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STEMI EQUIVALENT
STEMI EQUIVALENT
 Represent coronary occlusion without meeting the traditional STE criteria
 Benefit from immediate percutaneous coronary intervention (PCI)
2017 AHA/ACC guidelines: STEMI equivalent
 Hyperacute T-wave changes
 True Posterior MI
 Multileads ST depression with coexistent ST elevation in lead aVR
 Characteristic diagnostic criteria in the setting of left bundle branch block.
CASE 1
HYPERACUTE T WAVE
 Hyperacute T-waves in ≥ 2 contiguous leads may be the first signs of a developing
infarct often preceding any STE
 Noted early after the onset of coronary occlusion and transmural infarction and
tend to be a short-lived structure that evolves rapidly into ST-segment elevation
 Hyperacute T waves have never been formally defined
• Look for excessively large T waves relative to the size of the preceding QRS complex, voltage
matters.
• Wide, broad and large relative to the QRS
• Look for changes in the size of T waves with symptoms
 Do SERIAL ECG
Hyperacute T wave
- Broad base, wide, blunted peak
Tall T wave (Hyperkalemia)
- Pointy, peaked or “tented” with a
narrow base, they have sharp apex
and symmetric
CASE 2
Upright T Wave V1
 Normal ECG has a flat or inverted T-wave in lead V1
 Upright T wave V1 can be variant, in LBBB, LVH ECG
 Upright T-wave in lead V1 is abnormal if:
 Loss of precordial T-wave balance. Height of upright T-wave in V1 taller than T-
wave in V6 (Type of hyperacute T wave)
 Or A NEW, upright T-wave in V1 (compare to old EKG) in the absence of a LBBB or
LVH
 Lesion: Left circumflex artery disease (44%), Right coronary artery (22%), Left
anterior descending artery (2%)
NORMAL ECG
CASE 3
Wellen’s Syndrome
 Use to describe these ECG changes, which represent a reperfusion pattern in the
setting of severe proximal LAD stenosis, when seen in an asymptomatic patient
who was recently symptomatic.
 Normal or mildly elevated trop
 Pain free patient with recent history of angina
 Patterns to look for (T wave morphology in precordial leads)
 Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)
 Isoelectric or slight ST elevation in precordial leads ( < 1mm)
 Preserved R wave progression
 Absence of Q waves
Wellen’s Syndrome
 2 pattern of T wave:
Type A – Biphasic, with initial positivity
and terminal negativity (25% of cases)
Type B – Deeply and
symmetrically inverted (75% of
cases)
***T wave changes can
evolve over time from
Type A to Type B pattern
Wellen’s Syndrome
Repeated ECG – Normal
Patient developed chest
pain at ED with
diaphoresis. Repeated
ECG as below.
Are you happy?
Wellen’s Syndrome
 Pseudonormalisation
 Apparent normalization of T wave in Wellen’s Syndrome.
 The T waves switch from biphasic/inverted to upright and
prominent.
 ECG changes can precede symptoms
 Accompanied by recurrent chest pain
 Sign of reocclusion of LAD artery
 If the artery remains occluded, the patient now develops
an evolving anterior STEMI
 Do SERIAL ECG in Wallen’s Syndrome
Wellen’s Syndrome
Wellen mimics
 There are both cardiac and non-cardiac causes of T wave inversions.
- PE (anterior ischemia)
- Toxicology: marijuana, PCP, or cocaine use.
- Takotsubo cardiomyopathy
- LVH and HTN
 Be aware and take into account the likelihood that the patient is presenting with
ACS.
CASE 4
De Winter’s ST/T Complex
 In 2% of proximal LAD lesion
 Patterns to look for
 Tall, prominent, symmetrical T waves in the precordial leads
 Upsloping ST segment depression > 1mm at the J-point in the precordial leads
 Absence of ST elevation in the precordial leads
 Reciprocal ST segment elevation (0.5mm – 1mm) in aVR
 “Normal” STEMI morphology may precede or follow the De Winter pattern
De Winter’s ST/T Complex
 An anterior STEMI equivalent that presents without obvious ST segment elevation
 Key diagnostic features include ST depression and peaked T waves in
the precordial leads
 Patients with the de Winter ECG pattern were younger, more likely to be male
and with a higher incidence of hypercholesterolaemia compared to patients with
a classic STEMI pattern.
