The document discusses atypical STEMI patterns and their equivalents, emphasizing the importance of recognizing these patterns for timely intervention in acute coronary syndrome (ACS). It outlines various ECG features indicative of atypical STEMI such as isolated posterior STEMI, st elevation in aVR, and hyperacute T waves, highlighting criteria for emergency catheter lab activation. The document stresses the need for proper ECG evaluation to differentiate between benign early repolarization and STEMI to avoid delays in treatment.

1. Atypical stemi patterns &
stemi equivalents
- Dr Varun Patel
Courtesy for References:
1. EM Docs website
2. Dr Stephen Smith’s Blog
3. ECG in Acute MI Book by Dr Stephen smith
4. Life in the Fast lane Website

2. Cardiac Action Potential

3. Classification of acs

4. Basic physiology of stemi
• Due to Ischemia -> Damage to Na/K ATPase Pump
occurs -> Decreased intracellular K levels ->
Delayed Phase 3 repolarization.
• The repolarization in normal cells start from the point
of Depolarization start. In Ischemic cells, it is the
other way round and repolarization begins from the
last point of depolarization.

5. Basic Physiology in stemi
• Hyperacute T waves
• ST segment Elevation:
Current of Injury Theory
Incomplete
Depolarization Theory
• Reciprocal Changes
• Q wave formation

6. Evolution of stemi

7. St changes but not mi
• Following are changes in ST segment that are not
considered as MI:
LVH with strain pattern
Early Repolarization
Pericarditis
LV Aneurysm (Persistent ST elevation after 6 weeks
of Transmural MI)

8. Atypical stemi patterns
• There are some patterns of ECG that are not typical
but are considered significant as Equivalents to
STEMI during diagnosis of ACS.
• These are divided for convenience into 2 sections:
1. Those causing ST depression and T wave changes
2. Those causing ST elevations
• The important question to answer is – Whether to
activate Cath Lab for PCI in these cases? We will
deal with it one by one.

9. Atypical Stemi patterns
1. Those causing ST depression and T wave
changes:
 Isolated Posterior STEMI
 Isolated ST depression in aVL
 Hyperacute T waves
 De-Winter’s pattern

10. Atypical Stemi patterns
2. Those causing ST elevations:
 ST elevations in aVR
 Presumed New LBBB
 STEMI Equivalents in a paced rhythm

11. Atypical Stemi patterns
I] Isolated Posterior STEMI:
Posterior heart is involved in 20% cases, but
Isolated Posterior STEMI is seen in 5% patients
only.
When to suspect Posterior STEMI?
1. When there is presence of Inferior & Lateral
STEMI, always do a Posterior ECG to rule out
Posterior STEMI.
2. ECG shows: Isolated ST Depressions in V1-V3

12. Atypical Stemi patterns
• ECG Signs of Isolated Posterior STEMI:
1. ST Depressions in leads V1-V3
2. Prominent T waves in leads V1-V3
3. R:S ratio in lead V2 is >1
• Lead Placement for Posterior STEMI:
First put the Electrode for lead V8 at Tip of Scapula and
then put V7 & V9 on either sides of V8
• On acquiring Posterior ECG, you can Diagnose Posterior
STEMI if there is >0.5mm ST elevations in Posterior
Leads.

13. Atypical Stemi patterns

14. Atypical Stemi patterns
• DD for ST depressions plus T inversions in V1-V3:
1. Isolated Posterior STEMI
2. Anterior wall Subendocardial Ischemia
3. RVH with Strain Pattern

15. Atypical Stemi patterns
• CASE STUDY:
A 54yr old Female with k/c/o DM & HTN with Chronic
Smoking, with complaints of Substernal Chest Pain
irradiating to both shoulders. The pain was persistent
since 3 hours. Following was the ECG taken:

16. Atypical Stemi patterns

17. Atypical Stemi patterns
• The patient was diagnosed as NSTEMI and loaded
with Inj Enoxaparin, Dual Antiplatelets and admitted
to ICU. In ICU, a 2D ECHO was done which
revealed Regional wall motion Abnormality in
Posterior wall. At this point, the patient was sent to
Cath lab for PPCI.
• CAG revealed a complete 100% occlusion in Left
Circumflex Artery (LCX)
• How can such delay be avoided?

18. Atypical Stemi patterns
• How common is Posterior STEMI? What is the
Significance of Precordial ST Depressions in ACS?
 As per many studies conducted, the average occurrence
rate of an Isolated Posterior STEMI is 3-11%. This is not
a less number!
 In all these patients, a study revealed that an average
time for Door to PCI in these patients was 29.4 hours.
None of the patients had Door to PCI time of less than 6
hours.
 However, note that 3/4th of the patients coming with ST
depressions in Ant Chest leads did not have a completely
occluded Artery. Thus, it is Important to properly evaluate
this ECG and not assume that it is Posterior STEMI.

