lowering treatments (e.g., ezetimibe, evolocumab, alirocumab) can be considered if
statins are contraindicated or in patients who are intolerant of statins.
• Eplerenone should be added to optimal medical therapy in eligible patients (creatinine <221
micromol/L [<2.5 mg/dL] in men and <177 micromol/L [<2.0 mg/dL] in women; potassium <5.0
mmol/L [<5.0 mEq/L]) 3 to 14 days after STEMI with ejection fraction <0.40, and either symptomatic
heart failure or diabetes mellitus. Earlier initiation of the drug (<7 days) has been shown to
significantly reduce the rates of all-cause mortality, sudden cardiac death, and cardiovascular
mortality/hospitalisation, whereas initiation >7 days has not been shown to have a significant effect
on outcomes.[53]

• Adequate analgesia with morphine is essential to relieve pain and its related sympathetic activity,
which can further increase myocardial oxygen demand. Nitroglycerin should also be given
immediately if the patient is not hypotensive.

• Supplemental oxygen is indicated only if oxygen saturation is less than 94%.[18] [26] Guidelines
recommend that oxygen should not be routinely administered in normoxic patients with suspected
or confirmed ACS.[18] [26]

• Glycaemic control, including the use of insulin where appropriate, should also be maintained,
although rigid control has not been shown to be beneficial in critically ill patients.[10]

• Non-steroidal anti-inflammatory drugs should be avoided, and stopped if possible in patients

already on them.[54]

Haemodynamically stable: >90 minutes after first medical contact

and within 12 hours of symptom onset with no contraindications
to thrombolysis
Thrombolysis is indicated if PCI is not available within 90 minutes of first medical contact and the patient
has no contra-indications to thrombolytic therapy.7[B]Evidence It should be initiated within 30 minutes
of presentation. Thrombolysis is used only once on initial diagnosis, and this must be within 12 hours
of symptom onset (ideally within 3 hours) as the efficacy of fibrinolytic agents in lysing the thrombus
diminishes over time. Therapy within the first 2 hours (particularly the first hour) can occasionally abort MI
and dramatically reduce mortality.[11] 8[B]Evidence

Absolute contra-indications for thrombolysis are any prior intracranial haemorrhage, known malignant
intracranial lesion or structural cerebral vascular lesion (e.g., arteriovenous malformations), ischaemic
stroke within previous 3 months, suspected aortic dissection, active bleeding or bleeding diathesis, and
significant closed head or facial trauma within previous 3 months.[11]

Thrombolytics can be associated with an increased risk of bleeding, in addition to the risk associated with
other antithrombotic and/or antiplatelet agents used, and can also cause intracranial haemorrhage.

Transfer to a PCI-capable hospital within 24 hours should be considered in all patients undergoing
fibrinolytic therapy. Angiography with intent to revascularise the culprit vessel should be considered within
24 hours in patients after successful fibrinolytic therapy.[37]
TREATMENT

Emergency PCI after thrombolysis is recommended in high-risk patients with: ongoing chest pain;
haemodynamic, mechanical, or electrical instability; or shock. Patients should be transferred for PCI
as soon as possible after thrombolysis.[55] Those transferred within 6 hours after thrombolytic therapy
had significantly fewer ischaemic complications than those who were only transferred if they had

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ST-elevation myocardial infarction Treatment
complications.[56] Rescue PCI is associated with improved clinical outcomes after failed fibrinolytic
therapy.[57] Facilitated PCI, that is administering half- or full-dose thrombolytic therapy prior to transfer in
patients being transferred to a centre for immediate PCI, has not been shown to be beneficial, and while
commonly performed, is highly controversial and is not universally recommended.[58]

Antiplatelet and anticoagulant agents (e.g., oral aspirin and clopidogrel; intravenous heparin) are
also indicated for the treatment of STEMI, as this limits secondary thrombosis by inhibiting platelet
activation and subsequent platelet aggregation. Prasugrel and ticagrelor are not recommended in patients
undergoing thrombolysis as they have not been adequately studied in this setting.[59] GPIIb/IIIa inhibitors
are not indicated in STEMI if thrombolytic therapy is indicated.9[C]Evidence Low molecular weight heparin
should be considered instead of unfractionated heparin in patients treated with thrombolysis.[60] [61]
10[A]Evidence

Supportive measures are the same as those for patients who undergo PCI within 90 minutes.

Haemodynamically stable: >90 minutes after first medical contact

and within 12 hours of symptom onset with contraindications to
thrombolysis
In patients with contraindications to thrombolysis, PCI is indicated even if it cannot occur within 90
minutes. Patients should be transferred for PCI as soon as possible.

Antiplatelet and anticoagulant agents (e.g., aspirin plus a P2Y12 inhibitor [clopidogrel, prasugrel,
ticagrelor, or cangrelor]; GPIIb/IIIa inhibitors; and intravenous heparin) are also indicated for the treatment
of STEMI, as this limits secondary thrombosis by inhibiting platelet activation and subsequent platelet
aggregation. Cangrelor, an intravenous P2Y12 inhibitor, can be used as an adjunct to PCI to reduce the
risk of periprocedural MI, repeat coronary revascularisation, and stent thrombosis in patients who have
not previously been treated with a P2Y12 inhibitor and are not being treated with a GPIIb/IIIa inhibitor.[28]
Bivalirudin can be used as a single-agent alternative to a GPIIb/IIIa inhibitor and heparin.[29] However,
choice of anticoagulation is based on clinician preference.

Supportive measures are the same as those for patients who undergo PCI within 90 minutes.

Haemodynamically stable: no access to PCI within 90 minutes and

>12 hours after symptom onset
Even beyond 12 hours, if there are persistent symptoms, it is possible to obtain benefits from
revascularisation, which would be best performed with percutaneous coronary revascularisation. Stable
patients in whom PCI or thrombolysis is not indicated are treated with pharmacotherapy only, including
beta-blockers and antiplatelet and anticoagulation therapy. If the patient becomes unstable, they should
undergo late PCI, which can be done up to 36 hours after the onset of symptoms.[62]

Supportive measures are the same as those for patients who undergo PCI within 90 minutes.

Ongoing pharmacotherapy
ACE inhibitors should be started early (i.e., when patient is haemodynamically stable, optimally on
TREATMENT

first day in hospital) for a favourable effect on ventricular remodelling, especially in patients with
large anterior wall MI.11[A]Evidence Statins and anti-platelet therapy should be continued. Beta-
blockers12[C]Evidence should be continued for 3 years - continuing use should then be evaluated on the
basis of comorbidities.[50] [63]

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 ST-elevation myocardial infarction Treatment
Chronic nitrate use is not routinely recommended after a MI, but may be used as part of the treatment
plan for CHF and for chronic angina.

Treatment details overview

Consult your local pharmaceutical database for comprehensive drug information including contraindications,
drug interactions, and alternative dosing. ( see Disclaimer )

Presumptive ( summary )
Patient group Tx line Treatment

suspected MI 1st aspirin plus ox ygen

ongoing chest pain plus morphine

ongoing chest pain adjunct glyceryl trinitrate

Acute ( summary )
Patient group Tx line Treatment

haemodynamically unstable 1st emergency revascularisation

plus anticoagulation

plus aspirin + P2Y12 inhibitor

plus morphine

adjunct ox ygen

adjunct glucose control

adjunct inotrope support or intra-aortic balloon

pump (IABP) or ventricular mechanical
circulatory support

electrically unstable post- 1st emergency revascularisation

cardiac arrest

electrically unstable post- plus hypothermia

cardiac arrest

electrically unstable post- plus anticoagulation

cardiac arrest

electrically unstable post- plus aspirin + P2Y12 inhibitor

TREATMENT

cardiac arrest

electrically unstable post- plus beta-blocker

cardiac arrest

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ST-elevation myocardial infarction Treatment

Acute ( summary )
electrically unstable post- plus statin
cardiac arrest

electrically unstable post- adjunct ezetimibe

cardiac arrest

electrically unstable post- adjunct evolocumab or alirocumab

cardiac arrest

electrically unstable post- adjunct eplerenone

cardiac arrest

electrically unstable post- adjunct morphine

cardiac arrest

electrically unstable post- adjunct glyceryl trinitrate

cardiac arrest

electrically unstable post- adjunct ox ygen

cardiac arrest

electrically unstable post- adjunct glucose control

cardiac arrest

access to PCI within 90 1st revascularisation

minutes

access to PCI within 90 plus anticoagulation

minutes

access to PCI within 90 plus aspirin + P2Y12 inhibitor

minutes

access to PCI within 90 plus beta-blocker

minutes

access to PCI within 90 plus statin

minutes

access to PCI within 90 adjunct ezetimibe

minutes

access to PCI within 90 adjunct evolocumab or alirocumab

minutes

access to PCI within 90 adjunct eplerenone

minutes

access to PCI within 90 adjunct morphine

minutes

access to PCI within 90 adjunct glyceryl trinitrate

minutes

access to PCI within 90 adjunct ox ygen

TREATMENT

minutes

access to PCI within 90 adjunct glucose control

minutes

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 ST-elevation myocardial infarction Treatment

Acute ( summary )
no access to PCI within 90 1st thrombolysis
minutes: within 12 hours
of symptom onset with
no contraindication to
thrombolysis

no access to PCI within 90 adjunct transfer for PCI after thrombolysis

minutes: within 12 hours
of symptom onset with
no contraindication to
thrombolysis

no access to PCI within 90 plus anticoagulation

minutes: within 12 hours
of symptom onset with
no contraindication to
thrombolysis

no access to PCI within 90 plus aspirin + clopidogrel

minutes: within 12 hours
of symptom onset with
no contraindication to
thrombolysis

no access to PCI within 90 plus beta-blocker

minutes: within 12 hours
of symptom onset with
no contraindication to
thrombolysis

no access to PCI within 90 plus statin

minutes: within 12 hours
of symptom onset with
no contraindication to
thrombolysis

no access to PCI within 90 adjunct ezetimibe

minutes: within 12 hours
of symptom onset with
no contraindication to
thrombolysis

no access to PCI within 90 adjunct evolocumab or alirocumab

minutes: within 12 hours
of symptom onset with
no contraindication to
thrombolysis

no access to PCI within 90 adjunct eplerenone

minutes: within 12 hours
of symptom onset with
no contraindication to
thrombolysis
TREATMENT

no access to PCI within 90 adjunct morphine

minutes: within 12 hours
of symptom onset with

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ST-elevation myocardial infarction Treatment

Acute ( summary )
no contraindication to
thrombolysis

no access to PCI within 90 adjunct glyceryl trinitrate

minutes: within 12 hours
of symptom onset with
no contraindication to
thrombolysis

no access to PCI within 90 adjunct ox ygen

minutes: within 12 hours
of symptom onset with
no contraindication to
thrombolysis

no access to PCI within 90 adjunct glucose control

minutes: within 12 hours
of symptom onset with
no contraindication to
thrombolysis

no access to PCI within 1st consider PCI

90 minutes: within 12
hours of symptom onset
with contraindication to
thrombolysis

no access to PCI within plus anticoagulation

90 minutes: within 12
hours of symptom onset
with contraindication to
thrombolysis

no access to PCI within plus aspirin + P2Y12 inhibitor

90 minutes: within 12
hours of symptom onset
with contraindication to
thrombolysis

no access to PCI within plus beta-blocker

90 minutes: within 12
hours of symptom onset
with contraindication to
thrombolysis

no access to PCI within plus statin

90 minutes: within 12
hours of symptom onset
with contraindication to
thrombolysis

no access to PCI within adjunct ezetimibe

90 minutes: within 12
TREATMENT

hours of symptom onset

with contraindication to
thrombolysis

no access to PCI within adjunct evolocumab or alirocumab

90 minutes: within 12

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27
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 ST-elevation myocardial infarction Treatment