De Winter’s ST/T Complex
CASE 5
Posterior MI
 Isolated posterior MI is less common (3-11% of infarcts) - ?missed diagnosed due to
lack of ST elevation
 Posterior infarction usually occurred in the context of an inferior or lateral infarction – larger
infarction
 How to spot posterior infarction
 Posterior infarction is confirmed by the presence of ST elevation and Q waves in the
posterior leads (V7-9).
 Not directly visualised by the standard 12-lead ECG
 Reciprocal changes of STEMI are sought in the anteroseptal leads V1-3.
 horizontal ST depression in the anteroseptal leads (V1-3) should raise the suspicion of posterior MI
 Lesion: RCA / left circumflex artery occlusion
Posterior MI
 Posterior MI is suggested by the
following changes in V1-V3:
 Horizontal ST depression
 Tall, broad R waves (>30ms)
 Upright T waves
 Dominant R wave (R/S ratio > 1) in V2
 Mirrored image at V1 – V3
 Confirmed by Posterior ECG (V7 – V9)
 At least 0.5mm ST elevation
Posterior MI
CASE 6
ST Elevation in aVR
 Indicates subendocardial ischemia due to O2 supply/demand mismatch. Not always indicate artery
stenosis
 Clinical causes include:
 Left main coronary artery critical stenosis
 Recent publication – recognized this pattern consistent with left main coronary artery sub-occlusion or complete
occlusion with collaterals
 Left proximal LAD disease
 Direct ischemia to the basal septum
 Triple vessel disease
 Subendocardial ischemia (taken in setting of something like severe tachycardia or sepsis)
 a reciprocal change to the global perfusion
 Repolarization abnormality (eg from LVH, LBBB)
 Metabolic/toxic causes (eg hypokalemia, digoxin)
ST Elevation in aVR
 In reality, ischemic ST elevation in aVR occurs in two broad categories:
1) in patients with recognized STEMI (due to coronary occlusion, usually of the LAD) and is
associated with higher mortality than in patients without STE in aVR
 majority of 100% left main occlusions do not make it alive to the ED, or arrive in arrest
 Left main stenosis results in an ECG with overlapping syndromes of proximal LAD occlusion (STE in
V1-V6, I, aVL) and circumflex occlusion (lateral STE and posterior STEMI, which has ST depression in
V1-V4, which may diminish the ST elevation of the anterior STEMI.
2) in patients without ischemic ST elevation, in which case there is always diffuse ST depression of
subendocardial ischemia (which can be due to supply-demand mismatch or due to ACS).
 GI bleed, sepsis, respiratory failure, severe anemia, tachydysrhythmias, severe hypertension, shock
ST Elevation in aVR
 Widespread horizontal ST depression, most prominent in
leads I, II and V4-6
 ST elevation in aVR ≥ 1mm
 ST elevation in aVR ≥ V1
In the context of widespread ST depression + symptoms of
myocardial ischaemia
 STE in aVR ≥ 1mm indicates proximal LAD / LMCA occlusion or
severe 3VD
 STE in aVR ≥ 1mm predicts the need for CABG
 STE in aVR ≥ V1 differentiates LMCA from proximal LAD occlusion
 Absence of ST elevation in aVR almost entirely excludes a
significant LMCA lesion
ST Elevation in aVR
CASE 7
LBBB WITH SGARBOSSA CRITERIA
LBBB: Left Bundle Branch Block
• V1: Dominant S wave
• V6: broad, notched (‘M’-shaped) R
wave
• QRS Duration>120ms
• Left axis deviation
• Poor R wave progression
LBBB WITH SGARBOSSA CRITERIA
 New or presumably new LBBB has been considered a STEMI equivalent.
 Most cases of LBBB at time of presentation, however, are “not known to be old”
because of prior electrocardiogram (ECG) is not available for comparison.
