STEMI mimics; A mnemonic

Simon Mark Daley (2018)

aised intracranial pressure (Such as 

R SAH or haemorrhagic stroke)

bberrant conduction (Left Bundle

A Branch Block)

pasm of the coronary arteries 

I nflammation (Pericarditis)
S
(Prinzmetal's/variant angina)

S
pontaneous coronary artery dissection
(SCAD) E
mbolism (Pulmonary)

E lectrolytes (Hyperkalaemia)
G
rief (Takotsubo cardiomyopathy)

D M
evice (Ventricular paced rhythm) yocardial infarction recently (leading to
ventricular aneurysm)

E
nlarged ventricle (Left ventricular
hypertrophy)

S odium channelopathy (Brugada
Syndrome) N ormal for them (Early repolarisation)

T horacic aortic dissection

T emperature (Hypothermia)
E nlarged ventricle (Left ventricular hypertrophy)

Accounts for up to 25% of ED presentations with chest pain.

The left ventricle hypertrophies in response to pressure secondary to conditions such as

hypertension and aortic stenosis, as well as aortic regurgitation, mitral regurgitation,
coarctation of the aorta, and hypertrophic cardiomyopathy.

This leads to the following ECG

features; 
Increased R wave amplitude in
leads I, aVL and v4-v6.
Increased S wave depth in leads
III, aVR,v1-v3.
The thickened LV wall leads to
prolonged depolarisation
increased R wave peak time and
delayed repolarisation (ST and T
wave abnormalities) in the
lateral leads.

Diagnostic criteria (Sokolov-Lyon);

 
S wave depth in v1 + tallest R wave
height in v5-v6 >35mm.

(Courtesy of LITFL)
A bberant conduction (Left bundle branch block)

Accounts for up to 15% of ED presentations with chest pain.

 
Caused by aortic stenosis, ischaemic heart disease, hypertension, anterior MI, primary
degenerative disease of the conducting system (Lenegre disease), hyperkalaemia, digoxin
toxicity.

Diagnostic criteria;
QRS duration >120ms.
Dominant S wave in v1.
Broad monophasic R wave in lateral leads (I, aVL, v5-v6.
Absence of Q waves in lateral leads (I, v5-v6 - Q waves are still allowed in aVL.
Prolonged R wave peak time >60ms in left precordial leads (v5-v6).

Associated features;
Appropriate discordance.
Poor R wave progression in the
chest leads.
Left axis deviation.
 

 
Can be assessed using Sgarbossa
criteria to exclude presence of
STEMI.
(Courtesy of LITFL)
N ormal for them (Early repolarisation)
Accounts for up to 12% of ED presentations with chest pain.
 
Most commonly seen in young, healthy patients <50. It produces widespread ST elevation
that may mimic pericarditis or AMI. Generally considered to be a normal variant not
indicative of cardiac disease. ER is less common in >50s, in whom STE is more likely to
represent myocardial ischaemia. It is rare in the >70s. Clinicians should avoid diagnosing ER
in patients >50, especially those with risk factors.

How to recognise ER;

Widespread concave STE, most prominent v2-v5.
Notching or slurring at the J-point.
Prominent, slightly asymmetrical T waves that are concordant with the QRS complexes.
The degree of STE is modest comparison to the T wave amplitude (less than 25% of the T
wave height in v6).
ST elevation is usually <2mm in the precordial leads and <0.5mm in the limb leads, although
precordial STE may be                                                                                                                     
up to 5mm.
No reciprocal ST                                                                                                               
depression to suggest                                                                                                                 
STEMI.
ST segment changes are                                                                                                   
relatively stable over                                                                                                                   
time (no
progressive                                                                                                                     
on serial ECG tracings).

(Courtesy of LITFL)
N ormal for them (Early repolarisation)

The degree of ST elevation may fluctuate in response to changes in autonomic tone:

diminishing with increased sympathetic tone / exercise / tachycardia or increasing when the
HR slows. 
The ST elevation may gradually disappear over time as the patient ages: up to 30% of
patients with ER will have resolution of ST elevation on ECGs taken several years later.

Early repolarisation no longer a "benign" finding devoid of clinical significance.

Studies have demonstrated a 2 to 3-fold increased risk of death vs those without.
Absolute risk remains exceedingly low in otherwise healthy individuals.
Incidental finding of ER should not be interpreted as a high-risk marker for arrhythmic
death due to the relatively low odds of SCD based on ER alone.