Acute ( summary )
hours of symptom onset
with contraindication to
thrombolysis

no access to PCI within adjunct eplerenone

90 minutes: within 12
hours of symptom onset
with contraindication to
thrombolysis

no access to PCI within adjunct morphine

90 minutes: within 12
hours of symptom onset
with contraindication to
thrombolysis

no access to PCI within adjunct glyceryl trinitrate

90 minutes: within 12
hours of symptom onset
with contraindication to
thrombolysis

no access to PCI within adjunct ox ygen

90 minutes: within 12
hours of symptom onset
with contraindication to
thrombolysis

no access to PCI within adjunct glucose control

90 minutes: within 12
hours of symptom onset
with contraindication to
thrombolysis

no access to PCI within 1st revascularisation

90 minutes: >12 hours of
symptom onset

no access to PCI within plus beta-blocker

90 minutes: >12 hours of
symptom onset

no access to PCI within plus anticoagulation

90 minutes: >12 hours of
symptom onset

no access to PCI within plus aspirin + P2Y12 inhibitor

90 minutes: >12 hours of
symptom onset

no access to PCI within plus statin

90 minutes: >12 hours of
symptom onset
TREATMENT

no access to PCI within adjunct ezetimibe

90 minutes: >12 hours of
symptom onset

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ST-elevation myocardial infarction Treatment

Acute ( summary )
no access to PCI within adjunct evolocumab or alirocumab
90 minutes: >12 hours of
symptom onset

no access to PCI within adjunct eplerenone

90 minutes: >12 hours of
symptom onset

no access to PCI within adjunct morphine

90 minutes: >12 hours of
symptom onset

no access to PCI within adjunct glyceryl trinitrate

90 minutes: >12 hours of
symptom onset

no access to PCI within adjunct ox ygen

90 minutes: >12 hours of
symptom onset

no access to PCI within adjunct glucose control

90 minutes: >12 hours of
symptom onset

Ongoing ( summary )
Patient group Tx line Treatment

post-STEMI 1st dual antiplatelet therapy

plus ACE inhibitor

plus beta-blocker

plus statin

adjunct ezetimibe

adjunct evolocumab or alirocumab

adjunct eplerenone
TREATMENT

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 ST-elevation myocardial infarction Treatment

Treatment options

Presumptive
Patient group Tx line Treatment

suspected MI 1st aspirin plus ox ygen

» Patient should be admitted to a unit with
continuous cardiac monitoring and started on
strict bed rest for the first 12 to 24 hours.

» Supplemental oxygen is indicated only if

oxygen saturation is less than 94%.[18] [26]
Guidelines recommend that oxygen not be
routinely administered in normoxic patients with
suspected or confirmed ACS.[18] [26]

» Aspirin is given immediately.1[A]Evidence

Primary options

» aspirin: 300 mg orally immediately, followed

by 75 mg once daily
ongoing chest pain plus morphine
» Adequate analgesia with morphine is essential
to relieve pain and its related sympathetic
activity, which can further increase myocardial
oxygen demand.

Primary options

» morphine sulfate: 2-4 mg intravenously

every 5-15 minutes until adequate pain
control is achieved
ongoing chest pain adjunct glyceryl trinitrate
» Should be given immediately, if the patient
is not hypotensive, as it reduces myocardial
oxygen demand and lessens ischaemia, and
may rarely abort MI if there is coronary spasm.
However, it should not be given in doses that
interfere with analgesic therapy. Sublingual
dosing should be given first to all patients, while
intravenous therapy is reserved for patients with
hypertension or heart failure.

Primary options

» glyceryl trinitrate: 0.3 to 1 mg sublingually

TREATMENT

every 5 minutes, maximum 3 doses; 5

micrograms/minute intravenously initially,
increase by 5-20 microgram/minute
increments every 3-5 minutes according to
response, maximum 200 micrograms/minute

30 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment

haemodynamically unstable 1st emergency revascularisation

» Invasive cardiac revascularisation within 48
hours of MI reduces mortality at 12 months
compared with medical treatment alone.[9]
2[C]Evidence

» If revascularisation fails, or there is persistent

pain or haemodynamic instability, urgent
coronary artery bypass graft (CABG) is
recommended.

plus anticoagulation
» A GPIIb/IIIa inhibitor plus heparin is indicated
for the treatment of STEMI as these agents
limit secondary thrombosis by inhibiting platelet
activation and subsequent platelet aggregation.

» Bivalirudin can be used as a single-agent

alternative to a GPIIb/IIIa inhibitor and
heparin.[29] It has been shown to significantly
reduce 30-day rates of major bleeding and
other adverse clinical events compared with
a combination of a GPIIb/IIIa inhibitor plus
heparin.[30] [31] 4[A]Evidence However,
choice of anticoagulation is based on clinician
preference. For patients who received
unfractionated heparin prior to procedure, wait
30 minutes before administering the bolus dose.

Primary options

» abciximab: 0.25 mg/kg intravenous bolus

initially, followed by 0.125 micrograms/kg/
minute infusion for 12 hours, maximum 10
micrograms/minute
-or-
» eptifibatide: 180 micrograms/kg intravenous
bolus initially at time of PCI, followed by 2
micrograms/kg/minute infusion for up to 18-24
hours and a second bolus of 180 micrograms/
kg/dose 10 minutes after the initial bolus
-or-
» tirofiban: 0.4 micrograms/kg/minute
intravenous infusion for 30 minutes initially,
followed by 0.1 micrograms/kg/minute
infusion
TREATMENT

--AND--
» enoxaparin: 30 mg intravenous bolus
initially, followed by 1 mg/kg subcutaneously
every 12 hours
-or-

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
31
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
» heparin: 60 units/kg intravenous bolus
initially, followed by 12 units/kg/hour infusion,
adjust dose to target aPTT

OR
Primary options

» bivalirudin: 0.75 mg/kg intravenous bolus

initially, followed by 1.75 mg/kg/hour infusion
for duration of procedure
plus aspirin + P2Y12 inhibitor
» Clopidogrel, prasugrel, and ticagrelor are oral
P2Y12 inhibitors indicated for the treatment
of STEMI in combination with aspirin. These
treatments limit secondary thrombosis by
inhibiting platelet activation and subsequent
platelet aggregation.

» Prasugrel was found to be superior to

clopidogrel in outcome measures when given for
at least 1 year; however, there is an increased
risk of bleeding in patients <60 kg or >74 years
of age. Lower doses are recommended in these
patients.[64] [65]

» Cangrelor, an intravenous P2Y12 inhibitor,

can be used as an adjunct to PCI to reduce
the risk of periprocedural MI, repeat coronary
revascularisation, and stent thrombosis in
patients who have not previously been treated
with a P2Y12 inhibitor and are not being treated
with a GPIIb/IIIa inhibitor.[28]

Primary options

» clopidogrel: 300-600 mg orally as a loading

dose, followed by 75 mg once daily
-or-
» prasugrel: 60 mg orally as a loading dose,
followed by 10 mg once daily
-or-
» ticagrelor: 180 mg orally as a loading dose,
followed by 90 mg twice daily
-or-
» cangrelor: 30 micrograms/kg intravenously
initially (before PCI), followed immediately by
4 micrograms/kg/minute infusion for at least
2 hours or the duration of PCI (whichever is
TREATMENT

longer)
--AND--
» aspirin: 300 mg orally immediately, followed
by 75 mg once daily

32 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
Doses >100 mg/day decrease effectiveness
of ticagrelor and are not recommended if this
drug is used concomitantly.
plus morphine
» Adequate analgesia with morphine is essential
to relieve ongoing chest pain and its related
sympathetic activity, which can further increase
myocardial oxygen demand.

Primary options

» morphine sulfate: 2-4 mg intravenously

every 5-15 minutes until adequate pain
control is achieved
adjunct ox ygen
» Supplemental oxygen is indicated only if
oxygen saturation is less than 94%.[18] [26]

» Guidelines recommend that oxygen not be

routinely administered in normoxic patients with
suspected or confirmed ACS.[18] [26]

adjunct glucose control

» If blood glucose is significantly elevated, an
intravenous insulin infusion may need to be
given, but rigid control has not been shown to be
necessary.[10]

» See local protocol for dosing guidelines.

adjunct inotrope support or intra-aortic balloon

pump (IABP) or ventricular mechanical
circulatory support
» Patients with low cardiac output states
and cardiogenic shock may benefit from a
dobutamine infusion.3[C]Evidence

» An intra-aortic balloon pump (IABP) or a

ventricular mechanical circulatory support device
is recommended if pharmacological measures
do not quickly improve shocked state.[11]
However, results from observational studies
appear to be conflicting for IABP in acute MI,
and in RCTs it has not been shown to reduce
mortality after acute MI even in patients with
cardiogenic shock.[27]
TREATMENT

Primary options

» dobutamine: 2.5 to 20 micrograms/kg/

minute intravenous infusion

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
33
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
electrically unstable post- 1st emergency revascularisation
cardiac arrest
» Emergency revascularisation is recommended
in patients who have had a cardiac arrest
and who have been resuscitated and are now
haemodynamically stable and show ECG
evidence for a STEMI.

» Guidelines recommend that multi-vessel

percutaneous coronary intervention (PCI) may
be considered either at the time of primary
PCI or as a planned staged procedure in
selected patients with STEMI and multi-vessel
disease who are haemodynamically stable.[41]
However, physicians should consider clinical
data, lesion severity/complexity, and risk of
contrast nephropathy to determine the optimal
PCI strategy (primary or staged).

» Emergency CABG is contraindicated in post-

cardiac arrest patients who are comatose.

» Thrombolysis is a potential option if PCI is

not readily available, but prolonged CPR is a
contraindication to the use of thrombolytics.

electrically unstable post- plus hypothermia

cardiac arrest
» Hypothermia is recommended for cardiac
arrest patients who have been resuscitated and
remain comatose.

electrically unstable post- plus anticoagulation

cardiac arrest
» A GPIIb/IIIa inhibitor plus heparin is indicated
for the treatment of STEMI as these agents
limit secondary thrombosis by inhibiting platelet
activation and subsequent platelet aggregation.

» Bivalirudin can be used as a single-agent

alternative to a GPIIb/IIIa inhibitor and
heparin.[29]It has been shown to significantly
reduce 30-day rates of major bleeding and
other adverse clinical events compared with
a combination of a GPIIb/IIIa inhibitor plus
heparin.[30] [31] 4[A]Evidence However,
choice of anticoagulation is based on clinician
preference. For patients who received
unfractionated heparin prior to procedure, wait
30 minutes before administering the bolus dose.
TREATMENT

Primary options

» abciximab: 0.25 mg/kg intravenous bolus

initially, followed by 0.125 micrograms/kg/

34 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
minute infusion for 12 hours, maximum 10
micrograms/minute
-or-
» eptifibatide: 180 micrograms/kg intravenous
bolus initially at time of PCI, followed by 2
micrograms/kg/minute infusion for up to 18-24
hours and a second bolus of 180 micrograms/
kg/dose 10 minutes after the initial bolus
-or-
» tirofiban: 0.4 micrograms/kg/minute
intravenous infusion for 30 minutes initially,
followed by 0.1 micrograms/kg/minute
infusion
--AND--
» enoxaparin: 30 mg intravenous bolus
initially, followed by 1 mg/kg subcutaneously
every 12 hours
-or-
» heparin: 60 units/kg intravenous bolus
initially, followed by 12 units/kg/hour infusion,
adjust dose to target aPTT

OR
Primary options

» bivalirudin: 0.75 mg/kg intravenous bolus

initially, followed by 1.75 mg/kg/hour infusion
for duration of procedure
electrically unstable post- plus aspirin + P2Y12 inhibitor
cardiac arrest
» Clopidogrel, prasugrel, and ticagrelor are oral
P2Y12 inhibitors indicated for the treatment
of STEMI in combination with aspirin. These
treatments limit secondary thrombosis by
inhibiting platelet activation and subsequent
platelet aggregation.