19. Atypical Stemi patterns
 Anterior Subendocardial Ischemia Vs Isolated Posterior
STEMI:
Following are few points that can be used to differentiate the two
on ECG:
• First, you should know that when there is precordial ST
depression due to subendocardial ischemia, it is not necessarily
due to anterior wall ischemia. Data from stress testing shows
that subendocardial ischemia DOES NOT LOCALIZE on the
ECG, and usually is in leads II, III, aVF and V4-V6. But, again,
this does not tell you which artery is involved.
• Second, ST depression in V1-V3, vs. V4-V6, is much more
likely to be posterior than subendocardial ischemia.

20. Atypical Stemi patterns
• Third, patients at higher risk of NSTEMI (older, more risk
factors, h/o angiogram with multivessel disease) are
much more likely to have subendocardial disease (vs.
younger smoker).
• Fourth, patients with reasons to have demand ischemia
(tachycardia, sepsis, GI Bleed, etc.) are much more likely
to have subendocardial ischemia (like in a stress test);
those with posterior MI are much more likely to present
with onset of chest pain and with normal vital signs.
• Fifth, look for tall R-waves in V1-V3 (the analog of Q-
waves in other locations).

21. Atypical Stemi patterns
• Sixth, placement of posterior leads. At least 0.5 mm of ST
elevation in just one lead appears to be the most sensitive
and specific single "criteria" for posterior MI.
• Seventh, an immediate echocardiogram can make the
distinction
• Eighth, Whether or not it is STEMI, the cath lab should be
activated if the ischemia cannot be controlled medically: aspirin,
nitro, beta blockers, clopidogrel, heparin/enoxaparin, GP IIb/IIIa
inhibitor.

22. Atypical Stemi patterns
II] Isolated ST depressions in aVL:
• ST depressions in aVL can be reciprocal to Inferior STEMI.
• Birbaum and Smith demonstrated in a study that Reciprocal ST
Depression in aVL can be apparent in absence of STEMI in
Inferior leads.
• In their study, they noted that 99% of patients with Inferior
STEMI have ST depressions in lead aVL as reciprocal
changes, 93% of which had prominent ST elevations in inferior
leads of >1mm. But 7% of patients had only Isolated ST
depressions in lead aVL, for which on further evaluation noted
that patient had Biomarker positive Inferior STEMI.
• As such, the evidence to prove this Hypothesis is still lacking
and Smith et al are still gathering enough evidence to prove it.
• As of now, this finding in ECG does not need immediate Cath
lab activation for PCI, but an Early Cardiologist consult is a
must.

23. Atypical Stemi patterns
III] Hyperacute T waves:
• Hyperacute T waves are a well defined ECG feature of Early
STEMI. They are noted anywhere between 5 min to 30 min of
onset of Chest Pain.
• They tend to be broad-based, taller than normal T-waves (>5-
10mm in precordial leads) and may be symmetric or asymmetric.
• Very often, reciprocal ST changes are seen in Inferior leads along
with Tall T waves.
• Possible common DD for Tall T waves:
1. Hyperkalemia
2. LVH
3. Benign Early Repolarization
4. Hyperacute Anterior STEMI

24. Atypical Stemi patterns
• How to Differentiate HATWs with other causes?
Following are the features of T-waves in DDs:
Hyperkalemia: narrow-based, symmetric, and peaked (sharp); may have
a widened QRS
BER: diffuse, peaked, associated with J-point elevation
LVH: look for voltage criteria and a strain pattern
Seen in BER – Note the associated J Point Elevation

25. Atypical Stemi patterns
• Note that Hyperacute T waves currently are considered as a criteria for activation
of Cath Lab along with positive clinical history. Before activation, following things
should be considered:
1. Rule out LVH and BER patterns as per ECG findings.
2. As Hyperkalemia T waves are very similar to HATWs, an urgent ABG should be
done to rule out Hyperkalemia before activation of Cath Lab for PCI.

26. Atypical Stemi patterns
IV] De-Winter’s Pattern:
• In 2008, De-Winter in a Dutch Registry, described a
pattern seen in ECG consistent with Anterior STEMI
and further complete occlusion in LAD found in CAG
in 2% of patients.
• De-Winter’s Pattern: Upsloping ST elevations in
aVR (>1mm) with ST-Depressions and tall T
waves in Precordial leads.

27. Atypical Stemi patterns

28. Atypical Stemi patterns
• Note that De-Winter’s Pattern is an indication to
Activate Cath Lab as it is a proven sign of Anterior
STEMI and LAD Occlusion on CAG.

29. Atypical Stemi patterns
V] ST elevations in aVR:
• Diffused ST depressions with ST elevations in aVR are
indicative of Subendocardial Ischemia and it indicates
that patient may have one of the following:
1. LMCA occlusion
2. LMEQ Disease (Significant stenosis in LAD and LCX)
3. Triple Vessel Disease
• Although studies have suggested that ST Elevations in
aVR have shown complete LMCA occlusion on CAG, still
the contradictory studies hamper the activation of Cath
Lab for such patients

30. Atypical Stemi patterns

31. Atypical Stemi patterns
• Current Guidelines for ST elevations in aVR:
1. If the patient is Unstable and has Subendocardial
Pattern of Ischemia with ST Elevations in aVR –
Activate Cath Lab immediately.
2. If the patient with similar ECG is stable – Do an
Emergency 2D ECHO and a Cardiology Consult
before activating Cath Lab.