A consensus paper in 2015 concluded that in the absence of syncope, or strong family history
of SCD, the finding of ER does not merit further investigation.
G rief (Takotsubo cardiomyopathy)

Only described within the last 20 years and increasingly recognised due to the increased use
and availability of coronary angiography. Also known as stress cardiomyopathy, or  broken
heart syndrome,Takotsubo is typically triggered by
emotional stress, or the death of a loved one.
 
Mayo clinic criteria (widely but not universally accepted);
New ECG changes and/or moderate troponin rise.
Transient akinesis/dyskinesis of LV (apical and mid-                                                        
ventricular segments) with regional wall abnormalities                                          
extending beyond a single vascular territory.
Absence of coronary artery stenosis >50% or culprit                                                  
lesion.

Clinically indistinct from STEMI in the ED and should be                                               

treated as such until proven otherwise -  although                                                       
Takotsubo may form an early differential.
 I nflammation (Pericarditis)

Inflammation of the pericardium produces characteristic chest pain (retrosternal, pleuritic,

worse laying flat, relieved sitting forward), tachycardia and dyspnoea. There may be an
associated pericardial rub or evidence of a pericardial effusion. Widespread ST segment
changes occur due to involvement of the underlying epicardium (ie myopericarditis).

Recognising pericarditis; Causes;

Widespread concave ST elevation and PR Infectious - mainly viral, occasionally
depression throughout most of the limb bacterial, fungal, TB
leads (I, II, III, aVL, aVF, and precordial Immunological
leads (v2-v6) Uraemia
Reciprocal ST depression and PR Post-MI / Dresslers
elevation in lead aVR (+v1)  Trauma
Post cardiac surgery
Paraneoplastic syndromes
Drug induced
Post radiotherapy

Features suggesting ER; Features suggesting pericarditis;

ST elevation limited to the precordial leads Generalised ST elevation
Absence of PR depression Presence of PR depression
Prominent T waves Normal T wave amplitude
ST segment / T wave ratio <0.25 ST segment / T wave ratio >0.25
Characteristic "fish-hook" appearance in v4 Absence of "fish-hook" appearance in v4
ECG changes usually stable over time (non- ECG changes evolve slowly over time
progressive)
S odium channelopathy (Brugada syndrome)
An ECG pattern with a high incidence of sudden death in patients with structurally normal
hearts. Diagnosis requires characteristic ECG finds AND clinical criteria. Further risk
stratification is controversial. Definitive treatment is ICD implantation. Brugada sign alone is
of questionable signficance.

BrS is a mutation of the cardiac sodium channel gene (often referred to as a sodium
channelopathy). ECG changes are often transient and can be unmasked or augmented by;
Fever
Ischaemia
Drugs
Hypokalaemia
Hypothermia
Post DCCV

Diagnostic criteria;
Only type 1 is potentially diagnostic.

But must be accompanied by one of the

following;
Documented VF or polymorphic VT
FH of SCD <45yrs
Brugada sign in family members ECG
Inducibility of VT with programmed
electrical stimulation Type 2 and 3 may warrant further
Syncope investigation.
Nocturnal agonal respiration
E mbolism (Pulmonary)

Ranges from asymptomatic to life-threatening catastrophe. PE occurs when a DVT migrates

to the pulmonary arterial tree.

Massive PE - Acute PE with obstructive shock or SBP <90mmHg

Sub-massive PE - Acute PE without symptomatic hypotension (SBP>90mmHg but with
either RV dysfunction or myocardial necrosis
Those without the above severe features are non-massive or low risk PEs

ECG features;
Non-specific ST changes or T wave changes(seen in up to 50% of cases)
Sinus tachycardia (44%)
s1 q3 t3 (less common than perceived, only around 20%)
Complete or incomplete RBBB (18%)
Right axis deviation (16%)
P pulmonale (right atrial enlargement) - Peaked P wave in lead II >2.5mm (9%)
Atrial arrhythmias (8%)
Dominant R wave in v1 - a manifestation of acute RV dilatation
Clockwise rotation - shift of the R/S transition point towards v6 ("pulmonary
disease pattern"), implying rotation of the heart due to RV dilatation
 T horacic aortic dissection
The most common catastrophe of the aorta (3:100,000): 3 times more common than
abdominal aneurysm rupture. Aortic dissection is a type of acute aortic syndrome (AAS)
characterised by blood entering the medial layer of the wall with the creation of a false
lumen.

