Non-ST-elevation Myocardial Infarction: The Right Clinical Information, Right Where It's Needed

Non-ST-elevation
myocardial infarction
The right clinical information, right where it's needed
Last updated: Dec 06, 2018

Table of Contents
Summary 3
Basics 4
Definition 4
Epidemiology 4
Aetiology 4
Pathophysiology 4
Classification 5
Prevention 8
Primary prevention 8
Secondary prevention 8
Diagnosis 10
Case history 10
Step-by-step diagnostic approach 10
Risk factors 14
History & examination factors 17
Diagnostic tests 19
Differential diagnosis 22
Diagnostic criteria 26
Treatment 29
Step-by-step treatment approach 29
Treatment details overview 34
Treatment options 36
Follow up 52
Recommendations 52
Complications 53
Prognosis 54
Guidelines 56
Diagnostic guidelines 56
Treatment guidelines 57
Evidence scores 61
References 63
Images 76
Disclaimer 78
Summary
◊ Part of the acute coronary syndrome spectrum. Usually caused by a partial or near-complete
occlusion of a coronary artery resulting in compromised blood flow to myocardium with subsequent
myocardial injury or infarction as demonstrated by elevation in troponin.
◊ There are differences in typical presentation between the sexes. Male patients typically present
with chest pressure/discomfort lasting at least several minutes, at times accompanied by sweating,
dyspnoea, nausea, and/or anxiety. Women present more commonly with middle/upper back pain or
dyspnoea and similar associated symptoms.
◊ Symptoms are indistinguishable from those of unstable angina. However, non-ST-elevation

myocardial infarction (MI) is differentiated from unstable angina by a rise of troponin.
◊ ECG is the first-line investigation in all patients and should not be delayed for history, examination, or
other tests.
◊ Early risk stratification and treatment with anti-ischaemic (beta-blockers, nitrates), anticoagulant
(heparin), and dual antiplatelet agents (aspirin plus a P2Y12 receptor inhibitor) is needed. Higher-
risk patients should be considered for an early invasive strategy (coronary angiography and
revascularisation in 12-24 hours).
◊ Complications are progression or worsening of MI, heart failure, cardiogenic shock, arrhythmias, and
death.
Non-ST-elevation myocardial infarction Basics
Definition
Non-ST-elevation myocardial infarction (NSTEMI) is an acute ischaemic event causing myocyte necrosis.
The initial ECG may show ischaemic changes such as ST depressions, T-wave inversions, or transient ST
BASICS
elevations; however, it may also be normal or show non-specific changes. If persistent ST elevation, evidence
of posterior MI, or a new left bundle-branch block is present, then the patient should be evaluated as an ST-
elevation myocardial infarction. NSTEMI, therefore, encompasses a broad spectrum of ischaemic injury to
the myocardium, which is detected by elevation of troponin.[1] It can be distinguished from unstable angina
pectoris by normal serial troponin.
Epidemiology
Cardiovascular disease (CVD) is the number one cause of death worldwide, accounting for 17.5 million
deaths per year. In 2012, the WHO estimated that one third of all deaths globally were attributable to CVD,
and 7.4 million of those deaths were from ischaemic heart disease.[8] Coronary heart disease mortality is
decreasing in many developed countries, but is increasing in developing and transitional countries, partly
as a result of increasing longevity, urbanisation, and lifestyle changes. Epidemiology data have shown
that acute coronary syndrome (ACS) cases with ST-elevation myocardial infarction (STEMI) appear to be
declining and that NSTEMI occurs more frequently than STEMI.[4] [6] In the US, it is estimated that >780,000
people will experience an ACS each year, and approximately 70% of these will have NSTEMI.[1] Trends from
the world's largest database of patients with ACS show that the percentage of patients with a diagnosis of
NSTEMI is rising dramatically.[9] This is likely to be due to the advent of more sensitive assays for myocardial
injury, earlier pharmacotherapy, and reperfusion (and prevention) of STEMI.[2] [9]
Aetiology
The classic mechanism of ST-elevation myocardial infarction (MI) is complete occlusion (typically thrombosis
or embolism) of a coronary artery. In contrast, NSTEMI is usually a result of a transient or near-complete
occlusion of a coronary artery or acute factor that deprives myocardium of oxygen.
Unstable plaques have soft, lipid-laden contents, with thin, often sclerotic fibrous caps infiltrated by
macrophages (foam cells). Release of the lipid-rich atherogenic core causes adhesion, activation, and
aggregation of platelets. This initiates the coagulation cascade. A superimposed thrombus forms, occluding
the coronary blood flow and resulting in myocardial ischaemia causing a type 1 MI.[10]
NSTEMI may also be caused by other mechanisms, such as dynamic obstruction (i.e., focal coronary artery
spasm or Prinzmetal's angina), severe progressive atherosclerosis, restenosis following percutaneous
coronary intervention (PCI), recreational drug use (e.g., cocaine or other stimulants), arterial inflammation, or
extrinsic causes leading to myocardial supply-demand mismatch (i.e., type 2 MI precipitated by acute blood
loss in a patient with underlying coronary artery disease).[1]
Pathophysiology
NSTEMI is a result of an acute imbalance between myocardial oxygen demand and supply, most commonly
due to a reduction in myocardial perfusion. Type 1 myocardial infarction (MI) is most commonly caused by
a non-occlusive thrombus that develops in a disrupted atherosclerotic plaque, and leads to non-occlusive or
near-complete thrombosis of a vessel supplying the myocardium.
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Dec 06, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
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subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
Several different sequences of events may lead to an NSTEMI:
• Plaque rupture with superimposed non-occlusive thrombus or embolic events leading to coronary
vascular obstruction
BASICS
• Dynamic obstruction, such as in vasospasm
• Progressive luminal narrowing (i.e., chronic arterial narrowing from restenosis)
• Inflammatory mechanisms (i.e., vasculitis)
• Extrinsic factors leading to poor coronary perfusion (such as hypotension, hypovolaemia, or hypoxia).
The most common cause is plaque rupture or obstructive atherosclerotic disease. In this setting, the release
of myocardial biomarkers in type 1 MI is thought to be due to atherosclerotic plaque fissuring or rupture with
resulting intra-coronary thrombus or platelet emboli leading to diminished myocardial blood flow.
Plaque rupture usually occurs at the weakest and thinnest part of the atherosclerotic cap (often at the
shoulder region). Ruptured plaques contain large numbers of inflammatory cells including monocytes,
macrophages, and T lymphocytes.[10] [11] Although one third of occlusions occur at a site with the greatest
stenosis, most (66% to 78%) arise from lesions with <50% stenosis, and <5% arise from lesions exhibiting
>70% stenosis.[11] Approximately 25% of patients with a diagnosis of NSTEMI have a 100% occlusion of the
affected artery on coronary angiography.[12]
The severity of myocardial damage in NSTEMI depends on:
• Duration of ischaemia and time to reperfusion

• Extent of underlying atherosclerosis
• Presence of collateral blood flow to the affected region (reserve blood flow)
• Diameter of affected coronary vessel
• Degree of occlusion
• Presence of other comorbidities (i.e., diabetes, renal failure, or hypertension).
Classification
Myocardial infarction redefined[2] [3] [4]
The development of myocardial tissue-specific biomarkers and sensitive cardiac imaging techniques
allows for early detection of very small amounts of myocardial injury or necrosis. Consequently, myocardial
infarction (MI) has been redefined to encompass any necrosis in the setting of myocardial ischaemia by any
of the following possible aetiologies. MI can be broken down into five different subtypes.
• Type 1: spontaneous MI caused by a pathological process in the wall of the coronary artery with
or without underlying CAD (e.g., plaque rupture). Presentations are consistent with acute coronary
syndrome-type symptoms.
• Type 2: MI secondary to an increase in oxygen demand or decrease in supply (i.e., imbalance caused
by severe anaemia or hypotension; also includes dynamic coronary artery spasm).
• Type 3: sudden unexpected cardiac death before cardiac biomarkers obtained.
• Type 4a: MI associated with percutaneous coronary intervention (PCI).
• Type 4b: MI associated with stent thrombosis.
• Type 4c: MI associated with re-stenosis.
• Type 5: MI associated with coronary bypass graft surgery.
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Dec 06, 2018.
5
Criteria required to meet the definition for acute MI (types 1, 2, and 3) include:[3]
1. Acute myocardial injury with clinical evidence of acute myocardial ischaemia and with detection of
a rise and/or fall of cardiac troponin values with at least one value above the 99th percentile upper
BASICS
reference limit (URL) and at least one of the following:
• Ischaemic symptoms
• New, or presumed new, ECG changes indicative of ischaemia (left bundle branch block, ST
elevation or depression)
• Development of pathological Q waves on the ECG
• Myocardial necrosis or regional wall motion abnormality evidenced by cardiac imaging
• Intra-coronary thrombus detected on angiography or autopsy.
2. Pathological findings of an acute MI.
The term 'myocardial injury' is used when there is evidence of elevated cardiac troponin values with at least
one value above the 99th percentile URL. The myocardial injury is considered acute if there is a rise and/or
fall of cardiac troponin values.[3]
There has been ongoing controversy in the literature and in clinical practice about distinguishing between
type 1 and type 2 MI. Type 1 MI occur spontaneously and are associated with symptoms of acute coronary
syndrome, typically have more significant elevations in troponin levels than type 2 MI, and are associated
with acute coronary arterial processes such as plaque rupture/ulceration/dissection noted at coronary
angiography. Type 2 MI are usually associated with elevated myocardial oxygen demand or decreased
myocardial blood flow such as occurs with tachycardia or hypotension. Troponin is elevated in type 2
MI, although not as elevated as in type 1 injuries. Although coronary artery disease may be present on
angiogram, there is absence of acute pathology. Some experts advocate for a separate category of 'non-
ischaemic myocardial injury' to describe biomarker elevation in the setting of critical illness, although this has
not been added to current European or American clinical guidelines.[5]
Acute coronary syndrome (ACS)[1]

ACS is a term used to describe a range of conditions resulting from sudden reduction in coronary blood
flow. Symptoms should be present suggestive of angina or anginal equivalent presentation. The presence
or absence of ST-segment elevation on presenting ECG indicates ST-elevation MI, or non-ST-elevation
acute coronary syndrome (NSTE-ACS). NSTE-ACS is further sub-divided into NSTEMI or unstable angina,
depending on elevation of troponin.
1. ST-elevation MI (STEMI): ECG demonstrates ST elevation of >1 mm in ≥2 anatomically contiguous

leads, usually associated by location. Repolarisation abnormalities often evolve over time from
hyperacute T waves to ST elevation to T-wave inversion to the development of Q waves. STEMI
patients typically have a rise and fall of serum cardiac biomarkers. While biomarkers are useful for
confirmatory and prognostic purposes, they are not required for the diagnosis of STEMI and should
not delay treatment. Clinicians must be careful to recognise other causes of ST elevation that mimic
a STEMI. These include left ventricular hypertrophy, left bundle-branch block, paced rhythm, benign
early repolarisation, pericarditis, and hyperkalaemia.
2. NSTEMI: ECG does not show persistent ST elevation, but may show ischaemic changes such as ST
depression or T-wave inversion. The ECG may also be normal. Serum levels of cardiac biomarkers are
elevated.
3. Unstable angina pectoris: cardiac biomarkers are normal.[6] [7]
BASICS
7
Non-ST-elevation myocardial infarction Prevention
Primary prevention
The most important preventive actions involve combined dietary and lifestyle changes (stopping smoking;
increasing physical activity; losing weight; increasing consumption of fish, fruits, vegetables, fibre, and nuts;
reducing salt intake).
If overweight, patients should lose weight and maintain a healthy body weight. Patients should consume
a diet rich in vegetables and fruits. Patients should be advised to choose wholegrain, high-fibre foods and
to eat fish, especially oily fish, at least twice a week. Excess sugars, trans-fats, salt, and foods with excess
cholesterol should be limited.
For a smoker, cessation is the single most crucial step that can be taken to reduce heart-related and
all-cause death. This also includes avoiding second-hand smoke. Many different support programmes,
medicines, and alternative therapies are available to help. It takes as little as 3 years of smoking cessation
in a smoker who has had an MI to reduce risk from cardiac death to the same level as that of someone who
has never smoked.
PREVENTION
Improving physical fitness through aerobic exercise is extremely important. It is recommended that patients
engage in ≥30 minutes of moderate-intensity physical activity 5 days/week or high intensity for more than 30
minutes 3 days per week.[26] Likewise, patients should engage in multiple short bouts of physical activity
daily, such as taking the stairs instead of the lift, or walking the dog.
Family members can be very helpful and should become involved along with other support systems to
help remind patients of and to reinforce lifestyle changes. Patients should use the resources that are
available (e.g., written materials, the Internet, educational classes, and regular counselling) and be in close
communication with healthcare providers.
Statin therapy in patients who are at risk for future development of coronary artery disease improves
survival and reduces future risk of cardiovascular events. Current guidelines recommend the use of a
cardiovascular risk calculator to identify those patients most at risk and guide initiation of statin therapy for
primary prevention.[35] The role of statins and other similar therapy in patients with minor or no risk factors is
currently being evaluated.[36]
Recent improvements in research, public awareness, and health education have demonstrated several
sex-specific differences in primary prevention of cardiovascular disease (CVD). In 2011, effectiveness-
based guidelines for the prevention of CVD in women were published.[37] The guidelines summarise current
knowledge, evidence, and rationale for prevention strategies in women.
Secondary prevention
The most important preventive actions involve combined dietary and lifestyle changes (stopping smoking;
increasing physical activity; losing weight; increasing consumption of fish, fruits, vegetables, fibre, and nuts;
reducing salt intake).
Patients should switch to a heart-healthy diet. If overweight, patients should lose weight and maintain a
healthy body weight. Patients should consume a diet rich in vegetables and fruits. Patients should be advised
to choose wholegrain, high-fibre foods and to eat fish, especially oily fish, at least twice a week. Excess
sugars, trans-fats, salt, and foods with excess cholesterol should be limited.
For a smoker, cessation is the single most crucial step that can be taken to reduce heart-related and all-
cause death. This includes avoiding second-hand smoke. Many different support programmes, medicines,
and alternative therapies are available to help. Data from the EVITA (Evaluation of Varenicline in Smoking
Cessation for patients post Acute Coronary Syndrome) trial suggest that pharmacotherapy with varenicline
Non-ST-elevation myocardial infarction Prevention
started in hospital at the time of an acute coronary syndrome may be efficacious for smoking cessation;
however, further studies to assess safety endpoints are needed.[145] It takes as little as 3 years of smoking
cessation in a smoker who has had a myocardial infarction to reduce risk from cardiac death to the same
level as that for someone who has never smoked.
Improving physical fitness through aerobic exercise is extremely important. It is recommended that patients
engage in ≥30 minutes of moderate-intensity physical activity on most, and preferably all, days of the week.
Likewise, patients should engage in multiple short bouts of physical activity daily, such as walking the dog or
taking the stairs instead of the lift.
Family members can be very helpful and should become involved along with other support systems to help
remind patients of, and to reinforce, lifestyle changes. Patients should use the resources that are available
(e.g., written materials, the Internet, educational classes, regular counselling) and be in close communication
with healthcare providers.
PREVENTION
9
Non-ST-elevation myocardial infarction Diagnosis
Case history
Case history #1
A 69-year-old man develops worsening substernal chest pressure after shovelling snow in the morning
before work. He tells his wife he feels a squeezing pain that is radiating to his jaw and left shoulder. He
appears anxious and his wife calls for an ambulance, as he is distressed and sweating profusely. Past
medical history is significant for hypertension and he has been told by his doctor that he has borderline
diabetes. On examination in the emergency department he is very anxious and diaphoretic. His heart rate
is 112 bpm and blood pressure is 159/93 mmHg. The ECG is significant for ST depression in the anterior
leads. Three doses of sublingual glyceryl trinitrate provide little relief.
Other presentations
Presentations of myocardial infarction (MI) can be diverse. Some patients do not have any chest
discomfort, whereas others may experience classical 'crushing' or severe pain. It is important to recognise
that atypical presentation such as dyspnoea, syncope, palpitations, isolated nausea/vomiting, abdominal
pain, and fatigue can indicate acute coronary syndrome. These atypical presentations are more common
in women, older people, people with diabetes, those with chronic kidney disease, and cardiac transplant
recipients. A feeling of indigestion may be the only symptom and occurs more often with inferior wall MI.
Highly specific presentations include substernal pressure/discomfort, which may radiate to the arm, neck,
and shoulder, associated with diaphoresis and anxiety.[1] Some patients present with jaw, neck, ear, arm,
or epigastric pain only. These symptoms should be considered equivalent to angina if they are clearly
related to stress or exertion, or are quickly relieved by glyceryl trinitrate or physical rest. A sharp, stabbing
pain or pain reproducible on palpation does not exclude acute coronary syndrome.[1]
Step-by-step diagnostic approach