» Prasugrel was found to be superior to

clopidogrel in outcome measures when given for
at least 1 year; however, there is an increased
risk of bleeding in patients <60 kg or >74 years
of age. Lower doses are recommended in these
patients.[64] [65]

» Cangrelor, an intravenous P2Y12 inhibitor,

can be used as an adjunct to PCI to reduce
the risk of periprocedural MI, repeat coronary
revascularisation, and stent thrombosis in
TREATMENT

patients who have not previously been treated

with a P2Y12 inhibitor and are not being treated
with a GPIIb/IIIa inhibitor.[28]

Primary options

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
35
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
» clopidogrel: 300-600 mg orally as a loading
dose, followed by 75 mg once daily
-or-
» prasugrel: 60 mg orally as a loading dose,
followed by 10 mg once daily
-or-
» ticagrelor: 180 mg orally as a loading dose,
followed by 90 mg twice daily
-or-
» cangrelor: 30 micrograms/kg intravenously
initially (before PCI), followed immediately by
4 micrograms/kg/minute infusion for at least
2 hours or the duration of PCI (whichever is
longer)
--AND--
» aspirin: 300 mg orally immediately, followed
by 75 mg once daily
Doses >100 mg/day decrease effectiveness
of ticagrelor and are not recommended if this
drug is used concomitantly.
electrically unstable post- plus beta-blocker
cardiac arrest
» Oral beta-blockers should be started as
soon as possible, as they decrease infarction
size, although care should be taken in patients
with evidence of heart failure, hypotension,
bradycardia, or asthma.[50] 6[A]Evidence

» Intravenous beta-blockers are recommended

only in patients who are hypertensive or have
ongoing ischaemia.[11] [51]

Primary options

» atenolol: 50-100 mg orally once daily

OR
Primary options

» metoprolol: 5 mg intravenously every 2

minutes for 3 doses, followed by 25-50 mg
orally (immediate-release) every 6 hours for
48 hours starting 15 minutes after the last
intravenous dose, followed by 50-100 mg
orally (immediate-release) twice daily
electrically unstable post- plus statin
cardiac arrest
» A high-dose statin should be initiated
TREATMENT

for plaque stabilisation if there are no

contraindications and if tolerated, whatever the
results of serum lipid measurements.[13]

» Other lipid-lowering treatments (e.g.,

ezetimibe, evolocumab, alirocumab) can be

36 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
considered if statins are contraindicated or the
patient is intolerant of statins.

Primary options

» atorvastatin: 40-80 mg orally once daily

OR
Primary options

» rosuvastatin: 20-40 mg orally once daily

electrically unstable post- adjunct ezetimibe
cardiac arrest
» Consider adding ezetimibe to a statin regimen
in patients who require additional lowering of
LDL.[52]

» Ezetimibe may also be used as an alternative

to statins if they are contraindicated or the
patient is intolerant of statins.

Primary options

» ezetimibe: 10 mg orally once daily

electrically unstable post- adjunct evolocumab or alirocumab
cardiac arrest
» Evolocumab and alirocumab are proprotein
convertase subtilisin/kexin type 9 (PCSK9)
antibody inhibitors approved as an adjunct
therapy to diet and maximally tolerated statin
therapy for adult patients with heterozygous
familial hypercholesterolaemia (HeFH), or clinical
atherosclerotic CVD, who require additional
lowering of LDL.

» Evolocumab and alirocumab may also be

used as an alternative to statins if they are
contraindicated or the patient is intolerant of
statins.

Primary options

» evolocumab: 140 mg subcutaneously once

every 2 weeks; 420 mg subcutaneously once
monthly

OR
Primary options
TREATMENT

» alirocumab: 75 mg subcutaneously once

every 2 weeks, increase according to
response, maximum 150 mg every 2 weeks
electrically unstable post- adjunct eplerenone
cardiac arrest

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
37
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
» Eplerenone should be added to optimal
medical therapy in eligible patients (creatinine
<221 micromol/L [<2.5 mg/dL] in men and <177
micromol/L [<2.0 mg/dL] in women; potassium
<5.0 mmol/L [<5.0 mEq/L]) 3 to 14 days after
STEMI with ejection fraction <0.40, and either
symptomatic heart failure or diabetes mellitus.
Earlier initiation of the drug (<7 days) has been
shown to significantly reduce the rates of all-
cause mortality, sudden cardiac death, and
cardiovascular mortality/hospitalisation, whereas
initiation >7 days has not been shown to have a
significant effect on outcomes.[53]

» Serum potassium levels should be monitored

regularly during therapy, especially during the
initiation of therapy.

Primary options

» eplerenone: 25 mg orally once daily initially,

increase gradually to 50 mg once daily as
tolerated within 4 weeks
electrically unstable post- adjunct morphine
cardiac arrest
» Adequate analgesia with morphine is essential
to relieve ongoing chest pain and its related
sympathetic activity, which can further increase
myocardial oxygen demand.

Primary options

» morphine sulfate: 2-4 mg intravenously

every 5-15 minutes until adequate pain
control is achieved
electrically unstable post- adjunct glyceryl trinitrate
cardiac arrest
» Should be given immediately, if the patient
is not hypotensive, as it reduces myocardial
oxygen demand and lessens ischaemia, and
may rarely abort MI if there is coronary spasm.
However, it should not be given in doses that
interfere with analgesic therapy. Sublingual
dosing should be given first to all patients, while
intravenous therapy is reserved for patients with
hypertension or heart failure.

Primary options

» glyceryl trinitrate: 0.3 to 1 mg sublingually

TREATMENT

every 5 minutes, maximum 3 doses; 5

micrograms/minute intravenously initially,
increase by 5-20 microgram/minute
increments every 3-5 minutes according to
response, maximum 200 micrograms/minute

38 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
electrically unstable post- adjunct ox ygen
cardiac arrest
» Supplemental oxygen is indicated only if
oxygen saturation is less than 94%.[18] [26]

» Guidelines recommend that oxygen not be

routinely administered in normoxic patients with
suspected or confirmed ACS.[18] [26]

electrically unstable post- adjunct glucose control

cardiac arrest
» If blood glucose is significantly elevated, an
intravenous insulin infusion may need to be
given, but rigid control has not been shown to be
beneficial in critically ill patients.[10]

» See local protocol for dosing guidelines.

access to PCI within 90 1st revascularisation

minutes
» Primary percutaneous coronary intervention
(PCI) with stent placement (using bare metal
stents or drug-eluting stents) is the preferred
method of revascularisation, and is indicated if
patient presents to the emergency department
within 90 minutes of first presentation.[11]
[35] [36] 5[C]Evidence Drug-eluting stents are
preferred.[38] Many hospitals have 24-hour
PCI capacity; however, in facilities without
catheterisation laboratories, routine transfer to a
PCI facility should be considered for all patients
within 30 minutes of presentation, and ideally
within 30 minutes of symptom onset, provided
that the transfer can be made within 120 minutes
at the latest.[36].

» Guidelines recommend that multi-vessel

PCI may be considered either at the time of
primary PCI or as a planned staged procedure
in selected patients with STEMI and multi-vessel
disease who are haemodynamically stable.[41]
However, physicians should consider clinical
data, lesion severity/complexity, and risk of
contrast nephropathy to determine the optimal
PCI strategy (primary or staged).

» Emergency revascularisation with CABG

should be strongly considered in patients who
fail PCI, and should be performed within 12
hours of symptom onset, ideally within 6 hours.
TREATMENT

access to PCI within 90 plus anticoagulation

minutes
» A GPIIb/IIIa inhibitor plus heparin is indicated
for the treatment of STEMI as these agents

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
39
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
limit secondary thrombosis by inhibiting platelet
activation and subsequent platelet aggregation.

» Bivalirudin can be used as a single-agent

alternative to a GPIIb/IIIa inhibitor and
heparin.[29] It has been shown to significantly
reduce 30-day rates of major bleeding and
other adverse clinical events compared with
a combination of a GPIIb/IIIa inhibitor plus
heparin.[30] [31] 4[A]Evidence However,
choice of anticoagulation is based on clinician
preference. For patients who received
unfractionated heparin prior to procedure, wait
30 minutes before administering the bolus dose.

Primary options

» abciximab: 0.25 mg/kg intravenous bolus

initially, followed by 0.125 micrograms/kg/
minute infusion for 12 hours, maximum 10
micrograms/minute
-or-
» eptifibatide: 180 micrograms/kg intravenous
bolus initially at time of PCI, followed by 2
micrograms/kg/minute infusion for up to 18-24
hours and a second bolus of 180 micrograms/
kg/dose 10 minutes after the initial bolus
-or-
» tirofiban: 0.4 micrograms/kg/minute
intravenous infusion for 30 minutes initially,
followed by 0.1 micrograms/kg/minute
infusion
--AND--
» enoxaparin: 30 mg intravenous bolus
initially, followed by 1 mg/kg subcutaneously
every 12 hours
-or-
» heparin: 60 units/kg intravenous bolus
initially, followed by 12 units/kg/hour infusion,
adjust dose to target aPTT

OR
Primary options

» bivalirudin: 0.75 mg/kg intravenous bolus

initially, followed by 1.75 mg/kg/hour infusion
for duration of procedure
access to PCI within 90 plus aspirin + P2Y12 inhibitor
TREATMENT

minutes
» Clopidogrel, prasugrel, and ticagrelor are oral
P2Y12 inhibitors indicated for the treatment
of STEMI in combination with aspirin. These
treatments limit secondary thrombosis by

40 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
inhibiting platelet activation and subsequent
platelet aggregation.

» Prasugrel was found to be superior to

clopidogrel in outcome measures when given for
at least 1 year; however, there is an increased
risk of bleeding in patients <60 kg or >74 years
of age. Lower doses are recommended in these
patients.[64] [65]

» Cangrelor, an intravenous P2Y12 inhibitor,

can be used as an adjunct to PCI to reduce
the risk of periprocedural MI, repeat coronary
revascularisation, and stent thrombosis in
patients who have not previously been treated
with a P2Y12 inhibitor and are not being treated
with a GPIIb/IIIa inhibitor.[28]

Primary options

» clopidogrel: 300-600 mg orally as a loading

dose, followed by 75 mg once daily
-or-
» prasugrel: 60 mg orally as a loading dose,
followed by 10 mg once daily
-or-
» ticagrelor: 180 mg orally as a loading dose,
followed by 90 mg twice daily
-or-
» cangrelor: 30 micrograms/kg intravenously
initially (before PCI), followed immediately by
4 micrograms/kg/minute infusion for at least
2 hours or the duration of PCI (whichever is
longer)
--AND--
» aspirin: 300 mg orally immediately, followed
by 75 mg once daily
Doses >100 mg/day decrease effectiveness
of ticagrelor and are not recommended if this
drug is used concomitantly.
access to PCI within 90 plus beta-blocker
minutes
» Oral beta-blockers should be started as
soon as possible, as they decrease infarction
size, although care should be taken in patients
with evidence of heart failure, hypotension,
bradycardia, or asthma.[50] 6[A]Evidence

» Intravenous beta-blockers are recommended

TREATMENT

only in patients who are hypertensive or have

ongoing ischaemia.[11] [51]

Primary options

» atenolol: 50-100 mg orally once daily

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
41
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
OR
Primary options

» metoprolol: 5 mg intravenously every 2

minutes for 3 doses, followed by 25-50 mg
orally (immediate-release) every 6 hours for
48 hours starting 15 minutes after the last
intravenous dose, followed by 50-100 mg
orally (immediate-release) twice daily
access to PCI within 90 plus statin
minutes
» A high-dose statin should be initiated
for plaque stabilisation if there are no
contraindications and if tolerated, whatever the
results of serum lipid measurements.[13]

» Other lipid-lowering treatments (e.g.,

ezetimibe, evolocumab, alirocumab) can be
considered if statins are contraindicated or the
patient is intolerant of statins.

Primary options

» atorvastatin: 40-80 mg orally once daily

OR
Primary options

» rosuvastatin: 20-40 mg orally once daily

access to PCI within 90 adjunct ezetimibe
minutes
» Consider adding ezetimibe to a statin regimen
in patients who require additional lowering of
LDL.[52]

» Ezetimibe may also be used as an alternative

to statins if they are contraindicated or the
patient is intolerant of statins.

Primary options

» ezetimibe: 10 mg orally once daily

access to PCI within 90 adjunct evolocumab or alirocumab
minutes
» Evolocumab and alirocumab are proprotein
convertase subtilisin/kexin type 9 (PCSK9)
antibody inhibitors approved as an adjunct
therapy to diet and maximally tolerated statin
therapy for adult patients with heterozygous
TREATMENT

familial hypercholesterolaemia (HeFH), or clinical

atherosclerotic CVD, who require additional
lowering of LDL.

» Evolocumab and alirocumab may also be

used as an alternative to statins if they are

42 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
contraindicated or the patient is intolerant of
statins.