32. Atypical Stemi patterns
V] Presumed New LBBB:
• Historically, it is clear that a new onset LBBB is
considered as a STEMI Equivalent.
• But, Studies by Chang et al in 2009 and Neeland et al in
2012 indicated that only about 40% of patients with New
Presumed LBBB have been found to have culprit lesion
on CAG.
• STEMI guidelines from 2013 have now removed
Presumed New LBBB as being Diagnostic for MI “In
Isolation”
• Further, a Presumed New onset LBBB might not be a
New onset LBBB and paperwork drawback may cause
problems.
• Thus, Presumed New Onset LBBB is not an indication for
Cath Lab Activation.

33. Atypical Stemi patterns
• Which patients should we activate Cath Lab call in
Presumed New Onset LBBB?
1. Patients who are Unstable and have Presumed
new LBBB
2. Patients with Positive 2D ECHO findings of
Regional wall motion abnormality with low EF
3. LBBB meeting Sgarbossa’s Criteria

34. Atypical Stemi patterns

35. Atypical Stemi patterns
VI] STEMI Equivalents in Paced Rhythms & Old LBBB:
• Most of the Pacemakers are inserted in Right Ventricle
and the pattern thus formed bypasses the Bundle of His,
ultimately mimicking LBBB pattern.
• Largest study till date for this has been published by
Sgarbossa et al in 32 patients with Pacemaker and
Coronary Occlusion.
• Sgarbossa Criteria: It states that LBBB or Pacemaker
with following signs on ECG are indicative of Coronary
Occlusion-
1. Concordant ST Elevation >1mm
2. Concordant ST Depression >1mm in V1-V3
3. Discordant ST Elevation >5mm

36. Atypical Stemi patterns
• Furthermore, Smith et al have made changes to this
criteria and published a Modified Sgarbossa Criteria:
1. Concordant ST Elevation >1mm
2. Concordant ST Depression >1mm in V1-V3
3. Discordant ST Elevation >25% of S-Wave
• Currently, the modified Sgarbossa Criteria is useful
in evaluating patients with Pacemaker and LBBB
with suspected Coronary Occlusion, and is enough
to activate Cath Lab if clinically indicated.

37. Atypical Stemi patterns

38. Benign early repolarization
(ber)

39. Benign early repolarization
(ber)

40. BER vs STEMI
• Case Study:
A 36yr old Male with history of Seizure Disorder. He
had a seizure in the morning and rolled out of bed. In
ER, patient is stable and has no complaints of Chest
Pain. His prehospital ECG was taken in Ambulance:

41. BER vs STEMI
What is the Diagnosis?

42. BER vs STEMI
• Smith et al have made a Formula to differentiate Benign Early
Repolarization from STEMI:
Formula: (1.96 x STE at 60ms after J point in V3) + (0.059 x
Computerized QTc) – (0.326 x R-wave amplitude in V4)
To use this Formula, following values are needed:
1. ST-elevation at 60ms after J point in V3
2. Computerized QTc
3. R-Wave Amplitude in V4
Interpretation: A value that you get from above formula, if more
than 23, it is indicative of a STEMI, whereas if less than 23, it is
indicative of BER.
A readymade calculator is available online named ‘Subtle
STEMI Calculator’

43. BER vs STEMI
There are certain Features you need to check if there is
confusion between BER and STEMI:

44. BER vs STEMI
• In the above case study, the formula revealed the
number as 22.883. This indicates more towards
BER. But, the closer to the number 23, the value will
not be specific enough.
• Later on, it was found that patient had a history of
fooling Ambulance and doctors repeatedly to gain
attention, as he knew that ECG had some changes.

45. Terminal qrs distortion
• During the evolution of the acute Anterior STEMI, you will see the
terminal S-wave begins to rise toward the baseline. When the
terminal S-wave rises above the baseline then it technically is no
longer an S-wave. When this occurs it is described as “terminal
QRS distortion”. This is highly suspicious of the Acute STEMI
(this statement holds especially true of Leads V2, V3).

46. Terminal qrs distortion
• NOTE: An exception to this rule occurs when the take off of the J-
point forms the shape of a “fish hook” (J-wave). If this J-wave is
present, the probability shifts in the direction of a benign normal
variant (early repolarization).

47. Terminal qrs distortion
• Progressive rise of Nadir of S-Wave shown below:
Note: For any case of ‘Terminal QRS Distortion’, do not waste time
in calculating the formula to differentiate BER vs STEMI. Activate
Cath lab Urgently and consider it as a STEMI Equivalent.

48. Conclusion
• Even though these Atypical STEMI Patterns are
relatively rare, an Emergency Physician should
know them correctly. This will allow to cut short the
delay in PPCI activation and can be useful in Early
Reperfusion of Occluded Coronary Artery.
THANK YOU