DIAGNOSIS
Patients with suspected acute coronary syndrome (ACS) require urgent evaluation. It is essential to establish
whether the symptoms are a manifestation of an ACS and, if so, how likely it is for an adverse clinical event
to occur.[1] Physicians need to first establish the patient's risk and follow current guidelines according to the
initial risk assessment to choose an appropriate management strategy. The initial risk assessment includes
the history, examination, ECG, and cardiac biomarkers.[1] [38]
ECG
ECG is indicated as the first-line investigation in all patients and should not be delayed to take the
history, carry out an examination, or do other diagnostic tests. A 12-lead ECG should be performed and
interpreted within 10 minutes of the patient arriving at the emergency facility. It is critical to immediate
management to exclude ST-elevation myocardial infarction (STEMI). NSTEMI is indistinguishable from
other types of ACS (STEMI or unstable angina) until ECG and biomarkers become available, because
their pathophysiology and presentation are similar.[1] Typical ECG findings may be present, but many
patients have a normal ECG at presentation and therefore serial ECGs, initially at 15- to 30-minute
intervals, should be performed to detect the potential for development of ST-segment elevation or
depression. ECG findings in NSTEMI may be highly variable. Typically >1 mm of ST depression is present
in 2 or more contiguous leads. Other potential findings include dramatic new T-wave inversions (Wellens
waves) or minor non-diagnostic changes, or the ECG may be normal. ECG changes of ST elevation or
new left bundle branch block should be evaluated as STEMI.
[Fig-1]
[Fig-2]
Continuous 12-lead ECG monitoring is a reasonable alternative to serial 12-lead recordings in patients
whose initial ECG is non-diagnostic.[1] Supplemental ECG leads V7 to V9 may be useful in patients with
non-diagnostic initial ECGs to rule out myocardial infarction (MI) due to left circumflex occlusion.[1] Less
commonly, the ECG may reveal a tachyarryhthmia or bradyarrhythmia precipitated by the MI.
History and examination

Patients presenting with chest pain or discomfort need immediate assessment for current or past history
of coronary artery disease (CAD) and traditional risk factors (e.g., age, sex, diabetes, hypertension,
cocaine use) to triage them as high priority.[1] ACS is highly likely if there is a history of chest or left arm
pain similar to previously documented angina pain, and a history of CAD (including MI). Angina pain
is typically deep, poorly localised chest or arm pain described as a sensation of tightness, heaviness,
aching, burning, pressure, or squeezing. The pain is most often retrosternal and can often radiate to the
left arm, but may also radiate to the lower jaw, neck, both arms, back, and epigastrium, where it may
mimic heartburn. It is associated with exertion or emotional stress (or less commonly with cold exposure)
and relieved by rest or sublingual glyceryl trinitrate.[1]
Diaphoresis is a common associated symptom. Shortness of breath is also common and is probably
secondary to diminished cardiac output. Patients may express anxiety or appear anxious. They may
also report a feeling of impending doom. Classically, events peak at around 8 a.m., presumably due
to haemodynamic stress caused by increased serum cortisol, adrenergic hormones, and platelet
aggregation.
Patients may present with a range of atypical symptoms, any of which may be the sole presenting
symptom. These include weakness, nausea, vomiting, abdominal pain, and syncope. These are more
common in women, older people, and those with diabetes or chronic kidney disease. Examination
DIAGNOSIS
findings are usually non-specific but may reveal hypertension or hypotension, the presence of third and
fourth heart sounds, and paradoxical splitting of the second heart sound. Signs of heart failure (raised
jugular venous pressure, bilateral crepitations on auscultation of the lungs) or cardiogenic shock may also
be present, and these signify a worse prognosis.
Initial tests (non-ECG)

In addition to the ECG, the following tests must also be performed in all patients.
• Therapeutic trial of sublingual glyceryl trinitrate: patients with ongoing ischaemic discomfort should
receive a trial of sublingual glyceryl trinitrate (0. 4 mg) every 5 minutes for a total of 3 doses, after
which the need for intravenous nitroglycerin should be assessed, if not contraindicated. Nitrates
should be avoided in patients with hypotension, suspected right ventricular infarction, or recent
phosphodiesterase inhibitor use.
• Cardiac troponins or other cardiac markers: a rise in the levels of cardiac troponins (>99th
percentile of normal) are diagnostic for the condition. The test should be repeated 3 to 6 hours
after symptom onset because levels may be normal initially. This test is readily available at most
institutions. If it is not available, the typical rise and fall of other cardiac markers (CK, CK-MB,
11
and/or myoglobin) can be used. Patients with a high index of suspicion who have negative serial
ECGs and cardiac enzymes should be closely monitored in a telemetry or chest pain unit, as it
may take time for cardiac markers to rise.[1] Additionally, there have been recent investigations into
novel cardiac biomarkers, such as cardiac myosin-binding protein C (cMyC), which may improve
discriminatory power of cardiac biomarkers, but these are not readily available.[39]
• Chest x-ray: indicated to determine whether congestive heart failure (CHF) is present and to
exclude non-cardiac causes for chest pain.
• FBC: haemoglobin and haematocrit measurements may help to evaluate a secondary cause of
NSTEMI (e.g., acute blood loss, anaemia) and to evaluate thrombocytopenia to estimate risk of
bleeding.
• Urea and serum creatinine: creatinine clearance should be estimated in NSTEMI patients and the
doses of renally cleared drugs should be adjusted appropriately. In chronic kidney disease patients
undergoing angiography, iso-osmolar contrast agents may be preferred.[1] [4]
• Serum electrolytes: electrolyte derangements may predispose to cardiac arrhythmias.
• Liver function tests: useful if treatment with drugs that undergo hepatic metabolism is considered.
Risk stratification
ACS management requires continuous risk stratification for death or recurrent MI. The American College
of Cardiology/American Heart Association recommend that patients with suspected ACS are risk stratified
based on the likelihood of ACS and adverse outcome(s) to further triage and assist in the selection
of treatment options.[1] A number of risk scores exist which incorporate a number of variables such
as clinical history, angina symptoms and equivalents, physical examination, ECG, renal function, and
troponin levels. These variables can be used to estimate the risk of death and non-fatal cardiac ischaemic
events, for example, using the TIMI risk score
[VIDEO: Thrombolysis in Myocardial Infarction (TIMI) Score for Unstable

Angina Non ST Elevation Myocardial Infarction ]
or the GRACE risk model.[1] [40]
DIAGNOSIS
[VIDEO: GRACE Score for Acute Coronary Syndrome Prognosis ]
The TIMI risk score is composed of 7 risk indicators rated on presentation. One point is awarded for the
presence of each of the following criteria:
• Age >65 years

• Presence of ≥3 CAD risk factors
• Prior coronary stenosis >50%
• ST-segment deviation on ECG
• Elevated serum cardiac biomarkers
• At least 2 anginal episodes in the past 24 hours
• Use of aspirin in the past 7 days.
Patients with a TIMI score of 0 to 2 are low risk, 3 to 4 are intermediate risk, and 5 to 7 are high risk. All-
cause mortality, rate of MI, and rate of urgent revascularisation at 14 days increase in proportion to the
number of risk factors present on the TIMI score.
The GRACE risk model is a web-based tool that can be used to predict in-hospital and post-discharge
mortality or MI in patients following an initial ACS.
The Killip classification is another tool that can be used for risk stratification. This classification system risk
stratifies patients with acute MI based on clinical evidence of left ventricular failure:
• Class I: no evidence of CHF

• Class II: presence of a third heart sound gallop, basilar rales, or elevated jugular venous pressure
• Class III: presence of pulmonary oedema
• Class IV: cardiogenic shock.
The HEART Score incorporates elements of the patient’s history, ECG, age, risk factors, and troponin
and is used for patients in the accident and emergency department setting to assess risk of acute MI,
percutaneous coronary intervention (PCI), coronary artery bypass graft (CABG), and death within 6
weeks of initial presentation.[41]
[VIDEO: HEART Score ]
Subsequent tests
Following initial work-up and risk stratification, a range of additional investigations may be considered.
• Brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-pro-BNP): measurement of BNP or
NT-pro-BNP may be considered to supplement assessment of global risk in patients with suspected
ACS, particularly cardiogenic shock associated with MI type 1.[1]
• Lipid profile: this test is indicated in the first 24 hours of admission to hospital to assess for lipid
abnormalities and therefore the need for any lipid-lowering therapy.
• Angiography: urgent and immediate angiography is indicated if patients do not stabilise with
intensive medical treatment.[1] Indications include recurrent symptoms (refractory angina),
ischaemia despite adequate medical treatment, high risk (e.g., CHF, malignant ventricular
arrhythmias), or non-invasive test findings (significant left ventricular dysfunction, ejection fraction
<0.35, large anterior or multiple perfusion defects). Patients with a history of anaphylaxis or allergy
to contrast must be pre-medicated prior to angiography.
[Fig-3]
DIAGNOSIS
[Fig-4]
• Echocardiography: cardiac ultrasound is also useful to evaluate ischaemic complications and
other causes of chest pain (i.e., pulmonary embolism, effusion, or acute valvular pathology) and is
indicated after initial assessment. Cardiac ultrasound can demonstrate ischaemic changes even
before ECG changes appear. The presence of regional wall motion abnormalities and decreased
left ventricular function provides evidence for ACS. Also important, normal cardiac function and
viability have a very high negative predictive value and practically exclude acute MI. Consequently,
cardiac ultrasound may be useful for early triage of patients with suspected MI.[3]
• Stress testing: stress testing, including treadmill exercise testing, may be useful and is
recommended in low and intermediate pre-test probability with a normal ECG and normal high
sensitivity biomarkers to assist with guiding the need for an invasive strategy.[1] [42] [43] The
sensitivity and specificity of these tests increase when combined with either nuclear imaging to look
for myocardial perfusion defects or echocardiography to assess wall motion abnormalities. The
key positive finding on nuclear imaging stress tests is the presence of a reversible defect. This is
an area of myocardium that becomes deprived of perfusion during increased myocardial demand
and reperfuses on stopping the activity. This signifies stenosis within the coronary circulation that
may be treated with percutaneous coronary intervention or CABG. Sub-maximal exercise testing
13
can be performed at 4 to 7 days after myocardial infarction, while symptom limited testing can be
performed at 14 to 21 days post-myocardial infarction, when the patient has been free of active
ischaemic or heart failure symptoms.[44]
• Coronary CT angiography (CCTA): this may provide non-invasive evaluation of coronary anatomy
and atherosclerosis. Renal failure is a relative contraindication. Patients with contrast allergy may
be pre-medicated prior to angiography.[45] Due to the high negative predictive value of CCTA,
evidence suggests that CCTA is useful in patients with low to moderate risk of NSTEMI. When
compared with the standard care of low-risk patients (observation, serial enzymes followed by
stress testing) CCTA reduced time to diagnosis, reduced length of emergency department stay,
and had similar safety.[46] CCTA is not indicated for patients with high-risk features (i.e., ischaemic
ECG changes, positive cardiac markers).[47]
[Fig-4]
[Fig-3]
Risk factors
Strong
atherosclerosis (history of angina, myocardial infarction, stroke, transient
ischaemic at tack, peripheral vascular disease)
• Atherosclerotic heart disease is the underlying mechanism in coronary artery disease (CAD). It
evolves over decades and can begin in childhood. One study found intimal lesions in the aorta in all
those aged 15-19 years, and in the right coronary artery in more than half of those of this age.[13]
Atherosclerosis is typically silent until an acute event occurs (e.g., acute coronary syndrome).
A sedentary lifestyle, excess caloric intake, and cigarette smoking are strongly associated with
atherosclerosis.
• In an acute setting, the presence or absence of the traditional risk factors for CAD are not specific or
sensitive for diagnosing NSTEMI. However, they do appear to be important in determining prognosis in
DIAGNOSIS
acute coronary syndrome and targeting secondary prevention strategies.[1]
diabetes
• Patients with diabetes mellitus are at increased risk of coronary artery disease (CAD). The
mechanisms are not fully known but they may reflect vascular abnormalities of inflammation, obesity,
hypertension, dyslipidaemia, and hypercoagulability.
• Approximately 20% to 25% of all patients with NSTEMI have diabetes and CAD accounts for 75% of
all deaths in the diabetic population.[1] [14] Diabetes is associated with more extensive CAD, unstable
lesions, and less favourable long-term outcomes (death, myocardial infarction [MI], acute coronary
syndrome re-admission), as well as with coronary revascularisation, especially percutaneous coronary
intervention.[1]
smoking
• Smoking causes nearly 1 in 5 deaths in the US. Cigarette smokers are substantially more likely than
non-smokers to develop coronary artery disease (CAD), to have a stroke, and to develop peripheral
vascular disease.[15] Smoking increases risk for CAD by direct promotion of atherosclerosis, reduced
oxygen delivery in the blood, increased thrombogenesis, and direct coronary artery spasm.
• Smoking results in a 2- to 3-fold increase in cardiac mortality.[6] Exposure to environmental tobacco
smoke also significantly increases risk for heart disease.[16] Surprisingly, current smoking is
associated with a lower risk of acute death in the setting of acute coronary syndrome.[1] This is
referred to as the 'smoker's paradox' and reflects the tendency for smokers to develop thrombi on less
severe plaques and at an earlier age than non-smokers.
dyslipidaemia
• Cholesterol is a main constituent of advanced atherosclerotic plaques. Western diet, excess calorie
intake, and sedentary lifestyle are the strongest contributors to dyslipidaemia. Large epidemiological
studies have firmly identified an increased risk of MI with serum lipid abnormalities (mainly increased
low-density lipoproteins [LDL], elevated triglycerides, and decreased high-density lipoproteins).[17] [18]
LDL levels have the strongest relationship.
• Lipid-lowering therapy reduces future ischaemic events and limits disease progression.[19] [20] Lower
LDL levels highly correlate with reduction of death from MI or recurrent acute coronary syndrome.[21]
family history of premature coronary artery disease (CAD)