Primary options

» evolocumab: 140 mg subcutaneously once

every 2 weeks; 420 mg subcutaneously once
monthly

OR
Primary options

» alirocumab: 75 mg subcutaneously once

every 2 weeks, increase according to
response, maximum 150 mg every 2 weeks
access to PCI within 90 adjunct eplerenone
minutes
» Eplerenone should be added to optimal
medical therapy in eligible patients (creatinine
<221 micromol/L [<2.5 mg/dL] in men and <177
micromol/L [<2.0 mg/dL] in women; potassium
<5.0 mmol/L [<5.0 mEq/L]) 3 to 14 days after
STEMI with ejection fraction <0.40, and either
symptomatic heart failure or diabetes mellitus.
Earlier initiation of the drug (<7 days) has been
shown to significantly reduce the rates of all-
cause mortality, sudden cardiac death, and
cardiovascular mortality/hospitalisation, whereas
initiation >7 days has not been shown to have a
significant effect on outcomes.[53]

» Serum potassium levels should be monitored

regularly during therapy, especially during the
initiation of therapy.

Primary options

» eplerenone: 25 mg orally once daily initially,

increase gradually to 50 mg once daily as
tolerated within 4 weeks
access to PCI within 90 adjunct morphine
minutes
» Adequate analgesia with morphine is essential
to relieve ongoing chest pain and its related
sympathetic activity, which can further increase
myocardial oxygen demand.

Primary options
TREATMENT

» morphine sulfate: 2-4 mg intravenously

every 5-15 minutes until adequate pain
control is achieved
access to PCI within 90 adjunct glyceryl trinitrate
minutes

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
43
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
» Should be given immediately, if the patient
is not hypotensive, as it reduces myocardial
oxygen demand and lessens ischaemia, and
may rarely abort MI if there is coronary spasm.
However, it should not be given in doses that
interfere with analgesic therapy. Sublingual
dosing should be given first to all patients, while
intravenous therapy is reserved for patients with
hypertension or heart failure.

Primary options

» glyceryl trinitrate: 0.3 to 1 mg sublingually

every 5 minutes, maximum 3 doses; 5
micrograms/minute intravenously initially,
increase by 5-20 microgram/minute
increments every 3-5 minutes according to
response, maximum 200 micrograms/minute
access to PCI within 90 adjunct ox ygen
minutes
» Supplemental oxygen is indicated only if
oxygen saturation is less than 94%.[18] [26]

» Guidelines recommend that oxygen not be

routinely administered in normoxic patients with
suspected or confirmed ACS.[18] [26]

access to PCI within 90 adjunct glucose control

minutes
» If blood glucose is significantly elevated, an
intravenous insulin infusion may need to be
given, but rigid control has not been shown to be
beneficial in critically ill patients.[10]

» See local protocol for dosing guidelines.

no access to PCI within 90 1st thrombolysis

minutes: within 12 hours
» Indicated if percutaneous coronary intervention
of symptom onset with
(PCI) is not available within 90 minutes of
no contraindication to
first medical contact and patient has no
thrombolysis
contraindications to therapy.7[B]Evidence

» Should be initiated within 30 minutes of

presentation.

» Used only once on initial diagnosis, and

this must be within 12 hours of symptom
onset (ideally within 3 hours) as the efficacy
of fibrinolytic agents in lysing the thrombus
TREATMENT

diminishes over time.

» Therapy within the first 2 hours (particularly

the first hour) can occasionally abort MI and
dramatically reduce mortality.[11] 8[B]Evidence

44 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
» Absolute contraindications: any prior
intracranial haemorrhage; known malignant
intracranial lesion or structural cerebral vascular
lesion (e.g., arteriovenous malformations);
ischaemic stroke within previous 3 months;
suspected aortic dissection; active bleeding or
bleeding diathesis; and significant closed head
or facial trauma within previous 3 months.[11]

» Associated with an increased risk of bleeding

and intracranial haemorrhage.

Primary options

» reteplase: 10 units intravenously as a single

dose, followed by a second dose of 10 units
30 minutes later

OR
Primary options

» alteplase: 15 mg intravenously as a single

dose, followed by 0.75 mg/kg (maximum
50 mg) over 30 minutes, then 0.5 mg/kg
(maximum 35 mg) over 60 minutes

OR
Primary options

» tenecteplase: body weight <60 kg: 30

mg intravenously as a single dose; body
weight 60-69 kg: 35 mg intravenously as
a single dose; body weight 70-79 kg: 40
mg intravenously as a single dose; body
weight 80-89 kg: 45 mg intravenously as
a single dose; body weight >90 kg: 50 mg
intravenously as a single dose
no access to PCI within 90 adjunct transfer for PCI after thrombolysis
minutes: within 12 hours
» Percutaneous coronary intervention (PCI)
of symptom onset with
after thrombolysis is recommended in high-
no contraindication to
risk patients with: ongoing chest pain;
thrombolysis
haemodynamic, mechanical, or electrical
instability; or shock. Routine PCI is not generally
recommended.

» Patients should be transferred for PCI as soon

as possible.[55] Those transferred within 6 hours
after thrombolytic therapy had significantly fewer
TREATMENT

ischaemic complications than those who were

only transferred if they had complications.[56]

» Rescue PCI is associated with improved

clinical outcomes after failed fibrinolytic
therapy.[57]

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
45
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
no access to PCI within 90 plus anticoagulation
minutes: within 12 hours
» Indicated for the treatment of STEMI as it limits
of symptom onset with
secondary thrombosis, by inhibiting platelet
no contraindication to
activation and subsequent platelet aggregation.
thrombolysis
GPIIb/IIIa inhibitors are not indicated in STEMI if
thrombolytic therapy is indicated.

» Low molecular weight heparin should be

considered instead of unfractionated heparin
in patients treated with thrombolysis.[60] [61]
10[A]Evidence

Primary options

» enoxaparin: 30 mg intravenous bolus

initially, followed by 1 mg/kg subcutaneously
every 12 hours

OR
Secondary options

» heparin: 60 units/kg intravenous bolus

initially, followed by 12 units/kg/hour infusion,
adjust dose to target aPTT
no access to PCI within 90 plus aspirin + clopidogrel
minutes: within 12 hours
» Indicated for the treatment of STEMI as they
of symptom onset with
limit secondary thrombosis, by inhibiting platelet
no contraindication to
activation and subsequent platelet aggregation.
thrombolysis
» Prasugrel and ticagrelor are not recommended
in patients undergoing thrombolysis as they have
not been adequately studied in this setting.[59].

Primary options

» clopidogrel: 300-600 mg orally as a loading

dose, followed by 75 mg once daily
-and-
» aspirin: 300 mg orally immediately, followed
by 75 mg once daily
Doses >100 mg/day decrease effectiveness
of ticagrelor and are not recommended if this
drug is used concomitantly.
no access to PCI within 90 plus beta-blocker
minutes: within 12 hours
» Oral beta-blockers should be started as
of symptom onset with
soon as possible, as they decrease infarction
no contraindication to
TREATMENT

size, although care should be taken in patients

thrombolysis
with evidence of heart failure, hypotension,
bradycardia, or asthma.[50] 6[A]Evidence

46 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
» Intravenous beta-blockers are recommended
only in patients who are hypertensive or have
ongoing ischaemia.[11] [51]

Primary options

» atenolol: 50-100 mg orally once daily

OR
Primary options

» metoprolol: 5 mg intravenously every 2

minutes for 3 doses, followed by 25-50 mg
orally (immediate-release) every 6 hours for
48 hours starting 15 minutes after the last
intravenous dose, followed by 50-100 mg
orally (immediate-release) twice daily
no access to PCI within 90 plus statin
minutes: within 12 hours
» A high-dose statin should be initiated
of symptom onset with
for plaque stabilisation if there are no
no contraindication to
contraindications and if tolerated, whatever the
thrombolysis
results of serum lipid measurements.[13]

» Other lipid-lowering treatments (e.g.,

ezetimibe, evolocumab, alirocumab) can be
considered if statins are contraindicated or the
patient is intolerant of statins.

Primary options

» atorvastatin: 40-80 mg orally once daily

OR
Primary options

» rosuvastatin: 20-40 mg orally once daily

no access to PCI within 90 adjunct ezetimibe
minutes: within 12 hours
» Consider adding ezetimibe to a statin regimen
of symptom onset with
in patients who require additional lowering of
no contraindication to
LDL.[52]
thrombolysis
» Ezetimibe may also be used as an alternative
to statins if they are contraindicated or the
patient is intolerant of statins.

Primary options
TREATMENT

» ezetimibe: 10 mg orally once daily

no access to PCI within 90 adjunct evolocumab or alirocumab
minutes: within 12 hours
» Evolocumab and alirocumab are proprotein
of symptom onset with
convertase subtilisin/kexin type 9 (PCSK9)
antibody inhibitors approved as an adjunct

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
47
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
no contraindication to therapy to diet and maximally tolerated statin
thrombolysis therapy for adult patients with heterozygous
familial hypercholesterolaemia (HeFH), or clinical
atherosclerotic CVD, who require additional
lowering of LDL.

» Evolocumab and alirocumab may also be

used as an alternative to statins if they are
contraindicated or the patient is intolerant of
statins.

Primary options

» evolocumab: 140 mg subcutaneously once

every 2 weeks; 420 mg subcutaneously once
monthly

OR
Primary options

» alirocumab: 75 mg subcutaneously once

every 2 weeks, increase according to
response, maximum 150 mg every 2 weeks
no access to PCI within 90 adjunct eplerenone
minutes: within 12 hours
» Eplerenone should be added to optimal
of symptom onset with
medical therapy in eligible patients (creatinine
no contraindication to
<221 micromol/L [<2.5 mg/dL] in men and <177
thrombolysis
micromol/L [<2.0 mg/dL] in women; potassium
<5.0 mmol/L [<5.0 mEq/L]) 3 to 14 days after
STEMI with ejection fraction <0.40, and either
symptomatic heart failure or diabetes mellitus.
Earlier initiation of the drug (<7 days) has been
shown to significantly reduce the rates of all-
cause mortality, sudden cardiac death, and
cardiovascular mortality/hospitalisation, whereas
initiation >7 days has not been shown to have a
significant effect on outcomes.[53]

» Serum potassium levels should be monitored

regularly during therapy, especially during the
initiation of therapy.

Primary options

» eplerenone: 25 mg orally once daily initially,

increase gradually to 50 mg once daily as
tolerated within 4 weeks
no access to PCI within 90 adjunct morphine
TREATMENT

minutes: within 12 hours

» Adequate analgesia with morphine is essential
of symptom onset with
to relieve ongoing chest pain and its related
no contraindication to
sympathetic activity, which can further increase
thrombolysis
myocardial oxygen demand.

48 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
Primary options

» morphine sulfate: 2-4 mg intravenously

every 5-15 minutes until adequate pain
control is achieved
no access to PCI within 90 adjunct glyceryl trinitrate
minutes: within 12 hours
» Should be given immediately, if the patient
of symptom onset with
is not hypotensive, as it reduces myocardial
no contraindication to
oxygen demand and lessens ischaemia, and
thrombolysis
may rarely abort MI if there is coronary spasm.
However, it should not be given in doses that
interfere with analgesic therapy. Sublingual
dosing should be given first to all patients, while
intravenous therapy is reserved for patients with
hypertension or heart failure.

Primary options

» glyceryl trinitrate: 0.3 to 1 mg sublingually

every 5 minutes, maximum 3 doses; 5
micrograms/minute intravenously initially,
increase by 5-20 microgram/minute
increments every 3-5 minutes according to
response, maximum 200 micrograms/minute
no access to PCI within 90 adjunct ox ygen
minutes: within 12 hours
» Supplemental oxygen is indicated only if
of symptom onset with
oxygen saturation is less than 94%.[18] [26]
no contraindication to
thrombolysis » Guidelines recommend that oxygen not be
routinely administered in normoxic patients with
suspected or confirmed ACS.[18] [26]

no access to PCI within 90 adjunct glucose control

minutes: within 12 hours
» If blood glucose is significantly elevated, an
of symptom onset with
intravenous insulin infusion may need to be
no contraindication to
given, but rigid control has not been shown to be
thrombolysis
beneficial in critically ill patients.[10]

» See local protocol for dosing guidelines.

no access to PCI within 1st consider PCI

90 minutes: within 12
» In patients with contraindications to
hours of symptom onset
thrombolysis, percutaneous coronary
with contraindication to
intervention (PCI) is indicated even if it cannot
thrombolysis
occur within 90 minutes. Patients should be
TREATMENT

transferred for PCI as soon as possible.

no access to PCI within plus anticoagulation

90 minutes: within 12
» A GPIIb/IIIa inhibitor plus heparin is indicated
hours of symptom onset
for the treatment of STEMI as these agents

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
49
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
with contraindication to limit secondary thrombosis by inhibiting platelet
thrombolysis activation and subsequent platelet aggregation.