 New or presumably new LBBB at presentation occurs infrequently, may interfere
with ST-elevation analysis, and should not be considered diagnostic of acute
myocardial infarction (MI) in isolation.
 Criteria for ECG diagnosis of acute STEMI in the setting of LBBB have been
propose  SGARBOSSA CRITERIA
LBBB WITH SGARBOSSA CRITERIA
 Other causes of Left Bundle Branch Block
 Aortic stenosis
 Ischaemic heart disease
 Hypertension
 Dilated cardiomyopathy
 Anterior MI
 Hyperkalaemia
 Digoxin toxicity
Original Sgarbossa
Criteria
The original three criteria used to diagnose infarction in
patients with LBBB are:
• Concordant ST elevation > 1mm in leads with a positive QRS
complex (score 5)
• Concordant ST depression > 1 mm in V1-V3 (score 3)
• Excessively discordant ST elevation > 5 mm in leads with a -
ve QRS complex (score 2)
These criteria are specific, but not sensitive (36%) for myocardial
infarction. A total score of ≥ 3 is reported to have a specificity of
90% for diagnosing myocardial infarction.
Smith-Modified
Sgarbossa Criteria:
ST elevation ≥5 mm discordant with the QRS complex
lacks adequate specificity
Smith et al used an ST/S ratio of <-0.25 as a replacement
for the absolute ST elevation of ≥5 mm.
In other words, if the discordant ST-segment deviation is
>25% of the amplitude of the QRS, ischemia should be
suspected.
This revised rule was found to be significantly more
accurate than the 3rd Sgarbossa criterion
STEMI EQUIVALENT
 HYPERACUTE T WAVE
 T WAVE UPRIGHT V1
 WELLENS SYNDROME
 DE WINTER ST/T COMPLEX
 POSTERIOR MI
 ST ELEVATION IN AVR
 LBB WITH SGARBOSSA CRITERIA
References
 https://www.aliem.com/tall-t-wave-lead-v1/
 https://www.resus.com.au/upright-t-wave-in-v1/
 https://umem.org/educational_pearls/2123/
 http://www.emdocs.net/hyperacute-t-waves/
 https://emergencymedicinecases.com/hyperacute-t-waves-occlusion-mi/
 https://litfl.com/t-wave-ecg-library/
 http://hqmeded-ecg.blogspot.com/2011/02/inferior-hyperacute-t-waves-clue-is-t.html
 https://www.maimonidesem.org/blog/wellens-syndrome-amp-pseudo-normalization
 https://www.resus.com.au/st-elevation-in-avr/
 https://emergencymedicinecases.com/ecg-cases-st-elevation-avr-stemi-equivalent/#
 https://litfl.com/wellens-syndrome-ecg-library/
 https://litfl.com/de-winter-t-wave/
 https://litfl.com/posterior-myocardial-infarction-ecg-library/
 https://litfl.com/sgarbossa-criteria-ecg-library/
 https://rebelem.com/modified-sgarbossa-criteria-ready-primetime/

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STEMI EQUIVALENT 1.pptx

  • 2. STEMI EQUIVALENT  Represent coronary occlusion without meeting the traditional STE criteria  Benefit from immediate percutaneous coronary intervention (PCI) 2017 AHA/ACC guidelines: STEMI equivalent  Hyperacute T-wave changes  True Posterior MI  Multileads ST depression with coexistent ST elevation in lead aVR  Characteristic diagnostic criteria in the setting of left bundle branch block.
  • 4. HYPERACUTE T WAVE  Hyperacute T-waves in ≥ 2 contiguous leads may be the first signs of a developing infarct often preceding any STE  Noted early after the onset of coronary occlusion and transmural infarction and tend to be a short-lived structure that evolves rapidly into ST-segment elevation  Hyperacute T waves have never been formally defined • Look for excessively large T waves relative to the size of the preceding QRS complex, voltage matters. • Wide, broad and large relative to the QRS • Look for changes in the size of T waves with symptoms  Do SERIAL ECG
  • 5.