• Defined as premature CAD in family members (men <55 years; women <65 years). Family history
includes a first-degree relative with a history of myocardial infarction (MI), sudden cardiac death, aortic
dissection, percutaneous coronary intervention, or coronary artery bypass graft. Inherited (primary)
disorders of lipoprotein metabolism are an important cause. On physical examination, patients may
have eruptive xanthomas, lipaemia retinalis (lipid accumulation within retinal vessels), or tendinous
xanthomas. In the acute setting of NSTEMI, presence or absence of family history does not help in
treatment, but presence of family history increases the probability of NSTEMI, and is associated with
an increased risk of 30-day cardiac events in patients with acute coronary syndrome.[1]
age >65 years

• Nearly 60% of people admitted to hospital with NSTEMI as the primary diagnosis are >65 years of
age.[22] Between 1990-1999, the mean age of NSTEMI patients rose from 65-68 years.[9] Older
patients have increased risks of underlying coronary artery disease (CAD) and multiple-vessel CAD.
They are at higher risk than younger patients for an adverse outcome.[1]
DIAGNOSIS
hypertension
• A major risk factor for poor outcomes in patients with acute coronary syndrome.[1] About 69% of
people who have a first myocardial infarction (MI) have BP >140/90 mmHg.[6] Hypertension is one of
the most prevalent risk factors for coronary artery disease in the US. Approximately 30% of Americans
have blood pressure >140/90 mmHg, placing them at greater risk of MI.[6] Effective treatment of
hypertension dramatically reduces the risk of cerebrovascular events, heart failure, and future MI.[6]
High blood pressure induces ventricular hypertrophy and endothelial dysfunction/damage, and
promotes atherosclerosis, all of which predispose patients to cardiac events.
obesity and metabolic syndrome phenotype

• Estimates suggest that more than half of adults in Western society will become overweight or
obese.[23] Excess calorie intake increases low-density lipoproteins, total cholesterol, and triglyceride
levels. Obesity and the metabolic phenotype (abdominal obesity with known history of hyperlipidaemia,
hypertension, and insulin resistance) predispose to coronary artery disease.[23] [24] [25] Cardiac
output and blood volume increase to supply the vascular-rich adipose tissue. Obesity is associated
15
with diastolic dysfunction and is a strong stimulus for left ventricular hypertrophy.[24] Adipokines and
other hormones secreted by adipose tissue are highly linked to inflammation and atherosclerosis.
physical inactivity
• The relative risk of coronary artery disease (CAD) associated with physical inactivity ranges from
1.5 to 2.4, an increase comparable to that for high cholesterol, high blood pressure, and cigarette
smoking.[26] Physical activity has anti-atherosclerotic, psychological, antithrombotic, anti-ischaemic,
and anti-arrhythmic effects that are important in primary and secondary prevention of CAD.[27]
Regular exercise increases cardiorespiratory fitness and lowers myocardial oxygen demand. This
correlates with lower mortality, and reduced risk of CAD and morbidity from NSTEMI. Sustained,
regular physical activity lowers blood pressure, reduces lipid levels, reduces adiposity, increases
insulin sensitivity, and decreases inflammation, stress, and adrenergic activity.[27]
cocaine use
• Cocaine accounts for up to 25% of acute myocardial infarctions (MI) in people aged 18-45 years.
The lifetime risk of non-fatal MI with cocaine use is 7 times the risk in non-users.[28] In the hour after
cocaine is used, the risk of MI is 24 times the baseline risk. It is probably due to cocaine-induced
coronary vasospasm and thrombosis, in addition to a direct effect on heart rate and arterial pressure.
Cocaine also has direct myocardial toxic properties.[1]
depression
• An independent predictor of future myocardial infarction in otherwise healthy people.[29] [30]
stent thrombosis or restenosis

• Stent thrombosis or in-stent restenosis may cause ST-elevation myocardial infarction (STEMI),
NSTEMI, or unstable angina. Both stent thrombosis and restenosis have complex causes, triggers,
pathophysiology, and risk factors. Of importance, premature cessation of antiplatelet agents in patients
with stents (drug-eluting and bare-metal) may trigger an acute coronary syndrome.[31]
chronic kidney disease

DIAGNOSIS
• Patients with chronic kidney disease have increased risk of NSTEMI and worsened prognosis following
an NSTEMI.[32]
surgical procedures (including intra-operative and postoperative periods)

• NSTEMI is a relatively common complication of all types of surgical and non-surgical procedures. Type
of surgery, patient risk factors, and prior patient history are important contributors to postoperative
NSTEMI. Often this is detected as a rise in cardiac markers in the days following the surgical
procedure. Preoperative risk assessment and additional steps to reduce the risk of myocardial
ischaemia/stress may prevent this complication or enable early recognition and therapy.[33]
sleep apnoea
• Untreated moderate to severe obstructive sleep apnoea (OSA) has been associated with a 17%
increase in relative risk of cardiovascular events compared to risk in patients without OSA.[34]
History & examination factors

Key diagnostic factors
presence of risk factors (common)
• Key risk factors include increasing age, previous cardiovascular disease, smoking, dyslipidaemia,
diabetes, and obesity.
chest pain (common)

• The most common symptom of NSTEMI is chest pain or discomfort. Described as a sensation of
tightness, heaviness, aching, burning, pressure, or squeezing.
• The pain is most often retrosternal and can often radiate to the left arm but may also radiate to the
lower jaw, neck, both arms, back, and epigastrium, where it may mimic heartburn.[1] [11]
diaphoresis (common)
• Classic sign or symptom of acute MI.
recent percutaneous coronary intervention or previous coronary artery

bypass graft (uncommon)
• Iatrogenic causes of NSTEMI, defined by degree of enzyme elevation following a procedure. For
percutaneous coronary intervention (PCI), a greater than 5-fold rise in troponin, and for coronary
artery bypass graft, a greater than 10-fold rise from normal baseline levels during the first 48 hours
following PCI plus any one of the following is considered NSTEMI:[3] symptoms include new ischaemic
changes; new pathological Q waves; angiographic findings consistent with procedural complication; or
imaging demonstration of new loss of viable myocardium or new regional wall motion abnormalities.
Other diagnostic factors

physical exertion (common)
DIAGNOSIS
• Acute alterations in haemodynamic stress that accompanies physical exertion may trigger unstable
plaque rupture.
• Increase in platelet activation and hyper-reactivity is also seen.
shortness of breath (common)

• Dyspnoea is frequent and is probably secondary to diminished cardiac output.
• Frank congestive heart failure, jugular venous distension, pulmonary oedema, and cardiogenic shock
can be present, and patients who present with these are at high risk for a poor outcome.[1]
weakness (common)
• More common presentation in women, older people, and those with diabetes.
anxiety (common)
• Patients may express anxiety or appear anxious. They may also report a feeling of impending doom.
nausea (common)
• May be the only symptom.
• Atypical symptoms are more common in women, older people, and those with diabetes.
17
vomiting (common)
abdominal pain (common)

hypertension (common)
• Depends on extent and location of infarction.
cold exposure (uncommon)

• Coronary and systemic vasoconstriction causes haemodynamic stress in the coronary arteries,
triggering rupture of unstable plaques.[11]
emotional upset (uncommon)

• May cause coronary and systemic arterial vasoconstriction, triggering rupture of unstable plaques.
early morning onset (uncommon)

• Events peak at around 8 a.m., presumably due to haemodynamic stress caused by increased serum
cortisol, adrenergic hormones, and platelet aggregation.
syncope (uncommon)
• More common in women, older people, and those with diabetes.
hypotension (uncommon)
• Depends on extent and location of infarction.
arrhythmias (uncommon)
DIAGNOSIS
• Presence of palpitations or tachy- or bradyarrhythmias.
abnormal heart sounds (uncommon)

• Presence of third and fourth heart sounds and paradoxical splitting of the second heart sound.
Diagnostic tests
1st test to order
Test Result
ECG non-specific ST-T wave
changes or ischaemic
• A 12-lead ECG should be performed and interpreted within 10
changes
minutes of the patient's arrival in the emergency facility. Classic ECG
findings of ischaemia in NSTEMI include horizontal or downsloping
ST depression >1.0 mm and/or symmetrically inverted T waves
(Wellens waves).
[Fig-1]
[Fig-2]
• In many patients the ECG may be normal.
• Serial ECGs, initially at 15- to 30-minute intervals, then at the
Doctor's discretion, should be taken in patients with chest pain, to
detect development of ST-elevation myocardial infarction (MI), or to
help guide reperfusion strategies.[1]
• Continuous 12-lead ECG monitoring is a reasonable alternative
to serial 12-lead recordings in patients whose initial ECG is non-
diagnostic.[1]
• Supplemental ECG leads V7 through V9 may be useful in patients
with non-diagnostic initial ECGs to rule out MI due to left circumflex
occlusion.[1]
trial of sublingual glyceryl trinitrate ongoing pain
• Patients with ongoing ischaemic discomfort should receive sublingual
glyceryl trinitrate (0. 4 mg) every 5 minutes for a total of 3 doses, after
which the need for intravenous glyceryl trinitrate should be assessed,
if it is not contraindicated.[1] Nitrates should be avoided in patients
with hypotension, suspected right ventricular infarction, or recent
phosphodiesterase inhibitor use.
DIAGNOSIS
cardiac troponins >99th percentile of normal
• Troponin levels confirm the diagnosis of infarction. Test is more
specific than CK-MB or myoglobin and is the best marker for
musculoskeletal injury, small myocardial infarction (MI), or late (>2-3
days) MI.
• The 99th percentile is the cut-off value used to determine acute
MI. Troponins rise 4-6 hours after onset of infarction, peak at 18-24
hours, and may persist for 14 days or longer.[1] Infarct size can be
estimated from the troponin value measured at 72 hours. Point-of-
care testing can provide quantitative results in as little as 10 minutes.
• Patients with negative cardiac biomarkers within 6 hours of the
onset of symptoms consistent with acute coronary syndrome should
have biomarkers remeasured in the time frame of 8-12 hours after
symptom onset.[1]
• Other conditions that may cause raised cardiac biomarkers include
trauma, renal failure, congestive heart failure, surgery, inflammatory
states, pulmonary embolism, sepsis, burns, rhabdomyolysis, and
drug toxicity.[48]
creatine kinase (CK) >99th percentile of normal
• Although not as sensitive as troponins, is very useful when troponin
assays are not available or if there is possible reinfarction.[48]
19
Test Result
CK-MB (cardiac isoforms) >99th percentile of normal
• Very useful when troponin assays are not available or if there is
possible re-infarction.
• CK-MB takes up to 72 hours to return to normal and is therefore
useful for detecting early re-infarction.
• The sensitivity of CK-MB for detection of very early acute myocardial
infarction (MI) is low. False-positive results can occur in the setting
of trauma, cardiopulmonary resuscitation, cardioversion, or cardiac
surgery.[1] [48]
• CK-MB has a short half-life (peaking about 1 day after infarction) in
comparison with troponins, which may stay elevated for 7 or more
days after MI. For this reason, CK-MB is a useful biomarker for
secondary increases.
FBC normal, anaemia,
• Haemoglobin and haematocrit measurements may help to evaluate a thrombocytopenia
secondary cause of NSTEMI (i.e., acute blood loss, anaemia) and to
evaluate thrombocytopenia to estimate risk of bleeding.
urea and serum creatinine normal or elevated
• Creatinine clearance should be estimated in NSTEMI patients and
the doses of renally cleared drugs should be adjusted appropriately.
In chronic kidney disease patients undergoing angiography, iso-
osmolar contrast agents may be preferred.[1] [4]
electrolytes normal or deranged
• Electrolyte derangements may predispose to cardiac arrhythmias.
liver function tests normal
• Useful if considering treatment with drugs that undergo hepatic
metabolism.
blood glucose normal or elevated
• There is controversy over whether tight glucose control may reduce
DIAGNOSIS
risk of death and morbidity.[49]

chest x-ray normal or may show
pulmonary oedema
• Pneumonia, oesophageal rupture, aortic dissection, and
pneumothorax can mimic cardiac ischaemia and may be diagnosed
with a chest x-ray.[1]
Other tests to consider
Test Result
lipids elevated, normal, or
• Lipid management should include assessment of a fasting lipid profile optimal
for all patients, within 24 hours of admission to hospital. Frequently, in
the acute phase of an acute coronary syndrome, lipid values may be
lower than normal for that patient.
Test Result
brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-pro- >99th percentile of normal
BNP)
• Measurement of BNP or NT-pro-BNP may be considered to
supplement assessment of global risk in patients with suspected
acute coronary syndrome.[1]
echocardiography regional wall motion
abnormality, depressed
• Cardiac ultrasound can demonstrate ischaemic changes even
left ventricular (LV)
before ECG changes appear. The presence of regional wall motion
function, or decreased
abnormalities and decreased LV function provide evidence for acute
ejection fraction
coronary syndrome. Cardiac ultrasound is also useful to evaluate
ischaemic complications and other causes of chest pain (i.e.,
pulmonary embolism, effusion, or acute valvular pathology).
angiography severe stenosis or
thrombosis
• Urgent and immediate angiography (without non-invasive risk
stratification) for failure of stabilisation with intensive medical
treatment is warranted.[1]
[Fig-4]
[Fig-3]
• Indications include recurrent symptoms (refractory angina),
ischaemia despite adequate medical treatment, high risk (e.g.,
congestive heart failure, malignant ventricular arrhythmias), or non-
invasive test findings (significant left ventricular dysfunction, ejection
fraction <0.35, large anterior or multiple perfusion defects).[1]
• Renal failure is a relative contraindication and patients with contrast
allergy must be pre-medicated prior to angiography.
stress testing ECG: ST-segment
depression >1mm (0.1
• Stress testing, including treadmill exercise testing, may be useful
mV); nuclear imaging:
and is recommended in patients with low and intermediate pre-test
probability with a normal ECG and normal high sensitivity biomarkers reversible or fixed
to assist with assessing need for an invasive strategy.[1] [42] [43] perfusion defect
DIAGNOSIS
• The sensitivity and specificity of these tests increase when combined
with either nuclear imaging to look for myocardial perfusion defects or
echocardiography to assess wall motion abnormalities.
• The key positive finding on nuclear imaging stress tests is the
presence of a reversible defect. This is an area of myocardium that
becomes deprived of perfusion during increased myocardial demand
and reperfuses on stopping the activity. This signifies stenosis within
the coronary circulation that may be treated with percutaneous
coronary intervention or coronary artery bypass graft.
• Sub-maximal exercise testing can be performed at 4-7 days after
myocardial infarction, while symptom limited testing can be performed
at 14-21 days post-myocardial infarction, when the patient has been
free of active ischaemic or heart failure symptoms.[44]
21
Test Result
coronary CT angiography (CCTA) occlusion or near-
occlusion
• May provide non-invasive evaluation of coronary anatomy and
atherosclerosis. Renal failure is a relative contraindication.
Patients with a contrast allergy should be pre-medicated prior to
angiography.[45]
[Fig-3]
[Fig-4]
• Due to the high negative predictive value of CCTA, evidence
suggests that CCTA is useful in patients with low to moderate risk of
NSTEMI. When compared with the standard care of low-risk patients
(observation, serial enzymes followed by stress testing) CCTA
reduced time to diagnosis, reduced length of emergency department
stay, and had similar safety.[46] CCTA is not indicated for patients
with high-risk features (i.e., ischaemic ECG changes, positive cardiac
markers).[47]
Differential diagnosis
Condition Differentiating signs / Differentiating tests

symptoms
Aortic dissection • Pain is described as a • Chest CT angiography with
'tearing' back pain. There contrast or MR angiography
may be BP differential may show the dissection or
between upper and lower an intimal flap. CXR may
extremities. reveal widened mediastinum.
• Aortic dissection often • Transoesophageal
occurs in patients who have echocardiography may show
collagen vascular disease a dissection depending on
(i.e., Marfan syndrome). the location.
DIAGNOSIS

