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
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
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
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
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
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
- 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
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
Elderly man, underlying HPT, DM, IHDpresented 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
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
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