» Bivalirudin can be used as a single-agent

alternative to a GPIIb/IIIa inhibitor and
heparin.[29] It has been shown to significantly
reduce 30-day rates of major bleeding and
other adverse clinical events compared with
a combination of a GPIIb/IIIa inhibitor plus
heparin.[30] [31] 4[A]Evidence However,
choice of anticoagulation is based on clinician
preference. For patients who received
unfractionated heparin prior to procedure, wait
30 minutes before administering the bolus dose.

Primary options

» abciximab: 0.25 mg/kg intravenous bolus

initially, followed by 0.125 micrograms/kg/
minute infusion for 12 hours, maximum 10
micrograms/minute
-or-
» eptifibatide: 180 micrograms/kg intravenous
bolus initially at time of PCI, followed by 2
micrograms/kg/minute infusion for up to 18-24
hours and a second bolus of 180 micrograms/
kg/dose 10 minutes after the initial bolus
-or-
» tirofiban: 0.4 micrograms/kg/minute
intravenous infusion for 30 minutes initially,
followed by 0.1 micrograms/kg/minute
infusion
--AND--
» enoxaparin: 30 mg intravenous bolus
initially, followed by 1 mg/kg subcutaneously
every 12 hours
-or-
» heparin: 60 units/kg intravenous bolus
initially, followed by 12 units/kg/hour infusion,
adjust dose to target aPTT

OR
Primary options

» bivalirudin: 0.75 mg/kg intravenous bolus

initially, followed by 1.75 mg/kg/hour infusion
for duration of procedure
no access to PCI within plus aspirin + P2Y12 inhibitor
TREATMENT

90 minutes: within 12
» Clopidogrel, prasugrel, and ticagrelor are oral
hours of symptom onset
P2Y12 inhibitors indicated for the treatment
with contraindication to
of STEMI in combination with aspirin. These
thrombolysis
treatments limit secondary thrombosis by

50 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
inhibiting platelet activation and subsequent
platelet aggregation.

» Prasugrel was found to be superior to

clopidogrel in outcome measures when given for
at least 1 year; however, there is an increased
risk of bleeding in patients <60 kg or >74 years
of age. Lower doses are recommended in these
patients.[64] [65]

» Cangrelor, an intravenous P2Y12 inhibitor,

can be used as an adjunct to PCI to reduce
the risk of periprocedural MI, repeat coronary
revascularisation, and stent thrombosis in
patients who have not previously been treated
with a P2Y12 inhibitor and are not being treated
with a GPIIb/IIIa inhibitor. [28]

Primary options

» clopidogrel: 300-600 mg orally as a loading

dose, followed by 75 mg once daily
-or-
» prasugrel: 60 mg orally as a loading dose,
followed by 10 mg once daily
-or-
» ticagrelor: 180 mg orally as a loading dose,
followed by 90 mg twice daily
-or-
» cangrelor: 30 micrograms/kg intravenously
initially (before PCI), followed immediately by
4 micrograms/kg/minute infusion for at least
2 hours or the duration of PCI (whichever is
longer)
--AND--
» aspirin: 300 mg orally immediately, followed
by 75 mg once daily
Doses >100 mg/day decrease effectiveness
of ticagrelor and are not recommended if this
drug is used concomitantly.
no access to PCI within plus beta-blocker
90 minutes: within 12
» Oral beta-blockers should be started as
hours of symptom onset
soon as possible, as they decrease infarction
with contraindication to
size, although care should be taken in patients
thrombolysis
with evidence of heart failure, hypotension,
bradycardia, or asthma.[50] 6[A]Evidence

» Intravenous beta-blockers are recommended

TREATMENT

only in patients who are hypertensive or have

ongoing ischaemia.[11] [51]

Primary options

» atenolol: 50-100 mg orally once daily

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
51
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
OR
Primary options

» metoprolol: 5 mg intravenously every 2

minutes for 3 doses, followed by 25-50 mg
orally (immediate-release) every 6 hours for
48 hours starting 15 minutes after the last
intravenous dose, followed by 50-100 mg
orally (immediate-release) twice daily
no access to PCI within plus statin
90 minutes: within 12
» A high-dose statin should be initiated
hours of symptom onset
for plaque stabilisation if there are no
with contraindication to
contraindications and if tolerated, whatever the
thrombolysis
results of serum lipid measurements.[13]

» Other lipid-lowering treatments (e.g.,

ezetimibe, evolocumab, alirocumab) can be
considered if statins are contraindicated or the
patient is intolerant of statins.

Primary options

» atorvastatin: 40-80 mg orally once daily

OR
Primary options

» rosuvastatin: 20-40 mg orally once daily

no access to PCI within adjunct ezetimibe
90 minutes: within 12
» Consider adding ezetimibe to a statin regimen
hours of symptom onset
in patients who require additional lowering of
with contraindication to
LDL.[52]
thrombolysis
» Ezetimibe may also be used as an alternative
to statins if they are contraindicated or the
patient is intolerant of statins.

Primary options

» ezetimibe: 10 mg orally once daily

no access to PCI within adjunct evolocumab or alirocumab
90 minutes: within 12
» Evolocumab and alirocumab are proprotein
hours of symptom onset
convertase subtilisin/kexin type 9 (PCSK9)
with contraindication to
antibody inhibitors approved as an adjunct
thrombolysis
therapy to diet and maximally tolerated statin
therapy for adult patients with heterozygous
TREATMENT

familial hypercholesterolaemia (HeFH), or clinical

atherosclerotic CVD, who require additional
lowering of LDL.

» Evolocumab and alirocumab may also be

used as an alternative to statins if they are

52 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
contraindicated or the patient is intolerant of
statins.

Primary options

» evolocumab: 140 mg subcutaneously once

every 2 weeks, or 420 mg subcutaneously
once monthly

OR
Primary options

» alirocumab: 75 mg subcutaneously once

every 2 weeks, increase according to
response, maximum 150 mg every 2 weeks
no access to PCI within adjunct eplerenone
90 minutes: within 12
» Eplerenone should be added to optimal
hours of symptom onset
medical therapy in eligible patients (creatinine
with contraindication to
<221 micromol/L [<2.5 mg/dL] in men and <177
thrombolysis
micromol/L [<2.0 mg/dL] in women; potassium
<5.0 mmol/L [<5.0 mEq/L]) 3 to 14 days after
STEMI with ejection fraction <0.40, and either
symptomatic heart failure or diabetes mellitus.
Earlier initiation of the drug (<7 days) has been
shown to significantly reduce the rates of all-
cause mortality, sudden cardiac death, and
cardiovascular mortality/hospitalisation, whereas
initiation >7 days has not been shown to have a
significant effect on outcomes.[53]

» Serum potassium levels should be monitored

regularly during therapy, especially during the
initiation of therapy.

Primary options

» eplerenone: 25 mg orally once daily initially,

increase gradually to 50 mg once daily as
tolerated within 4 weeks
no access to PCI within adjunct morphine
90 minutes: within 12
» Adequate analgesia with morphine is essential
hours of symptom onset
to relieve ongoing chest pain and its related
with contraindication to
sympathetic activity, which can further increase
thrombolysis
myocardial oxygen demand.

Primary options
TREATMENT

» morphine sulfate: 2-4 mg intravenously

every 5-15 minutes until adequate pain
control is achieved
no access to PCI within adjunct glyceryl trinitrate
90 minutes: within 12
hours of symptom onset

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
53
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
with contraindication to » Should be given immediately if the patient
thrombolysis is not hypotensive, as it reduces myocardial
oxygen demand and lessens ischaemia, and
may, rarely, abort MI if there is coronary spasm.
However, it should not be given in doses that
interfere with analgesic therapy. Sublingual
dosing should be given first to all patients, while
intravenous therapy is reserved for patients with
hypertension or heart failure.

Primary options

» glyceryl trinitrate: 0.3 to 1 mg sublingually

every 5 minutes, maximum 3 doses; 5
micrograms/minute intravenously initially,
increase by 5-20 microgram/minute
increments every 3-5 minutes according to
response, maximum 200 micrograms/minute
no access to PCI within adjunct ox ygen
90 minutes: within 12
» Supplemental oxygen is indicated only if
hours of symptom onset
oxygen saturation is less than 94%.[18] [26]
with contraindication to
thrombolysis » Guidelines recommend that oxygen not be
routinely administered in normoxic patients with
suspected or confirmed ACS.[18] [26]

no access to PCI within adjunct glucose control

90 minutes: within 12
» If blood glucose is significantly elevated, an
hours of symptom onset
intravenous insulin infusion may need to be
with contraindication to
given, but rigid control has not been shown to be
thrombolysis
beneficial in critically ill patients.[10]

» See local protocol for dosing guidelines.

no access to PCI within 1st revascularisation

90 minutes: >12 hours of
» If there are persistent symptoms it is possible
symptom onset
to obtain benefits from revascularisation even
beyond 12 hours.

» Revascularisation would be best performed

with percutaneous coronary intervention (PCI).

» There is no evidence that revascularisation is

beneficial in stable patients beyond 12 hours.

no access to PCI within plus beta-blocker

90 minutes: >12 hours of
TREATMENT

» Oral beta-blockers should be started as

symptom onset
soon as possible, as they decrease infarction
size, although care should be taken in patients
with evidence of heart failure, hypotension,
bradycardia, or asthma.[50] 6[A]Evidence

54 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
» Intravenous beta-blockers are recommended
only in patients who are hypertensive or have
ongoing ischaemia.[11] [51]

Primary options

» atenolol: 50-100 mg orally once daily

OR
Primary options

» metoprolol: 5 mg intravenously every 2

minutes for 3 doses, followed by 25-50 mg
orally (immediate-release) every 6 hours for
48 hours starting 15 minutes after the last
intravenous dose, followed by 50-100 mg
orally (immediate-release) twice daily
no access to PCI within plus anticoagulation
90 minutes: >12 hours of
» Indicated for the treatment of STEMI as it limits
symptom onset
secondary thrombosis, by inhibiting platelet
activation and subsequent platelet aggregation.

Primary options

» enoxaparin: 30 mg intravenous bolus

initially, followed by 1 mg/kg subcutaneously
every 12 hours

OR
Primary options

» heparin: 60 units/kg intravenous bolus

initially, followed by 12 units/kg/hour infusion,
adjust dose to target aPTT
no access to PCI within plus aspirin + P2Y12 inhibitor
90 minutes: >12 hours of
» Clopidogrel, prasugrel, and ticagrelor are oral
symptom onset
P2Y12 inhibitors indicated for the treatment
of STEMI in combination with aspirin. These
treatments limit secondary thrombosis by
inhibiting platelet activation and subsequent
platelet aggregation.

» Prasugrel was found to be superior to

clopidogrel in outcome measures when given for
at least 1 year; however, there is an increased
risk of bleeding in patients <60 kg or >74 years
of age. Lower doses are recommended in these
TREATMENT

patients.[64] [65]

» Cangrelor, an intravenous P2Y12 inhibitor,

can be used as an adjunct to PCI to reduce
the risk of periprocedural MI, repeat coronary
revascularisation, and stent thrombosis in

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
55
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
patients who have not previously been treated
with a P2Y12 inhibitor and are not being treated
with a GPIIb/IIIa inhibitor.[28]

Primary options

» clopidogrel: 300-600 mg orally as a loading

dose, followed by 75 mg once daily
-or-
» prasugrel: 60 mg orally as a loading dose,
followed by 10 mg once daily
-or-
» ticagrelor: 180 mg orally as a loading dose,
followed by 90 mg twice daily
-or-
» cangrelor: 30 micrograms/kg intravenously
initially (before PCI), followed immediately by
4 micrograms/kg/minute infusion for at least
2 hours or the duration of PCI (whichever is
longer)
--AND--
» aspirin: 300 mg orally immediately, followed
by 75 mg once daily
Doses >100 mg/day decrease effectiveness
of ticagrelor and are not recommended if this
drug is used concomitantly.
no access to PCI within plus statin
90 minutes: >12 hours of
» A high-dose statin should be initiated
symptom onset
for plaque stabilisation if there are no
contraindications and if tolerated, whatever the
results of serum lipid measurements.[13]

» Other lipid-lowering treatments (e.g.,

ezetimibe, evolocumab, alirocumab) can be
considered if statins are contraindicated or the
patient is intolerant of statins.