symptoms
Pulmonary embolism • Patients often present with • For patients with a high
dyspnoea, pleuritic chest probability of pulmonary
pain, cough, or haemoptysis. embolism (PE) on clinical
Hypoxia may be present. scoring (i.e., PE likely)
Lower limbs should be or an abnormal D-dimer,
examined for deep vein imaging is required. The
thrombosis (enlarged, multiple-detector computed
tender, erythematous tomographic pulmonary
calves). angiography (CTPA)
scanning of the chest is the
imaging study of choice for
acute pulmonary embolism.
• For patients with renal
insufficiency or iodinated
contrast allergies, ventilation-
perfusion scan ± peripheral
venous doppler exam are
recommended.
• Chest CT scan may show
central filling defects within
the vascular lumen, sharp
cut-off of the artery, or a
'tram track' appearance of
the artery in non-occlusive
embolism.
Peptic ulcer disease • Pain is described as burning • Endoscopy may show ulcers,
epigastric pain that occurs erosion, or gastropathy.
hours after meals or with
hunger. It often wakes
the patient at night and
is relieved by food and
antacids.
DIAGNOSIS
• There may be a previous
history of reflux or medicines
that can cause peptic
ulcer (i.e., recent use of
steroid or non-steroidal anti-
inflammatory drugs).
23

symptoms
Acute pericarditis • Pain is relieved by sitting • ECG may show diffuse ST
forwards. Friction rub or elevations (although PR
distant heart sounds may be elevation in aVR is most
heard on auscultation. specific finding).
• A history of a recent • Echocardiogram and
cardiac procedure (Dressler chest CT scan may
syndrome), renal failure, or show pericardial effusion
preceding illness (fever or or thickening of the
diarrhoea) may be present. pericardium. Cardiac MRI
is useful and has high
sensitivity for detection
of pericardial effusion,
loculations, and pericardial
thickening.
• Blood tests may indicate
systemic inflammation
(e.g., elevated WBC count,
elevated erythrocyte
sedimentation rate [ESR]
or CRP). Renal failure can
cause uraemic pericarditis.
Oesophageal spasm • Usually diagnosed after • The oesophagus may have

ruling out other causes of a corkscrew appearance
chest pain. A past history on barium swallow. This
of oesophageal spasm is represents simultaneous
typical and there may be a rings of contraction in the
precipitating event. distal oesophagus.[50]
• Pain due to oesophageal
spasm is often relieved by
glyceryl trinitrate, making it
difficult to differentiate from
cardiac pain.
DIAGNOSIS
Costochondritis • Diagnosis is made on the • There are no specific studies

history or exclusion of or imaging to diagnose
other causes. There may costochondritis.
be a history of recent or
repeated trauma. The pain is
typically localised with point
tenderness, sharp in nature,
and relieved by non-steroidal
anti-inflammatory drugs.
Panic at tack • Most often diagnosed after • No tests or procedures can

exclusion of other causes. diagnose anxiety disorders.
Patients often have other
psychiatric illness. Women
are affected more than
men. Panic attacks may be
situational.

symptoms
Stable ischaemic heart • Angina pain is recurrent and • Diagnosis is most
disease reproducible with exertion, often made on history
and is relieved by rest or alone. Coronary artery
glyceryl trinitrate. catheterisation may show the
typical fixed coronary artery
luminal wall narrowing.
• Intravascular ultrasound
during cardiac
catheterisation may reveal
the typical stable plaque of
stable angina (calcified, thick
fibrous caps) rather than
the unstable plaques (lipid-
laden, thin caps) that cause
acute coronary syndrome.
Myocarditis • There is a wide spectrum • The definitive test is

of presentation from endomyocardial biopsy,
asymptomatic to cardiogenic which shows lymphocyte
shock. Patients may infiltration and myocyte
present with a history of necrosis.
recent influenza-like illness • Cardiac enzymes or brain
associated with arthralgias natriuretic protein may be
and malaise. The symptoms raised.
of heart failure may be • Leukocytosis, eosinophilia,
present. elevated ESR and CRP, and
• Myocarditis may be a rise in serum viral titres are
idiopathic or caused by common.
infections (viral, bacterial,
or fungal), drugs (e.g.,
chemotherapy agents, anti-
hypertensives, and anti-
epileptics), and autoimmune
DIAGNOSIS
disorders (e.g., systemic
lupus erythematosus,
sarcoidosis, and rheumatoid
arthritis).
Acute cholecystitis • On physical examination • Ultrasound may show a

there is constant right upper distended gallbladder and
quadrant pain with or without gallstones.[51] If ECG
Murphy's sign (inhibition of changes accompany
inspiration due to pain on cholecystitis, these would
palpation). There may be most likely include ST
a history of gallstones or elevation.
previous episodes of biliary
colic.
25

symptoms
Boerhaave syndrome • Caused by oesophageal • CXR shows
rupture with mediastinitis. pneumomediastinum >90%
It typically follows retching of the time. Oesophagram
or vomiting, aggravated and CT scan can confirm
by swallowing. Patients diagnosis or reveal the
may have subcutaneous condition. CT may show
emphysema and a hoarse pneumomediastinum
voice. and peri-oesophageal air
tracks. Oesophagram may
show an oesophageal
tear.[52] Endoscopy is not
recommended for Boerhaave
syndrome.
Brugada syndrome • More common in Asian • ECG shows saddle-shaped

people and men aged 30 to ST elevation in leads V1
50 years. Patients typically to V3. These changes are
present after an episode associated with complete
of polymorphic ventricular or incomplete right bundle-
tachycardia or a cardiac branch block and T-wave
arrest. inversions.
Acute stress • Clinical features are similar • Often these patients present
cardiomyopathy to NSTEMI and may include with ECG changes, cardiac
chest pain, shortness of biomarker elevations, and
breath, and left ventricular left ventricular dysfunction
wall motion abnormalities. on cardiac imaging that
A characteristic feature is are indistinguishable from
that often the clinical state NSTEMI but on coronary
is triggered by a severe angiography will have no
extracardiac stressor (e.g., obstructive lesion. Coronary
intracranial haemorrhage, angiography remains the
phaeochromocytoma, definitive test for diagnosis of
DIAGNOSIS
exogenous catecholamine this condition.

administration, severe
emotional stress, takotsubo
cardiomyopathy, apical
ballooning syndrome).
Diagnostic criteria
American College of Cardiology/American Heart Association[1] [3]
The Fourth Universal Definition of Myocardial Infarction (2018) provides criteria for 5 distinct clinical
presentations of myocardial infarction (MI), which are based on pathological, clinical, and prognostic
factors.[3]
Evaluation begins with clinical history, obtaining an ECG(s), and assessing cardiac biomarkers. It is
important to note that ECG abnormalities and elevated cardiac biomarkers do not alone establish the
definition of NSTEMI. The ECG can be relatively normal but this does not exclude acute coronary syndrome
(ACS). More commonly associated findings in NSTEMI include ST depression, transient ST elevation, and/
or prominent T-wave inversions. While these findings are frequently present, they are not required for a
diagnosis of NSTEMI.
If the diagnosis of ACS is indicated by history and ECG, the diagnosis of NSTEMI may be established
if a biomarker of myocardial injury has been released (i.e., troponin elevation). If there is no evidence of
biochemical marker release suggestive of myocardial necrosis in a patient with suspected ACS, they may be
considered to have experienced unstable angina.[1]
Risk stratification scores[1]

ACS diagnosis and management requires continuous risk stratification for death or recurrent MI. Initial risk
assessment includes the history, examination, ECG, and cardiac biomarkers, all of which can be compiled to
estimate risk using the TIMI Risk Score, GRACE risk model, or the Killip Classification.
High-risk clinical features in patients with suspected ACS include ongoing chest pain, severe dyspnoea,
syncope/pre-syncope, or palpitations.
TIMI Risk Score[40]
[VIDEO: Thrombolysis in Myocardial Infarction (TIMI) Score for Unstable

Angina Non ST Elevation Myocardial Infarction ]
All-cause mortality, rate of MI, and rate of revascularisation at 14 days increase in proportion to the number
of risk factors present on the TIMI score. One point is awarded for the presence of each of the following
criteria (patients with a score of 0 to 2 are low risk, 3 to 4 are intermediate risk, and 5 to 7 are high risk):
• Age >65 years

• Presence of ≥3 coronary artery disease risk factors
• Prior coronary stenosis >50%
• ST-segment deviation on ECG
DIAGNOSIS
• Elevated serum cardiac biomarkers
• At least 2 anginal episodes in the past 24 hours
• Use of aspirin in the past 7 days.
The Global Registry of Acute Coronary Events (GRACE) risk model
[VIDEO: GRACE Score for Acute Coronary Syndrome Prognosis ]

The GRACE risk model is a web-based tool that can be used to predict in-hospital and post-discharge
mortality or MI in patients following an initial ACS.
Killip Classification
The Killip classification risk stratifies patients with acute MI based on clinical evidence of left ventricular
failure.
• Class I: no evidence of congestive heart failure

• Class II: presence of a third heart sound gallop, basilar rales, or elevated jugular venous pressure
• Class III: presence of pulmonary oedema
27
• Class IV: cardiogenic shock.
Heart Score
[VIDEO: HEART Score ]

Incorporates elements of the patient's history, ECG, age, risk factors, and troponin and is used for patients
in the accident and emergency department setting to assess risk of acute MI, percutaneous intervention,
coronary artery bypass graft, and death within 6 weeks of initial presentation.
DIAGNOSIS
Non-ST-elevation myocardial infarction Treatment
Step-by-step treatment approach

The following management approach should be applied to patients with acute coronary syndrome NSTEMI
(type 1 NSTEMI). Ideal treatments of the other types of NSTEMI are currently evolving and are beyond the
scope of this topic.
The aim of initial assessment is to relieve pain, identify and treat life-threatening instability, and then admit
the patient for further treatment/observation.[1] The goal of treatment is to relieve ischaemia, prevent further
thrombosis or embolism, and correct haemodynamic abnormalities. All patients should undergo early risk
estimation based on the medical history, physical examination, ECG findings, and cardiac markers.
Initial management
Initial medical therapy is indicated in all patients, with variation in some choices of agent according to risk
stratification.
Oxygen
All patients require oxygen saturation measurement using pulse oximetry.[1] Guidelines recommend
supplemental oxygen therapy only in patients who are hypoxaemic (arterial oxygen saturation <90%),
or in those who have respiratory distress or other high-risk features for hypoxaemia.[1] [4] Liberal use of
oxygen is associated with increased mortality in patients with acute coronary syndrome.[53] [54]
Antiplatelet therapy
Aspirin is indicated immediately for all patients suspected of having an acute coronary syndrome unless
contraindicated or already taken.[1] Healthcare personnel providing pre-hospital emergency services
should similarly give aspirin (chewed) to chest pain patients suspected of having an acute coronary
syndrome, again unless contraindicated or already taken by the patient.[1] Aspirin should be continued at
a daily maintenance dose thereafter.[1] 1[A]Evidence Aspirin, an irreversible COX-1 inhibitor, suppresses
thromboxane A2 production preventing platelet aggregation, and reduces the incidence of death and non-
fatal myocardial infarction (MI) in patients with unstable angina[55] [56] or acute MI.[56] Aspirin has been
shown to achieve a 30% to 51% reduction in future coronary events.[57] High-dose aspirin is associated
with an increased risk of bleeding when compared with low-dose aspirin in the absence of improved
outcomes.[1]
Similarly, P2Y12 receptor inhibitors (e.g., clopidogrel, ticagrelor, prasugrel) are indicated in early hospital
medical treatment of NSTEMI, providing powerful tools against platelet adhesion, activation, and
aggregation. P2Y12 receptor inhibitors can reduce mortality and morbidity, but they are associated with
an increased risk of bleeding.[58] [59] Ticagrelor and prasugrel are newer P2Y12 agents, which trials
have shown to have a faster onset of action and greater efficacy compared with clopidogrel.[1] [60] [61]
However, the risk of bleeding is also greater with these two P2Y12 agents compared with clopidogrel.[62]
[63] All patients should be given dual antiplatelet therapy with a P2Y12 receptor inhibitor in addition
to aspirin. If the patient is intolerant of aspirin or it is otherwise contraindicated, a P2Y12 receptor
inhibitor can be given instead of aspirin, but two different P2Y12 receptor inhibitors should not be given
TREATMENT
together. Clopidogrel or ticagrelor are suitable for patients on either non-invasive or invasive strategies,
while prasugrel is recommended only for patients on an invasive strategy since existing data come
from patients treated by percutaneous interventions.[64] There are variable responses to antiplatelet
inhibition with clopidogrel based on loss-of-function alleles for the CYP219C enzyme, which is required
to convert clopidogrel to its active drug metabolite. The presence of at least one loss-of-function mutation
29
for CYP219C may be as high as 30% in some populations. In a single-centre, retrospective study of
clopidogrel resistance it appeared that patients with clopidogrel resistance who remain on clopidogrel
are at a 4-fold increase for major adverse cardiovascular or cerebrovascular events compared with those
placed on a different P2Y12 inhibitor.[65]
Clinicians need to tailor therapy to strike a balance between a newer agent that may have a faster onset
of action and greater antiplatelet effect, but could potentiate bleeding (especially in those with prior TIA
or stroke). Regardless of which P2Y12 receptor inhibitor is chosen, a loading dose should be given
as soon as possible in most patients and then a maintenance dose continued for a minimum of 12
months.[66] Note that P2Y12 receptor inhibitors should not be given if urgent coronary artery bypass graft
(CABG) is anticipated or planned within 5 to 7 days, so it may be necessary to delay starting a P2Y12
receptor inhibitor until diagnostic angiography clarifies whether early CABG is indicated. For patients
receiving chronic clopidogrel therapy prior to presentation, there is some evidence to suggest decreased
periprocedural MI with clopidogrel reloading at the time of percutaneous coronary intervention (PCI).[67]
Pain relief
Pain relief is indicated in the initial management of all patients. Sublingual glyceryl trinitrate (GTN)
reduces myocardial oxygen demand and enhances myocardial oxygen delivery. GTN is contraindicated
if there is a history of recent phosphodiesterase-5 inhibitor use (e.g., sildenafil); it should not be given
if systolic BP is <90 mmHg or there is a concern about right ventricular infarction. Intravenous GTN is
recommended in patients with no symptom relief after 3 sublingual GTN tablets or sprays taken 5 minutes
apart.2[C]Evidence If the patient does not respond after taking 3 sublingual GTN tablets or has recurrent
symptoms despite sufficient anti-ischaemic treatment, intravenous morphine can be administered in
the absence of any contraindications.[1] Morphine causes vasodilation and may produce reductions in
heart rate (through increased vagal tone) and systolic BP to further reduce myocardial oxygen demand. It
should be given instead of GTN when GTN is contraindicated. Limited data (largely observational studies)
investigate morphine use for NSTEMI with evidence of potential safety concerns, thus it should be used
with caution.[68] One randomised, double-blind trial found that morphine delays and attenuates ticagrelor
exposure and action in patients with MI.[69]
Beta-blockers
Oral beta-blockers are recommended for routine use in all patients unless contraindicated.3[C]Evidence
Contraindications include heart rate <60 bpm, systolic blood pressure <100 mmHg, moderate or severe
associated left ventricular failure, PR interval on the ECG >0.24 seconds, second- or third-degree heart
block, active asthma/reactive airways disease, severe COPD, right ventricular infarction, and cardiogenic
shock. Randomised trials with threatened or evolving MI have shown lower rates of progression to
MI with beta-blocker treatment.[70] [71] Comparative studies between the various beta-blockers in
the acute setting are lacking. However, beta-blockers without intrinsic sympathomimetic activity (e.g.,
metoprolol, propranolol, and atenolol) are preferred. Cardioselective beta-blockers are preferred in the
initial management of NSTEMI, but guidelines recommend metoprolol, bisoprolol, or carvedilol for post-
NSTEMI management in patients with stabilised heart failure and reduced systolic function.[1]
The selection of a long-term beta-blocker often depends on the clinician's familiarity with the agent. The
TREATMENT
goal resting heart rate is 50 to 60 bpm. Intravenous administration of beta-blockers has shown harm,
especially for patients with evidence of heart failure or shock, and is generally avoided.[1] [72]
Calcium-channel blockers
Calcium-channel blockers can be given in patients with continuing or recurrent ischaemic symptoms after
being given adequate nitrate and beta-blocker therapy or in those who cannot tolerate beta-blockers.[1]
Although they are often used, there is good-quality evidence that calcium-channel blockers are no more
effective than control at reducing mortality or MI rates in people with unstable angina.4[C]Evidence
Patients treated acutely with a calcium-channel blocker for acute angina do not need to continue these
drugs, provided there is no recurrent angina on drug cessation or another indication for these drugs (i.e.,
hypertension). These drugs can start to be tapered after 24 hours at the discretion of the clinician. Short-
acting dihydropyridines (e.g., nifedipine) should be avoided in the absence of adequate beta-blocker
therapy because they may be associated with adverse outcomes.[1] Verapamil or diltiazem should be
avoided in severe left ventricular dysfunction.[1] In the UK, use of calcium channel blockers as add-on
therapy is not routine, unless beta-blockers are not tolerated or contraindicated.
Choice of invasive or conservative management