  • 6. Hyperacute T wave - Broad base, wide, blunted peak Tall T wave (Hyperkalemia) - Pointy, peaked or “tented” with a narrow base, they have sharp apex and symmetric
  • 8. Upright T Wave V1  Normal ECG has a flat or inverted T-wave in lead V1  Upright T wave V1 can be variant, in LBBB, LVH ECG  Upright T-wave in lead V1 is abnormal if:  Loss of precordial T-wave balance. Height of upright T-wave in V1 taller than T- wave in V6 (Type of hyperacute T wave)  Or A NEW, upright T-wave in V1 (compare to old EKG) in the absence of a LBBB or LVH  Lesion: Left circumflex artery disease (44%), Right coronary artery (22%), Left anterior descending artery (2%) NORMAL ECG
  • 10. Wellen’s Syndrome  Use to describe these ECG changes, which represent a reperfusion pattern in the setting of severe proximal LAD stenosis, when seen in an asymptomatic patient who was recently symptomatic.  Normal or mildly elevated trop  Pain free patient with recent history of angina  Patterns to look for (T wave morphology in precordial leads)  Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)  Isoelectric or slight ST elevation in precordial leads ( < 1mm)  Preserved R wave progression  Absence of Q waves
  • 11. Wellen’s Syndrome  2 pattern of T wave: Type A – Biphasic, with initial positivity and terminal negativity (25% of cases) Type B – Deeply and symmetrically inverted (75% of cases) ***T wave changes can evolve over time from Type A to Type B pattern
  • 12. Wellen’s Syndrome Repeated ECG – Normal Patient developed chest pain at ED with diaphoresis. Repeated ECG as below. Are you happy?
  • 13. Wellen’s Syndrome  Pseudonormalisation  Apparent normalization of T wave in Wellen’s Syndrome.  The T waves switch from biphasic/inverted to upright and prominent.  ECG changes can precede symptoms  Accompanied by recurrent chest pain  Sign of reocclusion of LAD artery  If the artery remains occluded, the patient now develops an evolving anterior STEMI  Do SERIAL ECG in Wallen’s Syndrome
  • 15. Wellen mimics  There are both cardiac and non-cardiac causes of T wave inversions. - PE (anterior ischemia) - Toxicology: marijuana, PCP, or cocaine use. - Takotsubo cardiomyopathy - LVH and HTN  Be aware and take into account the likelihood that the patient is presenting with ACS.
  • 17. De Winter’s ST/T Complex  In 2% of proximal LAD lesion  Patterns to look for  Tall, prominent, symmetrical T waves in the precordial leads  Upsloping ST segment depression > 1mm at the J-point in the precordial leads  Absence of ST elevation in the precordial leads  Reciprocal ST segment elevation (0.5mm – 1mm) in aVR  “Normal” STEMI morphology may precede or follow the De Winter pattern
  • 18. De Winter’s ST/T Complex  An anterior STEMI equivalent that presents without obvious ST segment elevation  Key diagnostic features include ST depression and peaked T waves in the precordial leads  Patients with the de Winter ECG pattern were younger, more likely to be male and with a higher incidence of hypercholesterolaemia compared to patients with a classic STEMI pattern.