Primary options

» atorvastatin: 40-80 mg orally once daily

OR
Primary options

» rosuvastatin: 20-40 mg orally once daily

no access to PCI within adjunct ezetimibe
90 minutes: >12 hours of
» Consider adding ezetimibe to a statin regimen
TREATMENT

symptom onset
in patients who require additional lowering of
LDL.[52]

» Ezetimibe may also be used as an alternative

to statins if they are contraindicated or the
patient is intolerant of statins.

56 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
Primary options

» ezetimibe: 10 mg orally once daily

no access to PCI within adjunct evolocumab or alirocumab
90 minutes: >12 hours of
» Evolocumab and alirocumab are proprotein
symptom onset
convertase subtilisin/kexin type 9 (PCSK9)
antibody inhibitors approved as an adjunct
therapy to diet and maximally tolerated statin
therapy for adult patients with heterozygous
familial hypercholesterolaemia (HeFH), or clinical
atherosclerotic CVD, who require additional
lowering of LDL.

» Evolocumab and alirocumab may also be

used as an alternative to statins if they are
contraindicated or the patient is intolerant of
statins.

Primary options

» evolocumab: 140 mg subcutaneously once

every 2 weeks; 420 mg subcutaneously once
monthly

OR
Primary options

» alirocumab: 75 mg subcutaneously once

every 2 weeks, increase according to
response, maximum 150 mg every 2 weeks
no access to PCI within adjunct eplerenone
90 minutes: >12 hours of
» Eplerenone should be added to optimal
symptom onset
medical therapy in eligible patients (creatinine
<221 micromol/L [<2.5 mg/dL] in men and <177
micromol/L [<2.0 mg/dL] in women; potassium
<5.0 mmol/L [<5.0 mEq/L]) 3 to 14 days after
STEMI with ejection fraction <0.40, and either
symptomatic heart failure or diabetes mellitus.
Earlier initiation of the drug (<7 days) has been
shown to significantly reduce the rates of all-
cause mortality, sudden cardiac death, and
cardiovascular mortality/hospitalisation, whereas
initiation >7 days has not been shown to have a
significant effect on outcomes.[53]

» Serum potassium levels should be monitored

regularly during therapy, especially during the
TREATMENT

initiation of therapy.

Primary options

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 ST-elevation myocardial infarction Treatment

Acute
Patient group Tx line Treatment
» eplerenone: 25 mg orally once daily initially,
increase gradually to 50 mg once daily as
tolerated within 4 weeks
no access to PCI within adjunct morphine
90 minutes: >12 hours of
» Adequate analgesia with morphine is essential
symptom onset
to relieve ongoing chest pain and its related
sympathetic activity, which can further increase
myocardial oxygen demand.

Primary options

» morphine sulfate: 2-4 mg intravenously

every 5-15 minutes until adequate pain
control is achieved
no access to PCI within adjunct glyceryl trinitrate
90 minutes: >12 hours of
» Should be given immediately, if the patient
symptom onset
is not hypotensive, as it reduces myocardial
oxygen demand and lessens ischaemia, and
may rarely abort MI if there is coronary spasm.
However, it should not be given in doses that
interfere with analgesic therapy. Sublingual
dosing should be given first to all patients, while
intravenous therapy is reserved for patients with
hypertension or heart failure.

Primary options

» glyceryl trinitrate: 0.3 to 1 mg sublingually

every 5 minutes, maximum 3 doses; 5
micrograms/minute intravenously initially,
increase by 5-20 microgram/minute
increments every 3-5 minutes according to
response, maximum 200 micrograms/minute
no access to PCI within adjunct ox ygen
90 minutes: >12 hours of
» Supplemental oxygen is indicated only if
symptom onset
oxygen saturation is less than 94%.[18] [26]

» Guidelines recommend that oxygen not be

routinely administered in normoxic patients with
suspected or confirmed ACS.[18] [26]

no access to PCI within adjunct glucose control

90 minutes: >12 hours of
» If blood glucose is significantly elevated, an
symptom onset
intravenous insulin infusion may need to be
given, but rigid control has not been shown to be
beneficial in critically ill patients.[10]
TREATMENT

» See local protocol for dosing guidelines.

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ST-elevation myocardial infarction Treatment

Ongoing
Patient group Tx line Treatment

post-STEMI 1st dual antiplatelet therapy

» Recommended for at least 12 months in
all patients whether they were stented or
not. Aspirin should be given indefinitely, and
clopidogrel (or prasugrel or ticagrelor) for at least
1 year. However, prasugrel and ticagrelor are not
recommended in patients who have undergone
thrombolysis as they have not been adequately
studied in this setting.[59]

» Prasugrel was found to be superior to

clopidogrel in outcome measures when given for
at least 1 year; however, there is an increased
risk of bleeding in patients <60 kg or >74 years
of age. Lower doses are recommended in these
patients.[64] [65]

Primary options

» clopidogrel: 75 mg orally once daily

-or-
» prasugrel: 10 mg orally once daily
-or-
» ticagrelor: 90 mg orally twice daily
--AND--
» aspirin: 75 mg orally once daily
plus ACE inhibitor
» Should be started early (i.e., when patient is
haemodynamically stable, optimally on first day
in hospital) for a favourable effect on ventricular
remodelling, especially in patients with large
anterior wall MI.11[A]Evidence

Primary options

» perindopril: 4-16 mg/day orally

OR
Primary options

» lisinopril: 5 mg orally once daily for 48 hours

initially, followed by 5-10 mg once daily

OR
TREATMENT

Primary options

» enalapril: 2.5 mg orally once daily for 48

hours initially, increase gradually to 10 mg
twice daily

OR

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 ST-elevation myocardial infarction Treatment

Ongoing
Patient group Tx line Treatment
Primary options

» ramipril: 2.5 mg orally twice daily initially,

increase gradually to 5 mg twice daily
according to response
plus beta-blocker
» Should be given for 3 years. Continuing use
can then be considered and should be evaluated
based on comorbidities.[50] [63] 12[C]Evidence

Primary options

» metoprolol: 100 mg orally (immediate-

release) twice daily

OR
Primary options

» atenolol: 100 mg orally once daily

plus statin
» Should be given indefinitely if tolerated and not
contraindicated.

Primary options

» atorvastatin: 10-80 mg orally once daily

OR
Primary options

» rosuvastatin: 5-40 mg orally once daily

adjunct ezetimibe
» Consider adding ezetimibe to a statin regimen
in patients who require additional lowering of
LDL.[52]

» Ezetimibe may also be used as an alternative

to statins if they are contraindicated or the
patient is intolerant of statins.

Primary options

» ezetimibe: 10 mg orally once daily

adjunct evolocumab or alirocumab
» Evolocumab and alirocumab are proprotein
TREATMENT

convertase subtilisin/kexin type 9 (PCSK9)

antibody inhibitors approved as an adjunct
therapy to diet and maximally tolerated statin
therapy for adult patients with heterozygous
familial hypercholesterolaemia (HeFH), or clinical

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BMJ Best Practice topics are regularly updated and the most recent version
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ST-elevation myocardial infarction Treatment

Ongoing
Patient group Tx line Treatment
atherosclerotic CVD, who require additional
lowering of LDL.

» Evolocumab and alirocumab may also be

used as an alternative to statins if they are
contraindicated or the patient is intolerant of
statins.

Primary options

» evolocumab: 140 mg subcutaneously once

every 2 weeks; 420 mg subcutaneously once
monthly

OR
Primary options

» alirocumab: 75 mg subcutaneously once

every 2 weeks, increase according to
response, maximum 150 mg every 2 weeks
adjunct eplerenone
» Eplerenone should be added to optimal
medical therapy in eligible patients (creatinine
<221 micromol/L [<2.5 mg/dL] in men and <177
micromol/L [<2.0 mg/dL] in women; potassium
<5.0 mmol/L [<5.0 mEq/L]) 3 to 14 days after
STEMI with ejection fraction <0.40, and either
symptomatic heart failure or diabetes mellitus.
Earlier initiation of the drug (<7 days) has been
shown to significantly reduce the rates of all-
cause mortality, sudden cardiac death, and
cardiovascular mortality/hospitalisation, whereas
initiation >7 days has not been shown to have a
significant effect on outcomes.[53]

» Serum potassium levels should be monitored

regularly during therapy, especially during the
initiation of therapy.

Primary options

» eplerenone: 25 mg orally once daily initially,

increase gradually to 50 mg once daily as
tolerated within 4 weeks
TREATMENT

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 ST-elevation myocardial infarction Treatment

Emerging
Factor Xa inhibitors
These are being studied for acute coronary syndromes.[66] Rivaroxaban is a factor Xa inhibitor that has been
shown to reduce cardiovascular events when given in addition to dual antiplatelet therapy to stabilised STEMI
patients, but increases bleeding events.[67]

Factor IX inhibitors
Pegnivacogin, a factor IX inhibitor that is reversible with anivamersen, has been shown to reduce the
incidence of ischaemic events in patients with acute coronary syndrome compared with intravenous heparin,
when given during coronary interventions. This was in a phase 2 study that did not include patients with
STEMI. A phase 3 trial including STEMI patients is currently underway.[68]

Vorapaxar
Vorapaxar, an anti-protease-activated receptor-1 (PAR-1) antiplatelet agent, showed a modest reduction in
post-MI clinical events but with an increase in bleeding events.[69]

L-carnitine
A meta-analysis of 13 placebo-controlled trials found L-carnitine to significantly reduce all-cause mortality,
ventricular arrhythmias, and angina symptoms in patients experiencing acute MI. Further evaluation is
needed.[70]

Bone marrow stem-cell therapy

Stem-cell therapy has been proposed as a potential therapy for the repair and regeneration of damaged
vascular and cardiac tissue following an acute MI. Although current evidence suggests that stem-cell therapy
is safe, its effect on mortality, quality of life, and myocardial function following an acute MI is unclear.[71]
This is based, however, on limited evidence from small clinical trials. One randomised controlled study found
intracoronary bone marrow cell therapy to be safe, but its effect on myocardial function and myocardial
salvage was unclear.[72]
TREATMENT

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ST-elevation myocardial infarction Follow up

Recommendations
Monitoring

FOLLOW UP
Survivors of acute MI should be closely followed up for adequate modification of risk factors and
development of complications. Patients should be evaluated within 2 to 3 weeks of discharge and
evaluated periodically based on the extent of myocardial damage and patient condition.
[Fig-11]

[Fig-12]

[Fig-13]

Initiating risk-factor modification and aggressive medical management prior to discharge has been
associated with increased patient adherence. All patients should continue the optimal medical regimen
indefinitely. This includes aspirin, clopidogrel or prasugrel (for at least 1 year), beta-blockers, statins, and
ACE inhibitors (especially in patients with decreased ejection fraction).

Ejection fraction is assessed by echocardiography 3 months after the acute episode and then periodically
thereafter, depending on LV function and symptoms. Patients with ejection fraction <35% at 3 months'
follow-up should be referred to an electrophysiologist for consideration of an ICD, as there is a high risk
for arrhythmias in this population. Patients who develop diminished LV function and congestive heart
failure should be followed up and managed appropriately.

Patients with a history of MI are at increased risk for recurrent infarction. They should be evaluated by
stress testing or cardiac catheterisation if symptoms develop. Routine periodic ischaemic evaluations with
stress echocardiography or myocardial perfusion studies are controversial.