Once initial management is instigated, the decision should be made as to whether the patient requires
treatment using an invasive or non-invasive approach. The decision to pursue an invasive approach
or medical management is made on an individual basis.[73] Guidelines recommend that high-risk
patients routinely undergo early (12-24 hours) coronary angiography and angiographically directed
revascularisation if possible unless patients have serious comorbidities, including cancer or end-stage
liver disease, or clinically obvious contraindications, including acute or chronic (chronic kidney disease
[CKD] 4 or higher) renal failure, multi-organ failure, or medical frailty.[1] [74] [75] [76] [77] There has been
recent evidence that early (<12 hours) intervention may be more effective at reducing cardiovascular
death and MI.[78] [79] However, an increasing amount of new data, systematic reviews, and expert
opinion question the benefit of routine invasive versus selective invasive approaches, especially in low-
risk patients; this is an evolving field in NSTEMI.[1] [77] [80] [81] [82] [83] [84] [85]
Guidelines recommend that an invasive approach is appropriate if any of the following high-risk features
are present:[1] [4]
• Recurrent angina or ischaemia at rest or with low-level activities despite intensive medical therapy
• Rise and fall in cardiac biomarkers (troponin T or I) consistent with MI
• New or dynamic ST-T wave changes
• Signs or symptoms of heart failure (pulmonary oedema, S3 gallop), or new or worsening mitral
regurgitation
• High-risk findings from non-invasive testing
• Haemodynamic instability
• Life-threatening arrhythmia, such as sustained ventricular tachycardia or cardiac arrest
• PCI within 6 months
• Prior CABG
• High-risk score (i.e., TIMI, GRACE)
• Mild to moderate renal dysfunction
• Diabetes mellitus
• Reduced left ventricular function (ejection fraction <40%).
TREATMENT
Note that these criteria do not exactly match the risk of death stratification.
A conservative, early medical management strategy may be appropriate in subsets of patients, especially
those without the above high-risk features and with a low risk score. Guidelines and data suggest
that some sub-populations do not benefit from early invasive management, and clinician discretion is
31
advocated.[74] [75] For example, a routine early invasive strategy in low-risk women with NSTEMI has
not shown benefit over a conservative strategy.[86] While traditionally not included in many clinical trials,
emerging data suggest that older patients may benefit as much, if not more, from an invasive strategy.[87]
[88] [89]
Invasive approach
Anticoagulation therapy (subcutaneous low molecular weight heparin [LMWH], intravenous unfractionated
heparin [UFH], or the alternative agent fondaparinux) should be started on earliest recognition of
NSTEMI.5[A]Evidence The anticoagulant is used in conjunction with antiplatelet therapy already
started (i.e., aspirin and a P2Y12 receptor inhibitor). If fondaparinux is used during angiography/PCI,
guidelines recommend that UFH be used in addition.[1] Anticoagulation should not be given if there
are contraindications: namely, major bleeding, or history of adverse drug reaction or heparin-induced
thrombocytopenia.6[A]Evidence
The antiplatelet and anticoagulation regimens should be started before the diagnostic angiogram (i.e.,
upstream). Addition of a glycoprotein IIb/IIIa inhibitor is only recommended if there is evidence of a no-
reflow or a thrombotic complication.
The PCI involves angioplasty, alone or in combination with placement of a stent, capable of relieving
coronary narrowing or occlusion.[90] Radial artery access is preferred when possible as it decreases
procedural site complications.[91] Complications of PCI include PCI-induced MI; coronary perforation,
dissection, or rupture; cardiac tamponade; malignant arrhythmias; cholesterol emboli; and bleeding
from the access site. Contrast-induced nephropathy is a common and potentially serious complication,
especially in patients with baseline impaired renal function.[92] Early and late stent thromboses are
catastrophic complications.
Conservative approach
Anticoagulation treatment should be added to aspirin and a P2Y12 receptor inhibitor at the earliest
recognition (or suspicion) of NSTEMI and continued for at least 48 hours to hospital discharge and/or
until symptoms abide and objective markers demonstrate a trend towards normal.[93] Agents include
subcutaneous LMWH, intravenous UFH, or fondaparinux, according to clinician choice.
Long-term management post-stabilisation

Long-term therapy consists of a range of pharmacological and non-pharmacological strategies. Cardiac
rehabilitation is a structured programme that provides heart attack survivors with the tools, motivation,
and support needed to change behaviour and increase chance of survival. Typically, cardiac rehabilitation
programmes use group therapy to supervise and promote beneficial exercise, as well as to provide
emotional support. The aims of cardiac rehabilitation are to:
• Increase functional capacity

• Stop cigarette smoking
• Modify lipids and lipoproteins

TREATMENT
• Decrease body weight and fat stores

• Reduce BP
• Improve psychosocial well-being
• Prevent progression and promote plaque stability
• Restore and maintain optimal physical, psychological, emotional, social, and vocational functioning.
Cardiac rehabilitation should be started on discharge and after clearance by an outpatient physician.
The basic prescription should include aerobic and weight-bearing exercise 4 to 5 times per week for >30
minutes. There is a risk of triggering a recurrent MI with physical activity. However, this is minimal and
reduced by using a structured programme to minimise (and treat) this risk.
Pharmacological strategies include the following.
• Aspirin should be continued indefinitely at a low dose if the patient is tolerant and not
contraindicated.
• A P2Y12 receptor inhibitor should be continued for up to 12 months. For patients with aspirin
allergy, long-term P2Y12 receptor inhibitor use is suggested.[1] [94] [95]
• Oral beta-blockers should be continued indefinitely, especially in patients with reduced left
ventricular function. Cardioselective beta-blockers are preferred in the initial management of
NSTEMI, but guidelines recommend metoprolol, bisoprolol, or carvedilol for post-NSTEMI
management in patients with stabilised heart failure and reduced systolic function.[1]
• All patients with NSTEMI should start high-intensity statin therapy (moderate-intensity if not
a candidate for high-intensity statin) in hospital regardless of cholesterol levels, and if there
are no contraindications.[96] Two trials demonstrated superior outcomes in patients treated
with atorvastatin within 12 hours of receiving PCI, and it may provide benefit when given early
in NSTEMI.[97] [98] A high-intensity statin is defined as a daily dose that lowers low-density
lipoprotein cholesterol (LDL-C) by approximately >50%, while a moderate-intensity statin daily dose
lowers LDL-C by approximately 30% to 50%. Statin therapy is particularly important in patients
who have hyperlipidaemia, diabetes, prior MI, or CAD. Statins inhibit the rate-limiting step in
cholesterol synthesis. They may also reduce vascular inflammation, improve endothelial function,
and decrease thrombus formation in addition to lowering LDL.[21] The addition of ezetimibe to the
statin regimen may also be considered to achieve lower LDL targets and has a modest decrease in
combined cardiovascular outcomes primarily driven by differences in non-fatal MI.[20] [99]
• The addition of proprotein convertase subtilisin/kexin type 9 (PCSK-9) inhibitors, alirocumab and
evolocumab, to maximally tolerated statin therapy may also be considered for patients who require
additional LDL lowering (<50% reduction in LDL-C; may also consider if LDL-C ≥2.59 mmol/L
[≥100 mg/dL]).[100] [101] Alirocumab is approved for use as adjunct therapy to diet and maximally
tolerated statin therapy for adult patients with heterozygous familial hypercholesterolaemia, or
clinical atherosclerotic cardiovascular disease, who require additional lowering of LDL. Evolocumab
is approved as an adjunct to diet and other lipid-lowering therapies (e.g., statins, ezetimibe)
in patients with primary hyperlipidaemia (including heterozygous hypercholesterolaemia) and
homozygous familial hypercholesterolaemia to reduce LDL. It is now also approved to reduce the
risk of MI in patients with established cardiovascular disease, and may be used for this indication
without adjunctive diet and lipid-lowering therapies. Evolocumab and alirocumab may also be used
as an alternative to statins if they are contraindicated or the patient is intolerant of statins.
• ACE inhibitors should be started in all patients with left ventricular systolic dysfunction (ejection
fraction <40%), heart failure, hypertension, diabetes, stable chronic kidney disease, or other high-
risk features, such as ongoing ischaemia with worsening heart failure, S3 gallop, new or worsening
TREATMENT
mitral regurgitation, or haemodynamic instability, without overt cardiogenic shock.[1] [4] [102] [103]
[104] They are started after 24 hours. The goal blood pressure is at least <140/90 mmHg (including
patients with chronic kidney disease or diabetes).[105] Angiotensin-II receptor antagonists may be
used if the patient is intolerant to an ACE inhibitor.[106] [107]
33
• Aldosterone antagonists (e.g., eplerenone, spironolactone) should be used in all patients with
left ventricular dysfunction (ejection fraction ≤40%), a history of diabetes mellitus, or evidence of
congestive heart failure (S3 gallop, rales). They should be started in patients receiving target doses
of ACE inhibitors or angiotensin-II receptor antagonists. Aldosterone blockade should not be used
in patients with serum creatinine >221 micromol/L (2.5 mg/dL) in men or >177 micromol/L (2.0 mg/
dL) in women, as well as in patients with hyperkalaemia (potassium >5.0 mmol/L [5.0 mEq/L]).[108]
• Oral anticoagulation may be indicated at discharge in selected patients with NSTEMI who are
considered to be high risk for recurrent thrombosis. Several new medications, particularly direct
thrombin inhibitors such as dabigatran and factor Xa inhibitors such as rivaroxaban and apixaban,
are currently being evaluated as potential alternatives to warfarin.[109] While direct thrombin and
factor Xa inhibitors may produce a modest reduction in ischaemic events when added to antiplatelet
therapy, results also suggest that they increase the risk of major bleeding, particularly when added
to dual antiplatelet therapy with aspirin and clopidogrel.[110] Low-dose rivaroxaban has been
demonstrated to reduce future cardiovascular events but causes an almost equivalent increase in
major bleeding events.[111] [112] It has been approved in some countries, although not in the US.
• Triple antithrombotic therapy should be kept to as short a duration as clinically feasible for the
patient, with full-dose oral anticoagulant indication after stent placement/acute coronary syndrome
event.[113] [114]
Treatment details overview

Consult your local pharmaceutical database for comprehensive drug information including contraindications,
drug interactions, and alternative dosing. ( see Disclaimer )
Acute ( summary )
acute presentation
1st antiplatelet therapy
adjunct ox ygen
plus glyceryl trinitrate ± morphine
plus beta-blocker
adjunct calcium-channel blocker
plus assess need for invasive or conservative

approach
invasive approach plus percutaneous coronary intervention

planned
plus anticoagulation
adjunct glycoprotein IIb/IIIa inhibitor
invasive approach not plus anticoagulation

TREATMENT
planned
Ongoing ( summary )
post-stabilisation
Ongoing ( summary )
1st cardiac rehabilitation
plus continue antiplatelet therapy
plus continue beta-blocker
plus statin
adjunct ezetimibe added to statin therapy
adjunct PCSK-9 inhibitor
adjunct ACE inhibitor or angiotensin-II receptor

antagonist
adjunct aldosterone antagonist
adjunct anticoagulation
TREATMENT
35
Treatment options
Acute
acute presentation
1st antiplatelet therapy

Primary options
aspirin-tolerant
» aspirin: 150-300 mg orally as a single dose,
followed by 75 mg once daily thereafter
--AND--
» clopidogrel: 300-600 mg orally as a loading
dose, followed by 75 mg once daily
-or-
» ticagrelor: 180 mg orally as loading dose,
followed by 90 mg twice daily
-or-
» prasugrel: 60 mg orally as a loading dose,
followed by 10 mg once daily
OR
aspirin-intolerant
» clopidogrel: 300-600 mg orally as a loading
dose, followed by 75 mg once daily
-or-
» ticagrelor: 180 mg orally as loading dose,
followed by 90 mg twice daily
-or-
» prasugrel: 60 mg orally as loading dose,
followed by 10 mg orally once daily
» All patients should be given dual antiplatelet

therapy with aspirin and a P2Y12 receptor
inhibitor. If the patient is intolerant of aspirin or it
is otherwise contraindicated, a P2Y12 receptor
inhibitor can be given alone, but two different
P2Y12 receptor inhibitors should not be given
together. Clopidogrel or ticagrelor are suitable
for patients on either noninvasive or invasive
strategies, while prasugrel is recommended
only for patients on an invasive strategy since
existing data come from patients treated by
percutaneous interventions.[64]
» Aspirin should be given on clinical suspicion

or diagnosis of acute coronary syndrome and
continued indefinitely.1[A]Evidence Healthcare
personnel providing pre-hospital emergency
TREATMENT
services should give patients a single loading

dose of aspirin as soon as possible to chest pain
patients suspected of having acute coronary
syndrome unless contraindicated or already
taken by the patient.[1] [74]
Acute
» High-dose aspirin is associated with an
increased risk of bleeding when compared with
low-dose aspirin and in the absence of improved
outcomes.[1]
» A loading dose of a P2Y12 receptor inhibitor

is given as soon as possible on admission and
then a maintenance dose is given for up to 12
months.[115] 7[A]Evidence One trial showed
that adding clopidogrel to aspirin therapy in
acute myocardial infarction (MI) prevents 10
major vascular events per 1000 treated.[116]
P2Y12 receptor inhibitors can reduce mortality
and morbidity, but they may be associated with
increased bleeding risk.[58] [59] Ticagrelor and
prasugrel are newer P2Y12 agents, which trials
have shown to have a faster onset of action and
greater efficacy compared with clopidogrel, but
with an increased risk of bleeding.[1] [60] [61]
» Note that P2Y12 receptor inhibitors should

not be given if urgent coronary artery bypass
graft (CABG) is anticipated or planned within 5-7
days, so it may be necessary to delay starting
a P2Y12 receptor inhibitor until diagnostic
angiography clarifies whether early CABG is
indicated.
» For patients receiving chronic clopidogrel