  • 21. Posterior MI  Isolated posterior MI is less common (3-11% of infarcts) - ?missed diagnosed due to lack of ST elevation  Posterior infarction usually occurred in the context of an inferior or lateral infarction – larger infarction  How to spot posterior infarction  Posterior infarction is confirmed by the presence of ST elevation and Q waves in the posterior leads (V7-9).  Not directly visualised by the standard 12-lead ECG  Reciprocal changes of STEMI are sought in the anteroseptal leads V1-3.  horizontal ST depression in the anteroseptal leads (V1-3) should raise the suspicion of posterior MI  Lesion: RCA / left circumflex artery occlusion
  • 22. Posterior MI  Posterior MI is suggested by the following changes in V1-V3:  Horizontal ST depression  Tall, broad R waves (>30ms)  Upright T waves  Dominant R wave (R/S ratio > 1) in V2  Mirrored image at V1 – V3  Confirmed by Posterior ECG (V7 – V9)  At least 0.5mm ST elevation
  • 25. ST Elevation in aVR  Indicates subendocardial ischemia due to O2 supply/demand mismatch. Not always indicate artery stenosis  Clinical causes include:  Left main coronary artery critical stenosis  Recent publication – recognized this pattern consistent with left main coronary artery sub-occlusion or complete occlusion with collaterals  Left proximal LAD disease  Direct ischemia to the basal septum  Triple vessel disease  Subendocardial ischemia (taken in setting of something like severe tachycardia or sepsis)  a reciprocal change to the global perfusion  Repolarization abnormality (eg from LVH, LBBB)  Metabolic/toxic causes (eg hypokalemia, digoxin)
  • 26. ST Elevation in aVR  In reality, ischemic ST elevation in aVR occurs in two broad categories: 1) in patients with recognized STEMI (due to coronary occlusion, usually of the LAD) and is associated with higher mortality than in patients without STE in aVR  majority of 100% left main occlusions do not make it alive to the ED, or arrive in arrest  Left main stenosis results in an ECG with overlapping syndromes of proximal LAD occlusion (STE in V1-V6, I, aVL) and circumflex occlusion (lateral STE and posterior STEMI, which has ST depression in V1-V4, which may diminish the ST elevation of the anterior STEMI. 2) in patients without ischemic ST elevation, in which case there is always diffuse ST depression of subendocardial ischemia (which can be due to supply-demand mismatch or due to ACS).  GI bleed, sepsis, respiratory failure, severe anemia, tachydysrhythmias, severe hypertension, shock
  • 27. ST Elevation in aVR  Widespread horizontal ST depression, most prominent in leads I, II and V4-6  ST elevation in aVR ≥ 1mm  ST elevation in aVR ≥ V1 In the context of widespread ST depression + symptoms of myocardial ischaemia  STE in aVR ≥ 1mm indicates proximal LAD / LMCA occlusion or severe 3VD  STE in aVR ≥ 1mm predicts the need for CABG  STE in aVR ≥ V1 differentiates LMCA from proximal LAD occlusion  Absence of ST elevation in aVR almost entirely excludes a significant LMCA lesion
  • 30. LBBB WITH SGARBOSSA CRITERIA LBBB: Left Bundle Branch Block • V1: Dominant S wave • V6: broad, notched (‘M’-shaped) R wave • QRS Duration>120ms • Left axis deviation • Poor R wave progression
  • 31. LBBB WITH SGARBOSSA CRITERIA  New or presumably new LBBB has been considered a STEMI equivalent.  Most cases of LBBB at time of presentation, however, are “not known to be old” because of prior electrocardiogram (ECG) is not available for comparison.  New or presumably new LBBB at presentation occurs infrequently, may interfere with ST-elevation analysis, and should not be considered diagnostic of acute myocardial infarction (MI) in isolation.  Criteria for ECG diagnosis of acute STEMI in the setting of LBBB have been propose  SGARBOSSA CRITERIA
  • 32. LBBB WITH SGARBOSSA CRITERIA  Other causes of Left Bundle Branch Block  Aortic stenosis  Ischaemic heart disease  Hypertension  Dilated cardiomyopathy  Anterior MI  Hyperkalaemia  Digoxin toxicity
  • 33. Original Sgarbossa Criteria The original three criteria used to diagnose infarction in patients with LBBB are: • Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5) • Concordant ST depression > 1 mm in V1-V3 (score 3) • Excessively discordant ST elevation > 5 mm in leads with a - ve QRS complex (score 2) These criteria are specific, but not sensitive (36%) for myocardial infarction. A total score of ≥ 3 is reported to have a specificity of 90% for diagnosing myocardial infarction.
  • 34. Smith-Modified Sgarbossa Criteria: ST elevation ≥5 mm discordant with the QRS complex lacks adequate specificity Smith et al used an ST/S ratio of <-0.25 as a replacement for the absolute ST elevation of ≥5 mm. In other words, if the discordant ST-segment deviation is >25% of the amplitude of the QRS, ischemia should be suspected. This revised rule was found to be significantly more accurate than the 3rd Sgarbossa criterion
  • 35.
  • 36.