Patient instructions
Patients should refrain from any physical exertion until re-evaluated by a cardiologist in 2 to 3 weeks,
which may include stress testing. Further activity should be based on the extent of myocardial damage
with the acute MI and the patient's condition. Patients should ideally increase their activity gradually in a
cardiac rehabilitation program, which has a proven role, under a monitored setting.[85]

Complications

Complications Timeframe Likelihood

sinus bradycardia, first-degree heart block, and type I short term medium
second-degree heart block

Usually develop with occlusion of the right coronary artery, and are caused by infarction of the
atrioventricular node and the conduction system above the His bundle or by increased vagal tone.

These arrhythmias are usually benign and transient and do not require any treatment. If the heart rate
goes below 50 bpm and the patient is symptomatic, give IV atropine.

Temporary pacing may be required if heart failure, syncope or angina develop.

complete heart block with anterior MI short term medium

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 ST-elevation myocardial infarction Follow up

Complications Timeframe Likelihood

Can develop acutely in patients with anterior infarcts and may lead to ventricular asystole.
FOLLOW UP

Complete heart block in anterior infarcts occurs because of infarction and necrosis of the bundle branches
in the septum.

Trans-cutaneous or, preferably, trans-venous pacing should be carried out in these patients immediately
after conduction defects are noticed. Permanent pacing is usually required.

recurrent chest pain short term medium

Chest pain may occur in as many as 50% of patients after percutaneous coronary intervention (PCI).[77]

Angina-like symptoms should be assessed with ECG changes for escalation of medical therapy, and IABP
and repeat angiography considered.[11]

type II second-degree heart block with anterior MI short term low

Usually occurs from a defect in the conduction system below the His bundle and can rapidly progress into
complete heart block in patients with anterior MI.

Trans-cutaneous or more preferably trans-venous cardiac pacing should be carried out in these patients
immediately after conduction defects are noted.

complete heart block with inferior MI short term low

Can develop in patients with inferior infarcts caused by vagal stimulation.

Usually transient or resolved with atropine.

Temporary pacing may be required if heart failure, syncope, or angina develop. Permanent pacing is rarely
required.

acute mitral regurgitation short term low

Inferior MI can cause rupture of the posteromedial papillary muscle, while anterolateral infarctions can
cause rupture of the anterolateral papillary muscle.

Right ventricular papillary muscle rupture is rare and can cause life-threatening tricuspid regurgitation.

Complete papillary muscle rupture causes wide-open mitral regurgitation and is fatal.

Patients with incomplete papillary muscle rupture require emergency cardiac surgery.

Inotropic support and IABP should be considered for transient stabilisation before emergency surgery.

ventricular septal defects (VSD) short term low

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ST-elevation myocardial infarction Follow up

Complications Timeframe Likelihood

Interventricular septal rupture causing a VSD can occur.

FOLLOW UP
Rupture associated with anterior infarction is more apical in location, while inferior infarctions are
associated with more basal septal perforations and a much worse prognosis.

Rupture of the septum is more likely to be associated with complete heart block or right bundle branch
block.

These patients require emergency cardiac surgery.

Survival depends on early recognition, defect size, and degree of impairment of ventricular function.

acute pericardial tamponade short term low

Ventricular free wall rupture causing acute pericardial tamponade accounts for up to 10% of in-hospital
mortality from STEMI.

Thinness of the apical wall with marked intensity of necrosis at the terminal end of blood flow and shearing
effect of muscular contraction are proposed causes.

Tamponade most often occurs in patients without previous infarction and usually occurs at the junction of
the infarct and normal muscle.

There is an increased risk of ventricular wall rupture involving anterior and lateral walls after anterior MI.
Incomplete rupture can result in the development of a pseudoaneurysm.

Acute or complete rupture is rarely treatable.

Patients require emergency surgery for surgical resection of necrotic myocardium and primary
reconstruction.

Inotropic support and intra-aortic balloon counterpulsation for transient stabilisation should be considered
before surgery.

post-infarction pericarditis (Dressler's syndrome) short term low

Occurs in 5% to 10% of patients with MI.

Aspirin is the treatment of choice, as other non-steroidal anti-inflammatory drugs (NSAIDs) impair scar
formation in animal studies.[78]

congestive heart failure long term high

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 ST-elevation myocardial infarction Follow up

Complications Timeframe Likelihood

Congestive heart failure caused by decreased LV function occurs frequently after MI because of
FOLLOW UP

myocardial damage, infarct progression, and LV remodelling after the acute episode.

Appropriate use of medications, including beta-blockers, ACE inhibitors, angiotensin-II receptor

antagonists, and diuretics, when appropriate, decreases the incidence and progression of congestive heart
failure.

Biventricular pacing should be considered if appropriate criteria are met.

ventricular arrhythmias variable high

Ventricular tachycardia and ventricular fibrillation can occur during ischaemia and reperfusion and can
be lethal. They can also occur at any stage following a MI because of re-entry circuits at the border of
myocardial scar and normal myocardium, and are commonly seen in patients with decreased ejection
fraction.

Electrolytes should be optimised, especially potassium and magnesium, as electrolyte imbalance

increases the risk of ventricular arrhythmias. Potassium should be maintained at >4 millimol/L (4 mEq/L)
and magnesium at >1 millimol/L (2 mEq/L).

Appropriate therapy should be initiated with DC cardioversion and anti-arrhythmic therapy.

Optimal medical management, in particular beta-blockers, decreases incidence of ventricular arrhythmias.

Implantable cardioverter defibrillator (ICD) should be considered for all patients with persistently
decreased LV ejection fraction (<35%) if there has been no response to 3 months of intensive medical
therapy after MI.[21]

recurrent ischaemia and infarction variable high

Patients with acute MI can have recurrent ischaemia or infarction caused by further plaque rupture and
progression of atherosclerosis.

Recurrence should be treated in the same manner as the initial presentation.

Aggressive risk factor modification after the initial presentation decreases incidence of recurrences.

depression variable high

Common complication post MI, and patients should routinely be screened for it.[76]

Management with antidepressants or psychological therapies may be necessary.

in-stent thrombosis variable low

Dual antiplatelet therapy is recommended for at least 12 months in all patients whether they have been
stented or not. In-stent thrombosis is often precipitated by premature cessation of dual antiplatelet
therapy, but can also be caused by technical factors and other comorbidities such as diabetes mellitus.
Patients and their family should be strongly cautioned in hospital and in follow-up appointments about the
importance of dual antiplatelet therapy for 12 months.[79]

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ST-elevation myocardial infarction Follow up

Complications Timeframe Likelihood

left ventricular thrombus variable low

FOLLOW UP
LV thrombus can be seen in the early days of acute MI, especially large anterior MI with dyskinesia of the
apex. In early studies, LV thrombus was visualised by echocardiography in about one third of patients
with large anterior MI[80] [81] [82] in the absence of early revascularisation. The rate of embolism was low
even in patients with LV thrombus (4.5%). In a more recent study, in the era of early reperfusion therapy,
LV thrombus was identified in 8.8% of patients with cardiac MRI.[83] The majority of patients (88%) had
resolution of LV thrombus on follow-up cardiac MRI. Large baseline infarct size is a risk factor for LV
thrombus formation. Anticoagulation with vitamin K antagonists may be considered in patients with LV
mural thrombus.[84]

left ventricular aneurysm variable low

The incidence of LV aneurysm formation after acute MI is low (<5%) in the era of reperfusion therapy,
and it is seen more frequently in large anterior MI. The presence of LV aneurysm may increase the risk
for thrombo-embolic complications and arrhythmia, although surgery is rarely needed to correct the
aneurysm.[84]

Prognosis

About 15% of people who have an acute MI in the US will die of it, half within the first hour of symptoms.[2]
Prognosis for patients with STEMI varies depending on time to presentation after onset of chest pain and
time to treatment after presentation. Prognosis is improved by early reperfusion, adherence to appropriate
medical therapy, and risk factor modification. Patients with elevated troponin levels have a worse prognosis
than those with normal troponin levels.[22] Adherence to evidence-based medicine has been shown to
have better patient outcomes.[73] In-hospital death and re-infarction can affect 5% to 10% of patients.[74]
Major bleeding as defined by the Bleeding Academic Research Consortium (BARC) or the Thrombolysis in
Myocardial Infarction (TIMI) bleeding score is associated with worse 1-year mortality.[75]

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 ST-elevation myocardial infarction Guidelines

Diagnostic guidelines

Europe

Acute coronary syndrome: a national clinical guideline

Published by: Scottish Intercollegiate Guidelines Network Last published: 2016

Management of acute myocardial infarction in patients presenting with ST-

segment elevation
Published by: European Society of Cardiology Last published: 2012

Third universal definition of myocardial infarction

Published by: European Society of Cardiology Last published: 2012

Chest pain of recent onset: assessment and diagnosis of recent onset chest
GUIDELINES

pain or discomfort of suspected cardiac origin

Published by: National Institute for Health and Care Excellence Last published: 2010

North America

ACR appropriateness criteria: chest pain suggestive of acute coronary

syndrome
Published by: American College of Radiology Last published: 2014

ACCF/AHA guideline for the management of ST-elevation myocardial

infarction
Published by: American College of Cardiology Foundation; American Last published: 2013
Heart Association

Appropriateness criteria for coronary revascularization

Published by: American College of Cardiology Foundation Last published: 2009
Appropriateness Criteria Task Force; Society for Cardiovascular
Angiography and Interventions; Society of Thoracic Surgeons; American
Association for Thoracic Surgery; American Heart Association; American
Society of Nuclear Cardiology

Appropriateness criteria for stress echocardiography

Published by: American College of Cardiology Foundation Last published: 2008
Appropriateness Criteria Task Force; American Society of
Echocardiography; American College of Emergency Physicians; American
Heart Association; American Society of Nuclear Cardiology; Society for
Cardiovascular Angiography and Interventions; Society of Cardiovascular
Computed Tomography; Society for Cardiovascular Magnetic Resonance

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ST-elevation myocardial infarction Guidelines

Treatment guidelines

Europe

European Resuscitation Council guidelines for resuscitation 2015. Section 8.

Initial management of acute coronary syndromes
Published by: European Resuscitation Council Last published: 2015

2014 ESC/EACTS guidelines on myocardial revascularization

Published by: European Society of Cardiology; European Association Last published: 2014
for Cardio-Thoracic Surgery

Myocardial infarction with ST-segment elevation

Published by: National Institute for Health and Care Excellence Last published: 2013

MI: secondary prevention

GUIDELINES
Published by: National Institute for Health and Care Excellence Last published: 2013

Management of acute myocardial infarction in patients presenting with

persistent ST-segment elevation
Published by: European Society of Cardiology Last published: 2012

Pre-hospital treatment of STEMI patients

Published by: Working Group Acute Cardiac Care of the European Last published: 2011
Society of Cardiology

Ticagrelor for the treatment of acute coronary syndromes

Published by: National Institute for Health and Care Excellence Last published: 2011

Bivalirudin for the treatment of ST-segment-elevation myocardial infarction

Published by: National Institute for Health and Care Excellence Last published: 2011

Chest pain of recent onset: assessment and diagnosis of recent onset chest
pain or discomfort of suspected cardiac origin
Published by: National Institute for Health and Care Excellence Last published: 2010

Endoaortic balloon occlusion for cardiac surgery

Published by: National Institute for Health and Care Excellence Last published: 2008

Guideline for emergency ox ygen use in adult patients

Published by: British Thoracic Society Last published: 2008

Risk estimation and the prevention of cardiovascular disease: a national

clinical guideline
Published by: Scottish Intercollegiate Guidelines Network Last published: 2007

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 ST-elevation myocardial infarction Guidelines

Europe

Acute coronary syndrome

Published by: Joint Royal Colleges Ambulance Liaison Committee Last published: 2007

North America

ACC/AHA/SCAI focused update on primary percutaneous coronary

intervention for patients with ST-elevation myocardial infarction: an update
of the 2011 ACCF/AHA/SCAI guideline for percutaneous coronary intervention
and the 2013 ACCF/AHA guideline for the management of ST-elevation
myocardial infarction
Published by: American College of Cardiology; American Heart Last published: 2015
Association; Society for Cardiovascular Angiography and Interventions;
American College of Emergency Physicians
GUIDELINES

Acute coronary syndromes: 2015 American Heart Association guidelines for

cardiopulmonary resuscitation and emergency cardiovascular care science
Published by: American Heart Association Last published: 2015