therapy prior to presentation, there is some
evidence to suggest decreased periprocedural
MI with clopidogrel reloading at the time of
percutaneous coronary intervention.[67]
» There are variable responses to antiplatelet

inhibition with clopidogrel based on loss-of-
function alleles for the CYP219C enzyme, which
is required to convert clopidogrel to its active
drug metabolite. The presence of at least one
loss-of-function mutation for CYP219C may
be as high as 30% in some populations. In a
single-centre retrospective study of clopidogrel
resistance, it appeared that patients with
clopidogrel resistance who remain on clopidogrel
are at a fourfold increase for major adverse
cardiovascular or cerebrovascular events
compared with those placed on a different
P2Y12 inhibitor.[65]
» Conflicting data regarding interactions between

proton-pump inhibitors and clopidogrel have
resulted in broad warnings by regulatory
TREATMENT
agencies. There are weak data documenting

decreased platelet assay responsiveness and
worse outcomes in retrospective clinical studies
of patients using clopidogrel and proton-pump
inhibitors together. The results of the only
large randomised trial appear to refute earlier
37
Acute
observational data and found no increase in risk
with co-administration of these agents. Proton-
pump inhibitors are recommended for patients
with a history of NSTEMI who also require triple
therapy, particularly when there is a history of
gastrointestinal bleeding. Clinical discretion is
advised, as guidelines do not fully address this
controversy.[117]
adjunct ox ygen
» All patients require oxygen

saturation measurement using pulse
oximetry.[1] Supplemental oxygen should be
administered only to patients with an arterial
oxygen saturation <90%, respiratory distress, or
other high-risk features for hypoxaemia.[1] [4]
» Liberal use of oxygen is associated with

increased mortality in patients with acute
coronary syndrome.[53]
plus glyceryl trinitrate ± morphine
Primary options
» glyceryl trinitrate translingual: 400-800

micrograms (1-2 sprays) every 5 minutes,
maximum 3 doses
OR
» glyceryl trinitrate: 0.3 to 0.6 mg sublingually

every 5 minutes, maximum 3 doses
Secondary options
» glyceryl trinitrate: 5 micrograms/min

intravenously initially, increase by 5-20
micrograms/min increments every 3-5
minutes, maximum 200 micrograms/min
Tertiary options
» morphine sulfate: 2-5 mg intravenously

every 5-30 minutes when required
-and-
» glyceryl trinitrate: 5 micrograms/min
intravenously initially, increase by 5-20
micrograms/min increments every 3-5
minutes, maximum 200 micrograms/min
OR
TREATMENT
» morphine sulfate: 2-5 mg intravenously

every 5-30 minutes when required
» Glyceryl trinitrate (GTN) is contraindicated if

there is a history of recent phosphodiesterase-5
Acute
inhibitor use (e.g., sildenafil); it should not be
given if systolic BP is <90 mmHg or there is a
concern about right ventricular infarct.
» Intravenous GTN is indicated if 3 doses

of sublingual GTN have not relieved the
pain.2[C]Evidence
» Morphine should be added early if GTN is not

sufficient. Morphine, in addition to its analgesic
and anxiolytic properties, has haemodynamic
effects that are potentially beneficial in unstable
angina and NSTEMI.
» Morphine causes vasodilation and may

produce reductions in heart rate (through
increased vagal tone) and systolic BP to further
reduce myocardial oxygen demand.[1] If GTN
is not effective or is contraindicated, morphine
can be given as an alternative in the absence
of any contraindications. Limited data (largely
observational studies) investigate morphine
use for NSTEMI with evidence of potential
safety concerns, thus it should be used with
caution.[68] One small, randomised, double-
blind trial found that morphine delays and
attenuates ticagrelor exposure and action in
patients with myocardial infarction.[69]
plus beta-blocker
Primary options
» metoprolol: 50-100 mg orally (regular-

release) twice daily
OR
» atenolol: 50-100 mg/day orally
OR
» propranolol: 180-320 mg/day orally

(immediate-release) given in 3-4 divided
doses
» Oral beta-blockers are indicated for all patients

unless contraindicated.3[C]Evidence
» Treatment should begin within a few days of

the event, if not initiated acutely, and should be
continued indefinitely, especially in patients with
TREATMENT
reduced left ventricular function.
» Contraindications to beta-blocker therapy

include heart rate <60 bpm, systolic BP <100
mmHg, moderate or severe left ventricular
failure, PR interval on the ECG >0.24 seconds,
39
Acute
second- or third-degree heart block, active
asthma/reactive airways disease, severe COPD,
right ventricular infarction, and cardiogenic
shock.[1] [70] [71]
» Randomised trials with threatened or evolving

myocardial infarction (MI) have shown lower
rates of progression to MI with beta-blocker
treatment.[70] [71] Comparative studies between
the various beta-blockers in the acute setting are
lacking. However, beta-blockers without intrinsic
sympathomimetic activity (e.g., metoprolol,
propranolol, and atenolol) are preferred for initial
management.
» Selection of a long-term beta-blocker often

depends on the clinician's familiarity with the
agent. The goal resting heart rate is 50 to 60
bpm.[1]
adjunct calcium-channel blocker
Primary options
» diltiazem: 30-90 mg orally (immediate-

release) four times daily
OR
» verapamil: 80-120 mg orally (immediate-

release) three times daily
OR
» amlodipine: 5-10 mg orally once daily
» Calcium-channel blockers can be given to

patients with continuing or recurrent ischaemic
symptoms after being given adequate nitrate
and beta-blocker therapy, or those who cannot
tolerate beta-blockers.[1] Although they are often
used, they are no more effective than control at
reducing mortality or myocardial infarction rates
in people with unstable angina.4[C]Evidence
» Patients treated acutely with a calcium-channel

blocker for acute angina do not need to continue
these drugs, provided there is no recurrent
angina on drug cessation or another indication
for these drugs (i.e., hypertension). These drugs
can be tapered after 24 hours at the discretion of
the clinician.
TREATMENT
» Short-acting dihydropyridines (e.g., nifedipine)

should be avoided in the absence of adequate
beta-blocker therapy because they may be
associated with adverse outcomes.[1]
Acute
» Verapamil or diltiazem should be avoided
in severe left ventricular dysfunction.[1] In the
UK, use of calcium channel blockers as add-on
therapy is not routine, unless beta-blockers not
tolerated or contraindicated.
plus assess need for invasive or conservative
approach
» The latest guidelines recommend that high-risk

patients routinely undergo early (12-24 hours)
coronary angiography and angiographically
directed revascularisation unless patients
have serious comorbidities. However, since
the release of these guidelines, an increasing
amount of new data, systematic reviews, and
expert opinion question the benefit of routine
invasive versus selective invasive approaches,
especially in low-risk patients; this is an evolving
field in NSTEMI.[83] [85] [118] [119] [120]
» An invasive approach is recommended if

any of the following high-risk features are
present: recurrent angina or ischaemia at rest
or with low-level activities despite intensive
medical therapy; elevated cardiac biomarkers
(troponin T or I); new or presumably new ST-
segment depression; signs or symptoms of heart
failure or new or worsening mitral regurgitation;
high-risk findings from non-invasive testing;
haemodynamic instability; sustained ventricular
tachycardia; percutaneous coronary intervention
within 6 months; prior coronary artery bypass
graft; high-risk score (i.e., TIMI, GRACE);
reduced left ventricular function (ejection fraction
<0.40).
» A conservative approach may be appropriate

in subsets of patients, especially those without
high-risk features and with a low risk score.
These include low-risk women [86] and older
patients with comorbidities.[121]
invasive approach plus percutaneous coronary intervention
planned
» Angioplasty is coupled with placement of
stents.[90]
» Complications of percutaneous coronary

intervention (PCI) include PCI-induced MI;
coronary perforation, dissection, or rupture;
cardiac tamponade; malignant arrhythmias;
cholesterol emboli; and bleeding from the access
TREATMENT
site. At experienced high-volume sites, radial

artery access is preferred due to decreased
access site complications.[91]
» Contrast-induced nephropathy is a common

and potentially serious complication, especially
41
Acute
in patients with baseline impaired renal
function.[92] Stent thromboses (early and late)
are a catastrophic complication.
plus anticoagulation
Primary options
» heparin: 60 units/kg intravenous bolus

initially, followed by 12 units/kg/hour infusion,
adjust dose to target aPTT of 50-75 seconds
OR
» enoxaparin: 30 mg intravenous bolus

initially, followed by 1 mg/kg subcutaneously
every 12 hours
OR
» dalteparin: 120 units/kg subcutaneously

every 12 hours, maximum 10,000 units twice
daily
OR
» fondaparinux: 2.5 mg subcutaneously once

daily
-and-
» heparin: 50-60 units/kg intravenous bolus
as a single dose during PCI
» Anticoagulation therapy can be subcutaneous

low molecular weight heparin (LMWH) (e.g.,
enoxaparin), intravenous unfractionated heparin
(UFH), or fondaparinux, irrespective of the
initial treatment strategy, and therapy can be
continued throughout hospitalisation or until
the time of percutaneous coronary intervention
(PCI).[122] In the event that the patient will
be treated medically, without plans for PCI,
fondaparinux may be used alone. However, for
patients undergoing PCI, UFH or bivalirudin
should be added to avoid catheter thrombosis.
Bivalirudin is to be used only in patients who are
to be managed with an early invasive strategy.[1]
[123]
» UFH and LMWH are thrombin

inhibitors.5[A]Evidence Like heparin, their
mechanism of action involves binding to
TREATMENT
antithrombin III to increase its anticoagulant

activity.
» UFH and LMWH are contraindicated in

patients with major bleeding, history of
Acute
adverse drug reaction, or heparin-induced
thrombocytopenia.
» Creatinine clearance should be assessed

before administering enoxaparin or
fondaparinux. Patients with severe renal
impairment (creatinine clearance <30 mL/
minute) should be considered for UFH over
enoxaparin, or a dose reduction may be
required in these patients. Fondaparinux is
contraindicated in patients with severe renal
impairment.
adjunct glycoprotein IIb/IIIa inhibitor
Primary options
» eptifibatide: 180 micrograms/kg intravenous

bolus initially at time of percutaneous
coronary intervention, followed by 2
micrograms/kg/min 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/min

intravenous infusion for 30 minutes, followed
by 0.1 micrograms/kg/min
» Glycoprotein (GB) IIb/IIIa inhibitors block

platelet binding of fibrinogen to the GP IIb/IIIa
receptor. This is the final stage before platelet
aggregation and the formation of thrombus.
» Tirofiban[103] or eptifibatide[124] are preferred

if GP IIb/IIIa inhibitor administration is planned;
however, addition of a GP IIb/IIIa inhibitor is only
recommended if there is evidence of a no-reflow
or a thrombotic complication.[118] [119] [125]
invasive approach not plus anticoagulation
planned
Primary options
» heparin: 60 units/kg intravenous bolus

initially, followed by 12-15 units/kg/hour
infusion, adjust dose to target aPTT of 50-75
seconds
OR
» enoxaparin: 30 mg intravenous bolus

TREATMENT
initially, followed by 1 mg/kg subcutaneously

every 12 hours
OR
43
Acute
» dalteparin: 120 units/kg subcutaneously
every 12 hours, maximum 10,000 units twice
daily
OR
» fondaparinux: 2.5 mg subcutaneously once

daily for up to 8 days
» Anticoagulation therapy can be subcutaneous

low molecular weight heparin (LMWH) (e.g.,
enoxaparin), or intravenous unfractionated
heparin (UFH), or fondaparinux.
» Anticoagulation is contraindicated in patients

with major bleeding, history of adverse drug
reaction, or heparin-induced thrombocytopenia.
» Creatinine clearance should be assessed

before administering enoxaparin or
fondaparinux. Patients with severe renal
impairment (creatinine clearance <30 mL/
minute) should be considered for UFH over
enoxaparin, or a dose reduction may be
required in these patients. Fondaparinux is
contraindicated in patients with severe renal
impairment.[1]
Ongoing
post-stabilisation
1st cardiac rehabilitation
» The aims of cardiac rehabilitation are to

increase functional capacity; stop cigarette
smoking; modify lipids and lipoproteins;
decrease body weight and fat stores; reduce
BP; improve psychosocial well-being; prevent
progression and promote plaque stability;
induce regression of underlying atherosclerosis;
and restore and maintain optimal physical,
psychological, emotional, social, and vocational
functioning.[126]
» Cardiac rehabilitation should be started on

discharge and after clearance by an outpatient
physician. The basic prescription should include
aerobic and weight-bearing exercise 4 to 5 times
per week for >30 minutes. There is a risk of
triggering a recurrent myocardial infarction with
TREATMENT
physical activity. However, this is minimal and

reduced by using a structured programme to
minimise (and treat) this risk.[126]
plus continue antiplatelet therapy
Ongoing
Primary options
aspirin-tolerant
» aspirin: 75 mg orally once daily
--AND--
» clopidogrel: 75 mg orally once daily
-or-
» ticagrelor: 90 mg orally twice daily
-or-
» prasugrel: 10 mg orally once daily
OR
aspirin-intolerant
» clopidogrel: 75 mg orally once daily
-or-
» ticagrelor: 90 mg orally twice daily
-or-
» prasugrel: 10 mg orally once daily
» In patients tolerant to aspirin, it should be

continued indefinitely at a low dose. In addition,
a P2Y12 receptor inhibitor should be continued
for up to 12 months in patients treated medically
(no stenting) or treated with a bare metal stent,
and for at least 12 months for those patients
treated with a drug-eluting stent.[66] Clopidogrel
or ticagrelor are suitable for patients on either
non-invasive or invasive strategies, while
prasugrel is recommended only for patients
on an invasive strategy since existing data
comes from patients treated by percutaneous
interventions.[64]
» In patients intolerant of aspirin, or if it is

otherwise contraindicated, a P2Y12 receptor
inhibitor can be given alone, in which case it too
should be continued indefinitely. Two different
P2Y12 receptor inhibitors should not be given
together.
» There are variable responses to antiplatelet

inhibition with clopidogrel based on loss-of-
function alleles for the CYP219C enzyme, which
is required to convert clopidogrel to its active
drug metabolite. The presence of at least one
loss-of-function mutation for CYP219C may
be as high as 30% in some populations. In a
single-centre retrospective study of clopidogrel,
resistance it appeared that patients with
TREATMENT
clopidogrel resistance who remain on clopidogrel

are at a fourfold increase for major adverse
cardiovascular or cerebrovascular events
compared with those placed on a different
P2Y12 inhibitor.[65]
45
Ongoing
plus continue beta-blocker
Primary options
» metoprolol: 25-200 mg orally (extended-

release) once daily
OR
» bisoprolol: 1.25 to 10 mg orally once daily
OR
» carvedilol: 12.5 mg orally twice daily for 2

days, followed by 25 mg twice daily
» Oral beta-blockers should be continued

indefinitely, especially in patients with reduced
left ventricular function.
» Cardioselective beta-blockers are preferred

in the initial management of NSTEMI, but
guidelines recommend metoprolol, bisoprolol,
or carvedilol for post-NSTEMI management in
patients with stabilised heart failure and reduced
systolic function.[1]
plus statin
Primary options
high-intensity statin
» atorvastatin: 40-80 mg orally once daily
OR
high-intensity statin
» rosuvastatin: 20-40 mg orally once daily
Secondary options
moderate-intensity statin
» atorvastatin: 10-20 mg orally once daily
OR
» rosuvastatin: 5-10 mg orally once daily
OR
TREATMENT
» lovastatin: 40 mg orally once daily
OR
Ongoing
» fluvastatin: 40 mg orally (immediate-
release) twice daily; 80 mg orally (extended-
release) once daily
OR
» simvastatin: 20-40 mg orally once daily
Doses higher than 40 mg/day are not
recommended due to the increased risk of
myopathy.
OR
» pravastatin: 40-80 mg orally once daily
OR
» pitavastatin: 2-4 mg orally once daily
» Statin therapy should be given before hospital