Inferior ST elevation Pericarditic changes Electrical alternans

(tamponade)
Classification by Stanford;
Type A - Involves the ascending aorta. Surgery usually indicated 
Type B - Involves the aorta beyond left subclavian artery. Managed medically

Typical presenting symptoms; Risk factors;

Retrosternal chest pain -anterior HTN, smoking, hyperlipidaemia
dissection Previous CV surgery
Interscapular pain - descending aorta Structural abnormalities (eg bicuspid AV,
Severe pain ("worse ever" described in aortic coarctation)
90% of presentations) Iatrogenic (eg recent cardiac
Sudden onset (90%) catheterisation)
Sharp (64%) or tearing (50%) Infection
Down the back (46%) Arteritis
Migrating pain (16%) Aortic dilatation / aneurysm
Maximal in onset (not crescendo build up, Wall thinning
as in AMI) 'Crack' cocaine (abrupt catcholamine-
induced HTN
Inherited diseases (eg Marfans, Ehlers-
Danlos)
Age
S pontaneous coronary artery dissection (SCAD)

Rare, sometimes fatal traumatic condition, with 80% of cases occurring in women.

One of the coronary arteries develops a tear, causing blood to flow between the layers which
forces them apart. Mortality may be as high as 70%.

A primary cause of MI in young, fit, healthy women (and some men) with no obvious risk
factors. These can occur during pregnancy, postpartum and peri-menopausal periods.

Coronary angiogram is the most common method to form diagnosis, typically using
intravascular ultrasound (IVUS).

pasm of the coronary arteries

S (Prinzmetal's/variant angina)

Pattern of ST elevation very similar to acute STEMI - localised ST elevation with reciprocal ST
depression occurring during episodes of chest pain. Unlike acute STEMI, changes are
transient, reversible with vasodilators and not usually associated with myocardial necrosis.

It may be impossible to differentiate these two conditions based on the ECG alone.
 yocardial infarction recently (Leading to
M ventricular aneurysm)
Seen in patients with previous/recent MI. Mechanism is thought to be related to incomplete
reperfusion and transmural scar formation following AMI.

Typical ECG pattern;

Residual/persistent STE>2 weeks post MI
Well formed Q or QS waves
T wave flattening or inversion
evice (Ventricular paced
D rhythm)
Ventricular pacing causes identical changes to those seen in LBBB. There is appropriate
discordance with the ST segment and T wave directed opposite to the main vector of the QRS
complex.

aised intracranial pressure (Such as in

R SAH or haemorrhagic stroke)
Raised intracranial pressure (eg due to intracranial haemorrhage or traumatic brain injury)
may cause ST elevation or depression that simulates myocardial ischaemia or pericarditis.
More commonly, raised ICP is associated with widespread, deep T wave inversions.
E lectrolytes (Hyperkalaemia)
Although not the most common ECG abnormality caused by hyperkalaemia, there is a large
body of case studies and anecdotal evidence of ST segment elevation in hyperkalaemia. The
tall/peaked T waves very typically seen in this context can also complicate the evaluation of
the ST segment.
Serum potassium > 7.0  mEq/L
• Prolonged QRS interval with bizarre QRS morphology
• High-grade AV block with slow junctional and
Serum potassium > 5.5 mEq/L ventricular escape rhythms
• Peaked T waves (usually the • Any kind of conduction block (bundle branch blocks,
earliest sign of hyperkalaemia) fascicular blocks)
• Sinus bradycardia or slow AF
Serum potassium > 6.5 mEq/L • Development of a sine wave appearance (a pre-
• P wave widens and flattens terminal rhythm)
• PR segment lengthens
• P waves eventually disappear Serum potassium level of > 9.0 mEq/L
• Asystole
• Ventricular fibrillation
• PEA with bizarre, wide complex rhythm

T emperature (Hypothermia)
Common ECG changes due to hypothermia;
• Bradyarrhythmia’s
• Osborne waves (J wave) – these may give the appearance of STE due to J point
elevation/positive deflection
                                                                           • Ventricular ectopics
• Prolonged PR, QRS and QT intervals
                                                                           • Cardiac arrest due to VT, VF, or asystole
• Shivering artefact