ACCF/AHA guideline for the management of ST-elevation myocardial

infarction
Published by: American College of Cardiology Foundation; American Last published: 2013
Heart Association

2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular

risk
Published by: American College of Cardiology; American Heart Last published: 2013
Association

2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce

atherosclerotic cardiovascular risk in adults
Published by: American College of Cardiology; American Heart Last published: 2013
Association

ACCP evidence-based clinical practice guidelines: antithrombotic therapy

and prevention of thrombosis
Published by: American College of Chest Physicians Last published: 2012

2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based

therapy of cardiac rhythm abnormalities
Published by: American College of Cardiology; American Heart Last published: 2012
Association

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ST-elevation myocardial infarction Guidelines

North America

AHA/ACCF secondary prevention and risk reduction therapy for patients with
coronary and other atherosclerotic vascular disease: 2011 update
Published by: American Heart Association; American College of Last published: 2011
Cardiology Foundation

2011 ACCF/AHA/SCAI guideline for percutaneous coronary intervention

Published by: American College of Cardiology Foundation; American Last published: 2011
Heart Association; Society for Cardiovascular Angiography and
Interventions

Effectiveness-based guidelines for the prevention of cardiovascular disease

in women - 2011 update
Published by: American Heart Association Last published: 2011

GUIDELINES
Focused updates to guidelines in ST-elevation myocardial infarction and
percutaneous coronary intervention: application to interventional cardiology
Published by: American College of Cardiology Interventional Scientific Last published: 2010
Council

Clinical policy: critical issues in the evaluation and management of adult

patients with non-ST-segment elevation acute coronary syndromes
Published by: American College of Emergency Physicians Last published: 2006

Clinical policy: indications for reperfusion therapy in emergency department

patients with suspected acute myocardial infarction
Published by: American College of Emergency Physicians Last published: 2006

Asia

API expert consensus document on management of ischemic heart disease

Published by: Association of Physicians of India Last published: 2006

Oceania

Guidelines for the management of acute coronary syndromes

Published by: National Heart Foundation of Australia; Cardiac Society Last published: 2006
of Australia and New Zealand

ST-elevation myocardial infarction: New Zealand management guidelines

Published by: ST-Elevation Myocardial Infarction Guidelines Group; Last published: 2005
New Zealand Branch of the Cardiac Society of Australia and New
Zealand

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 ST-elevation myocardial infarction Evidence scores

Evidence scores
1. Mortality: there is good-quality evidence that aspirin reduces mortality, re-infarction, and stroke at 1
month compared with placebo in people with acute MI.
Evidence level A: Systematic reviews (SRs) or randomized controlled trials (RCTs) of >200
participants.

2. Mortality: there is poor-quality evidence that early invasive cardiac revascularisation may reduce
mortality at 1 and 6 months compared with medical treatment alone in people with cardiogenic shock
within 48 hours of acute MI.
Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomized
controlled trials (RCTs) of <200 participants.

3. Mortality: there is no direct evidence on positive inotropes for the treatment of cardiogenic shock after
acute MI. However, there is consensus that they are beneficial.
Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomized
controlled trials (RCTs) of <200 participants.

4. Bleeding: there is good-quality evidence that anticoagulation with bivalirudin alone significantly
reduces major bleeding and adverse clinical events compared with a GPIIb/IIIa inhibitor plus heparin in
patients with ST-segment elevation MI undergoing percutaneous coronary intervention (PCI).[30]
Evidence level A: Systematic reviews (SRs) or randomized controlled trials (RCTs) of >200
participants.

5. Mortality: there is poor-quality evidence that primary percutaneous transluminal coronary angioplasty
(PTCA) may reduce mortality rates compared with thrombolysis alone in people with acute MI.
Primary PTCA has been associated with increased major bleeding at 4 to 6 weeks compared with
thrombolysis.
Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomized
controlled trials (RCTs) of <200 participants.

6. Cardiovascular events: there is good-quality evidence that beta-blockers reduce re-infarction rates at
28 days compared with placebo in people with acute MI.
Evidence level A: Systematic reviews (SRs) or randomized controlled trials (RCTs) of >200
participants.
EVIDENCE SCORES

7. Mortality: there is medium-quality evidence that, compared with placebo, thrombolytic treatment
reduces mortality in people with acute MI. Thrombolytic treatment has been associated with increased
risk of stroke compared with control.

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ST-elevation myocardial infarction Evidence scores
Evidence level B: Randomized controlled trials (RCTs) of <200 participants, methodologically
flawed RCTs of >200 participants, methodologically flawed systematic reviews (SRs) or good quality
observational (cohort) studies.

8. Timing: there is medium-quality evidence that the earlier thrombolytic treatment is given after the onset
of symptoms in people with acute MI, the greater the benefit of treatment compared with placebo.
Thrombolytic treatment has been associated with an increased risk of stroke compared with control.
Evidence level B: Randomized controlled trials (RCTs) of <200 participants, methodologically
flawed RCTs of >200 participants, methodologically flawed systematic reviews (SRs) or good quality
observational (cohort) studies.

9. Mortality: there is poor-quality evidence that adding a glycoprotein IIb/IIIa inhibitor to thrombolytic
therapy within 6 hours of an acute MI may be no more effective at reducing mortality or other
cardiovascular events at 30 days compared with thrombolysis alone. The combined treatment has
been associated with increased bleeding complications, particularly extracranial haemorrhage.
Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomized
controlled trials (RCTs) of <200 participants.

10. Re-infarction rates: there is good-quality evidence that adding low weight molecular heparin
(enoxaparin) to thrombolytic therapy (streptokinase) reduces re-infarction rates compared with
thrombolytic therapy alone in people with acute MI; however, is no more effective at reducing mortality.
Evidence level A: Systematic reviews (SRs) or randomized controlled trials (RCTs) of >200
participants.

11. Mortality: there is good-quality evidence that angiotensin-converting enzyme (ACE) inhibitors are more
effective at reducing overall mortality and sudden cardiac death after 2 to 42 months compared with
placebo, when started within 14 days of an acute MI.
Evidence level A: Systematic reviews (SRs) or randomized controlled trials (RCTs) of >200
participants.

12. Mortality: there is poor-quality evidence that beta-blockers may reduce mortality rates at 6 weeks to 3
years after MI compared with placebo.
Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomized
controlled trials (RCTs) of <200 participants.
EVIDENCE SCORES

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BMJ Best Practice topics are regularly updated and the most recent version
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 ST-elevation myocardial infarction References

Key articles
• O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-
REFERENCES

elevation myocardial infarction: a report of the American College of Cardiology Foundation/American

Heart Association Task Force on Practice Guidelines. Circulation. 2013;127:e362-e425. Full text
Abstract

• Windecker S, Kolh P, Alfonso F, et al. 2014 ESC/EACTS Guidelines on myocardial revascularization.

Eur Heart J. 2014;35:2541-2619. Full text Abstract

• Cannon CP, Blazing MA, Giugliano RP, et al. Ezetimibe added to statin therapy after acute coronary
syndromes. N Engl J Med. 2015;372:2387-2397. Full text Abstract

• Montalescot G, Pitt B, Lopez de Sa E, et al; REMINDER Investigators. Early eplerenone treatment in

patients with acute ST-elevation myocardial infarction without heart failure: the Randomized Double-
Blind Reminder Study. Eur Heart J. 2014;35:2295-2302. Abstract

• Cantor WJ, Fitchett D, Borgundvaag B, et al. Routine early angioplasty after fibrinolysis for acute
myocardial infarction. N Engl J Med. 2009;360:2705-2718. Abstract

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53. Montalescot G, Pitt B, Lopez de Sa E, et al; REMINDER Investigators. Early eplerenone treatment in
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therapy for patients with coronary and other atherosclerotic vascular disease: 2011 update: a guideline
from the American Heart Association and American College of Cardiology Foundation. Circulation.
2011;124:2458-2473. Full text Abstract

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 ST-elevation myocardial infarction Images

Images

Figure 1: 12-Lead ECG with ST-segment elevation lead V1 to V4

IMAGES

From the personal collection of Dr Mahi Ashwath; used with permission

Figure 2: 12-Lead ECG with ST-segment elevation in the inferior leads (II, III, and aVF)
From the personal collection of Dr Mahi Ashwath; used with permission

82 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
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ST-elevation myocardial infarction Images

IMAGES
Figure 3: 12-Lead ECG with normal ST segments and without any abnormal Q waves
From the personal collection of Dr Mahi Ashwath; used with permission

Figure 4: 12-Lead ECG 1 week later with borderline anterolateral ST-elevation and reciprocal ST-depression
in the inferior leads; also noted is the poor R-wave progression and the presence of septal Q waves
From the personal collection of Dr Mahi Ashwath; used with permission

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
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of the topics can be found on [Link] . Use of this content is
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IMAGES ST-elevation myocardial infarction Images

Figure 5: 12-Lead ECG 1 hour later with obvious anterolateral ST-elevation and reciprocal ST-depression in
the inferior leads, absence of anterior R waves, and the development of anterior Q waves
From the personal collection of Dr Mahi Ashwath; used with permission

Figure 6: 12-Lead ECG 3 hours later with completed anterolateral infarct, absence of anterolateral R waves,
and the development of anterolateral Q waves; the ST segments are returning to normal
From the personal collection of Dr Mahi Ashwath; used with permission

84 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
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ST-elevation myocardial infarction Images

IMAGES
Figure 7: 12-Lead ECG the next day with completed anterolateral infarct; ST segments are completely back to
baseline
From the personal collection of Dr Mahi Ashwath; used with permission

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IMAGES ST-elevation myocardial infarction Images

Figure 8: Angiogram showing occluded right coronary artery

From the personal collection of Dr Mahi Ashwath; used with permission

86 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
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ST-elevation myocardial infarction Images

IMAGES
Figure 9: Angiogram showing an attempt to open the occluded right coronary artery with an angioplasty
balloon
From the personal collection of Dr Mahi Ashwath; used with permission

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IMAGES ST-elevation myocardial infarction Images

Figure 10: Angiogram after balloon angioplasty and stenting showing an open right coronary artery
From the personal collection of Dr Mahi Ashwath; used with permission

88 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
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ST-elevation myocardial infarction Images

Figure 11: 12-Lead ECG showing inferior and anterior ST-elevation with reciprocal changes in the lateral
leads

IMAGES
From the personal collection of Dr Mahi Ashwath; used with permission

Figure 12: 12-Lead ECG immediately after successful revascularisation showing ST segments returning to
baseline
From the personal collection of Dr Mahi Ashwath; used with permission

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IMAGES ST-elevation myocardial infarction Images

Figure 13: 12-Lead ECG on follow-up 7 months later with normal ST segments and the absence of Q waves
From the personal collection of Dr Mahi Ashwath; used with permission

90 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 13, 2017.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on [Link] . Use of this content is
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ST-elevation myocardial infarction Disclaimer

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Contributors:

// Authors:

Mahi L. Ashwath, MD, FACC, FASE

Director of Noninvasive Cardiology
Healthspan Cardiology, Board Member, Healthspan Physicians Inc., Cleveland, OH
DISCLOSURES: MLA declares that she has no competing interests.

Sanjay Gandhi, MD, FACC, FAHA, FSCAI

Director, Endovascular Cardiology
Associate Professor of Medicine, Endovascular Cardiology, Case Western Reserve University, Cleveland,
OH
DISCLOSURES: SG declares that he has no competing interests.

// Acknowledgements:
Dr Mahi L. Ashwath and Dr Sanjay Gandhi would like to gratefully acknowledge Dr Thomas Vrobel, a
previous contributor to this monograph. TV declares that he has no competing interests.

// Peer Reviewers:

Dale Adler, MD, FACC

Vice Chairman of Medicine for Network Development and Strategic Planning
Brigham and Women's Hospital, Boston, MA
DISCLOSURES: DA declares that he has no competing interests.

Deepak L. Bhat t, MD
Associate Professor of Medicine
Department of Cardiovascular Medicine, Cleveland Clinic, OH
DISCLOSURES: DLB declares that he has no competing interests.

Gregory Lip, MD, FRCP, FACC, FESC

Consultant Cardiologist and Professor of Cardiovascular Medicine
University Department of Medicine, City Hospital, Birmingham, UK
DISCLOSURES: GL declares that he has no competing interests.