discharge to all patients with acute coronary
syndrome.[127]
» All patients with NSTEMI should receive a

high-intensity statin (moderate intensity if not
candidate for high-intensity statin) regardless
of cholesterol levels, and if there are no
contraindications.[96] A high-intensity statin is
defined as a daily dose that lowers low-density
lipoprotein cholesterol (LDL-C) by approximately
>50%, while a moderate-intensity statin daily
dose lowers LDL-C by approximately 30% to
50%.
» Statin therapy is particularly important in

patients who have hyperlipidaemia, diabetes,
prior myocardial infarction, or coronary artery
disease. Statins inhibit the rate-limiting step in
cholesterol synthesis. They may also reduce
vascular inflammation, improve endothelial
function, and decrease thrombus formation in
addition to lowering LDL.[21]
» Patients should be monitored for jaundice,

malaise, fatigue, and lethargy.[128]
» Fractionated bilirubin should be used rather

than alanine aminotransferase (ALT) or
TREATMENT
aspartate transaminase (AST) to detect liver

dysfunction. If evidence of liver injury is found,
the statin should be stopped. If ALT or AST
exceeds 3 times the upper limit of normal, the
levels can be repeated but there is no need to
stop the statin.[128]
47
Ongoing
adjunct ezetimibe added to statin therapy
Primary options
» ezetimibe: 10 mg orally once daily
» The addition of ezetimibe to the statin regimen

may also be considered to achieve lower low-
density lipoprotein targets.[20] [99]
adjunct PCSK-9 inhibitor
Primary options
» alirocumab: 75-150 mg subcutaneously

once every two weeks, or 300 mg
subcutaneously once monthly
OR
» evolocumab: 140 mg subcutaneously once

every two weeks, or 420 mg subcutaneously
once monthly
» The addition of alirocumab and evolocumab to

maximally tolerated statin therapy may also be
considered for patients who require additional
low-density lipoprotein (LDL) lowering (<50%
reduction in LDL-C; may also consider if LDL-C
≥2.59 mmol/L [≥100 mg/dL]).[100] [101]
» Alirocumab is approved for use as adjunct

therapy to diet and maximally tolerated statin
therapy for adult patients with heterozygous
familial hypercholesterolaemia, or with clinical
atherosclerotic cardiovascular disease, who
require additional lowering of LDL.
» Evolocumab is approved as an adjunct to

diet and other lipid-lowering therapies (e.g.,
statins, ezetimibe) in patients with primary
hyperlipidaemia (including heterozygous
hypercholesterolaemia) and homozygous
familial hypercholesterolaemia to reduce LDL.
It is now also approved to reduce the risk of
myocardial infarction in patients with established
cardiovascular disease, and may be used for
this indication without adjunctive diet and lipid-
lowering therapies.
» Evolocumab and alirocumab may also be

used as an alternative to statins if they are
contraindicated or the patient is intolerant of
TREATMENT
statins.
adjunct ACE inhibitor or angiotensin-II receptor
antagonist
Primary options
Ongoing
» enalapril: 2.5 mg orally once daily for 48
hours, increase gradually to 10 mg twice daily
OR
» lisinopril: 5 mg orally once daily for 48

hours, followed by 5-10 mg once daily
OR
» captopril: 6.25 mg orally three times daily

starting on day 3 post-MI, increase gradually
to 50 mg three times daily
Secondary options
» valsartan: 20 mg orally twice daily initially,

increase gradually to 160 mg twice daily
OR
» losartan: 50 mg orally once daily initially,

increase gradually to 100 mg once daily
OR
» candesartan: 4 mg orally once daily initially,

increase gradually to 32 mg once daily
» Angiotensin-converting enzyme (ACE)

inhibitors should be used in all patients with left
ventricle systolic dysfunction (ejection fraction
<40%), heart failure, hypertension, diabetes,
stable chronic kidney disease, or other high-
risk features, such as ongoing ischaemia with
worsening heart failure, S3 gallop, new or
worsening mitral regurgitation, or haemodynamic
instability, without overt cardiogenic shock.
» Angiotensin-II receptor antagonists may

be used in cases of intolerance to ACE
inhibitors.[129]
» ACE inhibitors or angiotensin-II receptor

antagonists may be started 24 hours post
myocardial infarction.
» Goal BP is at least <140/90 mmHg (including

patients with chronic kidney disease or
diabetes).[105]
TREATMENT
adjunct aldosterone antagonist

Primary options
» eplerenone: 25 mg orally once daily initially,

increase gradually to 50 mg once daily within
4 weeks
49
Ongoing
OR
» spironolactone: 12.5 to 25 mg orally once

daily
» Aldosterone antagonists (e.g., eplerenone,

spironolactone) should be used in all patients
with left ventricular dysfunction (ejection
fraction ≤40%), a history of diabetes mellitus,
or evidence of congestive heart failure (S3
gallop, rales). They should be started in patients
receiving target doses of angiotensin-converting
enzyme (ACE) inhibitors or angiotensin-II
receptor antagonists. Aldosterone blockade
should not be used in patients with serum
creatinine >221 micromol/L (2.5 mg/dL) in men
or >177 micromol/L (2.0 mg/dL) in women,
as well as in patients with hyperkalaemia
(potassium >5.0 mmol/L [5.0mEq/L]).[108]
adjunct anticoagulation
Primary options
» warfarin: consult specialist for guidance on

dose
OR
» rivaroxaban: consult specialist for guidance

on dose
OR
» apixaban: consult specialist for guidance on

dose
» Most patients do not need to continue

anticoagulation after hospitalisation. A subset
of patients who are high risk for a repeat
thrombotic event may be put on chronic oral
anticoagulation.
» Rivaroxaban can be given to patients who

have experienced an acute coronary syndrome
at the discretion of the physician. Data from the
ATLAS ACS 2-TIMI 51 trial (Anti-Xa Therapy
to Lower Cardiovascular Events in Addition to
Aspirin with/without Thienopyridine Therapy
in Subjects with Acute Coronary Syndrome
2-Thrombolysis in Myocardial Infarction 51)
TREATMENT
indicated that low doses of rivaroxaban (i.e.,

5 mg/day) reduced the risk of the composite
end point of death from cardiovascular causes,
myocardial infarction, or stroke in addition to
aspirin and clopidogrel. There is an increased
risk of non-fatal bleeding that was observed in
Ongoing
these trials.[111] [112] It has been approved in
some countries, although not in the US.
» Patients with prior history of stroke/transient

ischaemic attack, age older than 75 years, or
<60 kg body weight should not be started on
rivaroxaban for this indication.
TREATMENT
51
Non-ST-elevation myocardial infarction Follow up
Recommendations
Monitoring
FOLLOW UP
Close monitoring and treatment is essential. An inpatient follow-up should be arranged within the first 1
to 2 weeks of discharge. Monthly visits should be scheduled thereafter. Lipids should be monitored at
least every 6 months until a target low-density lipoprotein <1.8 mmol/L (<70 mg/dL) is reached in patients
who have had a myocardial infarction or have coronary artery disease. The need for follow-up cardiac
ultrasounds is at the discretion of the physician. However, cardiac ultrasounds are necessary to evaluate
and monitor ventricular function.[1]
It is crucial to assist smoking cessation efforts and promote a physical activity regimen. If available,
cardiac rehabilitation is extremely helpful. Psychosocial risk factors such as anxiety and depression
should be addressed. Depression in particular has been associated with a poor prognosis.[30] All
medicines should be reviewed at every follow-up visit to encourage patient compliance and optimal
dosing.[1]
In patients who have undergone direct reperfusion, further non-invasive stress testing or further imaging
is indicated only if stenosis of intermediate severity (luminal narrowing of 50% to 70%) is present in a non-
culprit artery. Patients with recurrent ischaemic-type pain after reperfusion may need angiography after
medical therapy to evaluate for further stenosis or occlusion.[90]
All patients, regardless of whether a stent was placed, should be treated with with a P2Y12 receptor
inhibitor for up to 12 months and low-dose aspirin daily as long as tolerated. There is some evidence
that patients treated with bare metal stents (BMS) are at an increased risk for repeat procedural care
compared to those treated with drug-eluting stents (DES). P2Y12 receptor inhibitors for patients with
acute coronary syndrome NSTEMI should be continued for at least 12 months in all patients despite
treatment strategy of medical management, balloon angioplasty, lytic therapy, BMS placement, or DES
placement. For patients with stable coronary artery disease receiving percutaneous coronary intervention,
shorter duration of dual antiplatelet therapies may be considered.[90] [144] A scientific advisory from
several major health organisations describes the risks of premature discontinuation of dual antiplatelet
therapy in patients with coronary artery stents.[142]
Patient instructions
Patients should schedule a follow-up appointment with their doctor in 1 to 2 weeks. Patients should
be given prescriptions and detailed discharge instructions including a list of medicines to take. These
instructions should inform the patient what to do if they experience any recurrent signs or symptoms and
should include restrictions on physical activity. Before discharge, patients should also receive instruction
and prescriptions for any additional testing that is needed by the physician. These medicines typically
consist of cholesterol-lowering drugs, blood pressure medicines, cardioprotective drugs, aspirin, and
other similar drugs. If one is available, patients should enter a cardiac rehabilitation programme. Cardiac
rehabilitation is a structured programme that provides myocardial infarction (MI) survivors with the tools,
motivation, and support needed to change behaviour and increase chance of survival. Typically, cardiac
rehabilitation programmes use group therapy to supervise and promote beneficial exercise, as well as to
provide emotional support.
Patients should return to the nearest emergency department or call their physician if they develop
recurring chest pain or discomfort, shortness of breath, sweating, gastrointestinal symptoms,
lightheadedness, palpitations, or other symptoms suggesting another MI or heart condition.
Complications
Complications Timeframe Likelihood
FOLLOW UP
cardiac arrhythmias short term medium
Arrhythmias (e.g., ventricular ectopy, atrial fibrillation, brady- or tachyarrhythmias, ventricular fibrillation
[VF], or ventricular tachycardia [VT]) occur from injury to the cardiac conduction system. They may cause
sudden death or induce cardiogenic shock.[140] Bradycardia is often seen in right-sided or posterior
infarction.
The incidence of VF is <2%. The majority of VT/VF occurs within the first 48 hours after admission.[141]
Electrolyte abnormalities should be monitored and corrected. Cardioversion or anti-arrhythmic therapy

may be needed. In patients with heart block or symptomatic bradycardia, transcutaneous or transvenous
pacing may be required.
congestive heart failure (CHF) short term low
CHF in the acute setting develops in about 8% of patients. It is most often secondary to compromised
left ventricular function from a large ischaemic event. Pump failure often results in pulmonary oedema,
hypotension, and oliguria.
CHF requires prompt diagnosis and aggressive stabilisation to prevent progression to shock. Therapy
includes diuresis, vasodilators, and staged pharmacotherapy (e.g., ACE inhibitors).
cardiogenic shock short term low
Develops in 4.5% of acute myocardial infarction (MI).[137] NSTEMI accounts for approximately 20% of
cardiogenic shock complicating MI. Typically, it occurs after a massive MI or repeated ischaemic events,
and it is predominantly caused by left ventricular failure.[138] Median time to development is about 7
hours. Associated mortality is 70% to 80%, with an in-hospital mortality of 59%.[138] [139]
Cardiogenic shock requires urgent percutaneous coronary intervention or CABG surgery if not already
carried out. The patient needs intensive care and pressor support and may need intra-aortic balloon pump
counterpulsation or other circulatory assist devices as a bridge towards definitive therapy.
ventricular rupture or aneurysm short term low
Occurs in 1% to 3% of all infarcts (STEMI more than NSTEMI), usually secondary to a weakened necrotic
wall.[138] It is associated with CHF, right-sided heart failure, pulmonary oedema, or cardiogenic shock.
Glucocorticoid administration has been associated with slightly higher risk of rupture.
Prompt diagnosis is the key to treatment of ventricular rupture or aneurysm. Therapy includes
management of complications (CHF or shock). Small ruptures can be managed without surgery. Larger
ruptures need surgery but the timing of surgery is controversial.
acute mitral regurgitation short term low
53
Complications Timeframe Likelihood

Most often secondary to papillary muscle rupture or acute left ventricle dilation. Acute mitral regurgitation
FOLLOW UP
predominantly occurs after inferior infarction.
Complete papillary muscle ruptures need emergency surgical correction. Moderate to severe mitral
regurgitation in association with left ventricular dysfunction is acutely managed as CHF.
post-MI pericarditis (Dressler syndrome) short term low
Dressler syndrome is mediated by inflammatory byproducts and the formation of ischaemic myocardium.
Inflammation involves the pericardium and is treated with non-steroidal anti-inflammatory drugs (NSAIDs)
or colchicine (preferably colchicine as it may reduce the risk of recurrence). If haemodynamic compromise
is present, pericardiocentesis or surgical intervention is required.
venous thromboembolism (VTE) short term low
MI has been associated with an increased risk of VTE, particularly for pulmonary embolism.[143]
depression variable medium
A risk factor for cardiovascular disease, but an acute cardiovascular event can also precipitate depression
in people without prior psychiatric conditions.[30] Data suggest that a combined psychosocial approach to
the treatment of depression improves outcome in patients. Exercise combined with pharmacotherapy may
be the most efficacious approach.[29]
in-stent thrombosis variable low
Often precipitated by cessation of dual antiplatelet therapy. Occurs more frequently with drug-eluting
stents.[142]
Prognosis
Patients who have experienced NSTEMI have a high risk of morbidity and death from a future event. The
rate of sudden death in patients who have had a myocardial infarction (MI) is 4 to 6 times the rate in the
general population.[130] Life-threatening ventricular arrhythmias (sustained ventricular tachycardia or
ventricular fibrillation) occurring after 48 hours from the index acute coronary syndrome portend a poor
prognosis, and are most frequently associated with left ventricular dysfunction. The benefit of implantable
cardioverter-defibrillators, for both primary and secondary prevention, in patients with significant left
ventricular dysfunction has been well demonstrated.[131] [132] Implantation for primary prevention should be
considered at a minimum of 40 days following hospital discharge based on current recommendations.[133]
This risk varies significantly and is widely dependent on patient characteristics and risk factors (diabetes
or smoking), presence of heart failure,[134] extent of infarction, treatment given (percutaneous coronary
intervention or coronary artery bypass graft), and compliance with long-term treatment regimens (cardiac
rehabilitation, lifestyle changes, and pharmacotherapy).
Modern therapy for NSTEMI, particularly statins and revascularisation, has decreased morbidity and mortality
by reducing the likelihood of cardiogenic shock, recurrent MI, and death. However, these benefits are
offset by the mortality associated with trends of older age in patients who present with acute coronary
syndrome.[135]
Data from the era prior to medical therapy and revascularisation suggest that the risk of cardiovascular death
following an MI in the absence of treatment is approximately 5% per year, with a death rate after hospital
discharge in the first year of about 10%. Pharmacotherapy, lifestyle changes, and cardiac rehabilitation are
well demonstrated to be beneficial and together are additive in reducing mortality.[136]
FOLLOW UP
55
Non-ST-elevation myocardial infarction Guidelines
Diagnostic guidelines
Europe
Cardiac arrhythmias in coronary heart disease