  • 37. STEMI EQUIVALENT  HYPERACUTE T WAVE  T WAVE UPRIGHT V1  WELLENS SYNDROME  DE WINTER ST/T COMPLEX  POSTERIOR MI  ST ELEVATION IN AVR  LBB WITH SGARBOSSA CRITERIA
  • 38. References  https://www.aliem.com/tall-t-wave-lead-v1/  https://www.resus.com.au/upright-t-wave-in-v1/  https://umem.org/educational_pearls/2123/  http://www.emdocs.net/hyperacute-t-waves/  https://emergencymedicinecases.com/hyperacute-t-waves-occlusion-mi/  https://litfl.com/t-wave-ecg-library/  http://hqmeded-ecg.blogspot.com/2011/02/inferior-hyperacute-t-waves-clue-is-t.html  https://www.maimonidesem.org/blog/wellens-syndrome-amp-pseudo-normalization  https://www.resus.com.au/st-elevation-in-avr/  https://emergencymedicinecases.com/ecg-cases-st-elevation-avr-stemi-equivalent/#  https://litfl.com/wellens-syndrome-ecg-library/  https://litfl.com/de-winter-t-wave/  https://litfl.com/posterior-myocardial-infarction-ecg-library/  https://litfl.com/sgarbossa-criteria-ecg-library/  https://rebelem.com/modified-sgarbossa-criteria-ready-primetime/

Editor's Notes

  1. 60 Y.O MALAY GENTELMAN, NKMI ACTIVE SMOKER P/W: CENTRAL CHEST PAIN AROUND 1 HOUR AGO, PS 10/10 + DIAPHORESIS AND SYNCOPAL ATTACK ECG AS SHOWN
  2. 48 YEARS OLD LADY UL: HPT P/W: CHEST PAIN LEFT SIDED PS 8/10, RADIATING TO LEFT ARM AND NECK, OCCURRED DURING PATIENT WAS PREPARING A MEAL + DIAPHORESIS + VOMITING X1 ECG AS SHOWN
  3. 57 YEARS OLD MALAY GENTLEMAN U/L DM, HPT, HPL P/W CHEST PAIN YESTERDAY RADIATING TO JAW CURRENTLY NO CHEST PAIN, PS 0/10 ECG AS SHOWN
  4. 38 YEARS OLD MALAY GENTLEMAN ACTIVE SMOKER, NKMI/NKDA P/W: CENTRAL CHEST PAIN TODAY PS 10/10, OCCURRED DURING PT WAS WORKING AT BALAI BOMBA SYNCOPAL ATTACK – REGAINED CONSCIOUS AT WORK PLACE SWEATING ECG AS SHOWN
  5. 44 YEARS OLD MALAY LADY NKMI/NKDA P/W: LEFT SIDED CHEST PAIN AFTER CYCLING ABOUT 20KM PS 7/10 PALPITATION AND SWEATING ECG AS SHOWN
  6. - replace leads V4-V6 with V7-V9 - with V9 having the best PPV - only 0.5 mm of ST elevation is required to make the diagnosis of posterior MI
  7. 70 YEARS OLD, MALAY LADY U/L DM, HPT, IHD P/W: CENTRAL CHEST PAIN, BURNING IN NATURE, RADIATING TO BACK SWEATING AND PALPITATION ECG AS SHOWN
  8. Elderly man, underlying HPT, DM, IHD presented with acute GI bleed + chest pain His ischaemic symptoms and ECG improved with blood transfusion. In this case the subendocardial ischaemia was likely due to cellular hypoxia (O2 supply < demand) from his acute anaemia, exacerbated by poor coronary blood flow
  9. 70 YEARS OLD MALAY GENTLEMAN U/L IHD, HPT, HPL P/W: CHEST PAIN, BURNING IN NATURE, CENTRAL PS 7/10, RADIATING TO BILATERAL UL SWEATING ECG AS SHOWN
  10. LBBB Concordant ST elevation ≥ 1 mm in ≥ 1 lead Concordant ST depression ≥ 1 mm in ≥ 1 lead of V1-V3 Proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1 mm STE, as defined by ≥ 25% of the depth of the preceding S-wave