Published by: Scottish Intercollegiate Guidelines Network Last published: 2018
Risk estimation and the prevention of cardiovascular disease

Acute coronary syndrome

Chest pain of recent onset: assessment and diagnosis

Published by: National Institute for Health and Care Excellence Last published: 2016
GUIDELINES
ESC guidelines for the management of acute coronary syndromes in patients

presenting without persistent ST-segment elevation
Published by: European Society of Cardiology Last published: 2016
A systematic review and economic evaluation of new-generation computed

tomography scanners for imaging in coronary artery disease and congenital
heart disease: Somatom Definition Flash, Aquilion ONE, Brilliance iCT and
Discovery CT750 HD
Published by: Health Technology Assessment NHS R&D HTA Last published: 2013
Programme
International
Fourth universal definition of myocardial infarction

Published by: European Society of Cardiology; American College Last published: 2018
of Cardiology Foundation; American Heart Association; World Heart
Federation
North America
ACC/AATS/AHA/ASE/ASNC/SCAI/SCCT/STS 2016 appropriate use criteria for

coronary revascularization in patients with acute coronary syndromes
Published by: American College of Cardiology; American Association Last published: 2016
for Thoracic Surgery; American Heart Association; American Society of
Echocardiography; American Society of Nuclear Cardiology; Society for
Cardiovascular Angiography and Interventions; Society of Cardiovascular
Computed Tomography; Society of Thoracic Surgeons
North America
Guideline for the management of patients with non-ST-elevation acute

coronary syndromes
Published by: American College of Cardiology Foundation; American Last published: 2014
Heart Association
Depression as a risk factor for poor prognosis among patients with acute
coronary syndrome
Published by: American Heart Association Last published: 2014
Appropriate use criteria for cardiac radionuclide imaging

Published by: American College of Cardiology; American Society Last published: 2009
of Nuclear Cardiology; American College of Radiology; American
Heart Association; American Society of Echocardiography; Society of
Cardiovascular Computed Tomography; Society for Cardiovascular
GUIDELINES
Magnetic Resonance; Society of Nuclear Medicine
Appropriate use criteria for cardiac computed tomography and cardiac

magnetic resonance imaging
Published by: American College of Cardiology; American College of Last published: 2006
Radiology; Society of Cardiovascular Computed Tomography; Society
for Cardiovascular Magnetic Resonance; American Society of Nuclear
Cardiology; North American Society for Cardiac Imaging; Society for
Cardiovascular Angiography and Interventions; Society of Interventional
Radiology
Treatment guidelines
Europe
Cardiac arrhythmias in coronary heart disease

Guidelines on myocardial revascularization

Published by: European Society of Cardiology; European Association Last published: 2018
for Cardio-Thoracic Surgery
BTS guideline for ox ygen use in healthcare and emergency set tings
Published by: British Thoracic Society Last published: 2017
Risk estimation and the prevention of cardiovascular disease: a national

clinical guideline
Cardiac rehabilitation
57
Europe
Acute coronary syndrome

ESC guidelines for the management of acute coronary syndromes in patients

presenting without persistent ST-segment elevation
Published by: European Society of Cardiology Last published: 2016
Endoscopic saphenous vein harvest for coronary artery bypass grafting

Implantable cardioverter defibrillators and cardiac resynchronisation therapy

for arrhythmias and heart failure
GUIDELINES
Myocardial infarction: cardiac rehabilitation and prevention of further

cardiovascular disease
Antithrombotics: indications and management

Unstable angina and NSTEMI: early management

Endoaortic balloon occlusion for cardiac surgery

Clinical effectiveness and cost-effectiveness of immediate angioplasty for

acute myocardial infarction: systematic review and economic evaluation
Published by: Health Technology Assessment NHS R&D HTA Last published: 2005
Programme
North America
2017 AHA/ACC clinical performance and quality measures for adults with ST-
elevation and non-ST-elevation myocardial infarction
Published by: American College of Cardiology; American Heart Last published: 2017
Association
North America
ACC/AATS/AHA/ASE/ASNC/SCAI/SCCT/STS 2016 appropriate use criteria for

coronary revascularization in patients with acute coronary syndromes
Published by: American College of Cardiology; American Association Last published: 2016
for Thoracic Surgery; American Heart Association; American Society of
Echocardiography; American Society of Nuclear Cardiology; Society for
Cardiovascular Angiography and Interventions; Society of Cardiovascular
Computed Tomography; Society of Thoracic Surgeons
Antithrombotic therapy for VTE disease

Published by: American College of Chest Physicians Last published: 2016
Guideline for the management of patients with non-ST-elevation acute

coronary syndromes
GUIDELINES
Heart Association
2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce

atherosclerotic cardiovascular risk in adults
Association
2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based

therapy of cardiac rhythm abnormalities
Heart Association
AHA/ACCF secondary prevention and risk reduction therapy for patients with
coronary and other atherosclerotic vascular disease: 2011 update
Effectiveness-based guidelines for the prevention of cardiovascular disease

in women: 2011 update
Prevention of premature discontinuation of dual antiplatelet therapy in

patients with coronary artery stents
Association; Society for Cardiovascular Angiography and Interventions;
American College of Surgeons; American Dental Association; American
College of Chest Physicians
Asia
API expert consensus document on management of ischemic heart disease

Published by: Association of Physicians of India Last published: 2006
59
Oceania
National Heart Foundation of Australia & Cardiac Society of Australia and

New Zealand: Australian clinical guidelines for the management of acute
coronary syndromes
Published by: National Heart Foundation of Australia; Cardiac Society Last published: 2016
of Australia and New Zealand
Non ST-elevation acute coronary syndromes: New Zealand management

guidelines
Published by: Cardiac Society of Australia and New Zealand Last published: 2012
GUIDELINES
Non-ST-elevation myocardial infarction Evidence scores
Evidence scores
1. Reduction in mortality: there is good-quality evidence that antiplatelet treatment (aspirin 75-325 mg/
day) reduces the risk of death, MI, and stroke compared with placebo in people with unstable angina.
The evidence suggests no added cardiovascular benefit, but possible added harm, from doses of
aspirin >325 mg daily.
Evidence level A: Systematic reviews (SRs) or randomized controlled trials (RCTs) of >200
participants.
2. Reduction in chest pain episodes: there is poor-quality evidence that glyceryl trinitrate reduces
episodes of chest pain in people with unstable angina.
Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomized
controlled trials (RCTs) of <200 participants.
3. Reduction in mortality: there is poor-quality evidence that propranolol reduces mortality, MI, and
requirement for CABG or percutaneous coronary interventions at 30 days compared with placebo in
people with unstable angina who are taking optimal doses of nitrates and nifedipine.
4. Reduction in mortality: calcium-channel blockers are no more effective than control at reducing
mortality or MI rates in people with unstable angina. Short-acting dihydropyridine calcium-channel
blockers (such as nifedipine) have been associated with increased mortality in people with coronary
heart disease.
5. Prevention of MI: there is good-quality evidence that low molecular weight heparin reduces MI
compared with unfractionated heparin in people with unstable angina. The evidence found no
difference between the two treatments for major bleeds.
participants.
6. Reduction in mortality: there is good-quality evidence that unfractionated heparin plus aspirin reduces
mortality and MI at 7 days compared with aspirin alone in people with unstable angina. Longer-term
follow-up suggests no difference between treatments at 12 weeks. Unfractionated heparin plus aspirin
has not been associated with an increased risk of major bleeding compared with aspirin alone.
EVIDENCE SCORES
participants.
7. Prevention of MI: there is good-quality evidence that clopidogrel plus aspirin reduces the risk of death,
MI, and stroke at 9 months in people with unstable angina. This combination has been associated
61
Non-ST-elevation myocardial infarction Evidence scores
with an increase in major bleeding, but not haemorrhagic stroke, compared with aspirin alone at 6 to 9
months.
participants.
EVIDENCE SCORES
Non-ST-elevation myocardial infarction References
Key articles
• Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of
REFERENCES
patients with non-ST-elevation acute coronary syndromes: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014
Dec 23;64(24):e139-228. Full text Abstract
• Thygesen K, Alpert JS, Jaffe AS, et al; Executive Group on behalf of the Joint European Society
of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/
World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction. Fourth
universal definition of myocardial infarction (2018). J Am Coll Cardiol. 2018 Aug 27 [Epub ahead of
print]. Full text Abstract
• Mozaffarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics - 2015 update: a report
from the American Heart Association. Circulation. 2015 Jan 27;131(4):e29-322. Full text Abstract
• Franklin BA, Kahn JK, Gordon NF, et al. Cardioprotective "polypill"? Independent and additive benefits
of lifestyle modification. Am J Cardiol. 2004 Jul 15;94(2):162-6. Abstract
• Squizzato A, Bellesini M, Takeda A, et al. Clopidogrel plus aspirin versus aspirin alone for preventing
cardiovascular events. Cochrane Database Syst Rev. 2017 Dec 14;(12):CD005158. Full text Abstract
• National Institute for Health and Care Excellence. Unstable angina and NSTEMI: early management.
Nov 2013 [internet publication]. Full text
References
1. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of
patients with non-ST-elevation acute coronary syndromes: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014
Dec 23;64(24):e139-228. Full text Abstract
2. Antman E, Bassand JP, Klein W, et al. Myocardial infarction redefined - a consensus document of The
Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of
myocardial infarction. J Am Coll Cardiol. 2000 Sep;36(3):959-69. Full text Abstract
3. Thygesen K, Alpert JS, Jaffe AS, et al; Executive Group on behalf of the Joint European Society
of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/
World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction. Fourth
universal definition of myocardial infarction (2018). J Am Coll Cardiol. 2018 Aug 27 [Epub ahead of
print]. Full text Abstract
4. Roffi M, Patrono C, Collet JP, et al. 2015 ESC guidelines for the management of acute coronary
syndromes in patients presenting without persistent ST-segment elevation: Task Force for the
Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment
63
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75
Non-ST-elevation myocardial infarction Images
Images
Figure 1: ECG showing ST depression

IMAGES
From the personal collection of Dr Syed W. Yusuf and Dr Iyad N. Daher, Department of Cardiology, University
of Texas, Houston; used with permission
Figure 2: ECG showing ST depression

From the personal collection of Dr. Syed W. Yusuf and Dr. Iyad N. Daher, Department of Cardiology,
University of Texas, Houston; used with permission
Non-ST-elevation myocardial infarction Images
IMAGES
Figure 3: 64-slice CT angiography (A) and conventional angiography (B) showing a high-grade lesion in the
mid-right coronary artery, indicated by the arrows. The arrowheads show artefacts that may be mistaken for
lesions
From: Schussler JM and Grayburn PA. Heart, 2007;93:290-297
Figure 4: 64-slice CT angiography of a patient with stable angina showing 3D reconstruction (A), curved
reformatted images (B) and confirmation of a high-grade lesion on conventional angiography (C). The
arrowheads show calcified plaques. Dx= diagnosis
From: Schussler JM and Grayburn PA. Heart, 2007;93:290-297
77
Non-ST-elevation myocardial infarction Disclaimer
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Contributors:
// Authors:
Cody S. Deen, MD
Assistant Professor of Medicine
Director of Cardiology, Hillsborough Hospital, University of North Carolina, Hillsborough, NC
DISCLOSURES: CSD was previously the Director of Cardiac Rehab for Chatham Hospital, which was
financially set up as a consultancy relationship, until 2017. CSD has spoken (unpaid) at the Update in
Cardiology and Update in Internal Medicine Conferences at UNC for the last 5 years. CSD has served as
the PI for the Dal-GeneE (site now closed) and the ACCELERATE Trials at the University of North Carolina
(trial now completed). Each trial required paid travel to an investigator meeting.
// Acknowledgements:
Dr Cody S. Deen would like to gratefully acknowledge Dr Sripal Bangalore, Dr Mina Owlia, Dr Thomas
Vanhecke, and Dr Dena Krishnan, the previous contributors to this topic.
DISCLOSURES: SB, MO, TEV, and DK declare that they have no competing interests.
// Peer Reviewers:
Nicholas Palaskas, MD, FACC

Assistant Professor
University of Texas MD Anderson Cancer Center, Houston, TX
DISCLOSURES: NP declares that he has no competing interests.
Edward Ullman, MD
Associate Professor
Department of Emergency Medicine, Beth Israel Medical Deaconess Center, Boston, MA
DISCLOSURES: EU 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.
Shrilla Banerjee, MBMD, MRCP

Consultant Cardiologist
East Surrey Hospital, Surrey and Sussex NHS Trust, Surrey, UK
DISCLOSURES: SB declares that she has no competing interests.

Non-ST-elevation Myocardial Infarction: The Right Clinical Information, Right Where It's Needed

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Non-ST-elevation Myocardial Infarction: The Right Clinical Information, Right Where It's Needed

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Non-ST-elevation

The right clinical information, right where it's needed

Last updated: Dec 06, 2018

◊ Symptoms are indistinguishable from those of unstable angina. However, non-ST-elevation

The severity of myocardial damage in NSTEMI depends on:

• Duration of ischaemia and time to reperfusion

reference limit (URL) and at least one of the following:

Acute coronary syndrome (ACS)[1]

1. ST-elevation MI (STEMI): ECG demonstrates ST elevation of >1 mm in ≥2 anatomically contiguous

Step-by-step diagnostic approach

History and examination

Initial tests (non-ECG)

[VIDEO: Thrombolysis in Myocardial Infarction (TIMI) Score for Unstable

[VIDEO: GRACE Score for Acute Coronary Syndrome Prognosis ]

• Age >65 years

• Class I: no evidence of CHF

[VIDEO: HEART Score ]

acute coronary syndrome and targeting secondary prevention strategies.[1]

family history of premature coronary artery disease (CAD)

age >65 years

obesity and metabolic syndrome phenotype

stent thrombosis or restenosis

chronic kidney disease

surgical procedures (including intra-operative and postoperative periods)

History & examination factors

chest pain (common)

recent percutaneous coronary intervention or previous coronary artery

Other diagnostic factors

shortness of breath (common)

abdominal pain (common)

cold exposure (uncommon)

emotional upset (uncommon)

early morning onset (uncommon)

• Presence of palpitations or tachy- or bradyarrhythmias.

abnormal heart sounds (uncommon)

risk of death and morbidity.[49]

Other tests to consider

Condition Differentiating signs / Differentiating tests

Condition Differentiating signs / Differentiating tests

Condition Differentiating signs / Differentiating tests

Oesophageal spasm • Usually diagnosed after • The oesophagus may have

Costochondritis • Diagnosis is made on the • There are no specific studies

Panic at tack • Most often diagnosed after • No tests or procedures can

Condition Differentiating signs / Differentiating tests

Myocarditis • There is a wide spectrum • The definitive test is

Acute cholecystitis • On physical examination • Ultrasound may show a

Condition Differentiating signs / Differentiating tests

Brugada syndrome • More common in Asian • ECG shows saddle-shaped

exogenous catecholamine this condition.

Risk stratification scores[1]

TIMI Risk Score[40]

[VIDEO: Thrombolysis in Myocardial Infarction (TIMI) Score for Unstable

• Age >65 years

The Global Registry of Acute Coronary Events (GRACE) risk model

[VIDEO: GRACE Score for Acute Coronary Syndrome Prognosis ]

• Class I: no evidence of congestive heart failure

[VIDEO: HEART Score ]

Step-by-step treatment approach

Choice of invasive or conservative management

Long-term management post-stabilisation

• Increase functional capacity

• Modify lipids and lipoproteins

• Decrease body weight and fat stores