1. The document discusses various ECG patterns that can mimic myocardial infarction (MI), including non-infarction ischemia, pericarditis, LVH, LBBB, pulmonary embolism, Brugada pattern, and hypothermia. 2. It also discusses ECG patterns in MI that can be masked or obscured by other conditions, such as WPW syndrome, LBBB, RBBB, ventricular pacing rhythms, and hypothermia. 3. Criteria are provided to help differentiate MI patterns from mimics in some challenging cases, such as with LBBB, RBBB, ventricular pacing, or hypothermia present.

1. MIMICS AND MASKS OF
ECG IN MI
DR VENKATESWARA RAO A
DRNB CARDIOLOGY RESIDENT
APOLLO HOSPITAL

2. Myocardial infarction
• Non infarction, transmural ischemia(prinzmetal angina, takotsubo syndrome)
• Acute myocardial infarction(obstructive coronary occlusion)
• Post-myocardial infarction(ventricular aneurism pattern)
Acute pericarditis
Normal variants(including early repolarization pattern)
LVH, LBBB(V1-V2 OR V3 only)
Other causes
Acute pulmonary embolism(right to mid chest leads)
Brugada pattern
Class IC antiarrhythmic drugs
Hypercalcemia
DC cardioversion( immediately after procedure)
Hyperkalemia
Hypothermia(J or Osborn wave)
Intracranial hemorrhage
Myocardial injury due to trauma or secondary to tumor invading the left ventricle
myocarditis

3. ECG pattern hinting for potentially high –risk criteria coronary artery stenosis or
occlusion.
De winter syndrome
J –point depression and
upsloping ST depression in V1-6 That
continues into tall positive symmetrical T waves, often
with 1-2mm ST segment elevation in aVR

4. POSTERIOR STEMI:
ST depression>0.05mV( horizontal or downsloping and
concave) in V1-3 or V4
Especially if there is a tall R in V1/V2 with R/S ratio >1 in
V2.

5. WALLENS SIGN A
Biphasic anterior T waves that not always
accompanied by chest pain.
WALLENS sign B
Deeply inverted anterior T waves, not always
accompanied by chest pain.

6. Hyperacute T waves
Tall
Often asymmetrical
Broad based
Anterior T waves
Associated with reciprocal ST depression.

7. ACUTE ISCHEMIA in LVH
• ST Segment elevation >25% of QRS amplitude
• and ( ST elevations in 3 contiguous leads, or
• T wave inversions in the anterior leads.)

9. Takotsubo cardiomyopathy:
Also called transient left ventricular ballooning syndrome or stress cardiomyopathy
Is reversible wall motion abnormalties of left ventricular apex and mid ventricle.
Pts usually post menopausal women may presents with
chest pain
ST segment elevation
Elevated cardiac enzymes
The syndrome typically is reported in setting of emotional or physiological stress.
The exact pathophysiology is not known but may be related to vasospasm or
neurologically mediated cardiac damage, resulting in transmural current injury
With ST segment elevation or depressions simulating coronary occlusion.

11. Prinzmetal variant angina
Ecg changes:
ST segment depression
ST segment elevation
Mechanism : vasospasm of
proximal coronary artery

12. Left ventricular aneurism
Ecg changes :
The Persistence of the typical pattern of the fully evolved phase of myocardial
infarction i. e
• Q wave
• ST segment elevation
• Inverted T wave
• For 3 months or longer after the acute attack

14. ACUTE PERICARDITIS:
ECG changes
Diffuse ST segment elevations in most of the chest leads and in leads I, aVL,II, aVF
with reciprocal ST depression in aVR.
Differentiation from M.I : frequent presence of PR segment elevations in aVR, with
reciprocal PR segment depression in other leads, caused by concomitant atrial
current of injury.
Abnormal Q waves do not occur and ST elevations followed by T wave inversion
after a variable period.

16. Normal variant
Persistent juvenile pattern
T waves commonly are inverted in all precordial leads at birth and usually become upright
as time passes.
This persistent juvenile pattern,with Inverted T waves in leads to the left of V1.
Occurs in 1% to 3% of adults and is more common in women than men and more common
in African American than in other racial or ethnic groups.

18. The ST segment can be significantly elevated in normal persons, especially in the right
and midprecordial leads.
Upwardly concave ST segment elevation,
Tall precordial R waves,
Distinctive J waves with slurring or notching of the terminal QRS complex,
Early R wave transition in the precordial leads
And asymmetric T waves with gradual upslope and rapid descent.

19. This pattern occurs in 1% to 13% of general population and is most prevalent in young
adults, especially African American men. Its appearance is labile, being most prominent
under conditions of increased vagal tone.
Studies shows that ST segment elevation plus both J waves and QRS notching associated
with ventricular tachyarrhythmias and sudden death due to ventricular fibrillation.
Another study shows that J point elevation above 0.2mV associated with increased risk of
arrhythmic deaths among asymptomatic adults with early repolarization pattern
characterized by horizontal or down sloping ST segments in the inferior leads.

20. Early repolarization pattern
ECG findings
QRS-ST junction [ so called J point] elevation of >1mm above baseline
With QRS slurring [ at the transition of QRS to the ST segment]
Or notching [ a positive deflection inscribed on the terminal S wave]
ST segment elevation with upper concavity,
Prominent T waves in two or more contiguous leads
cardiac arrest secondary to idiopathic ventricular fibrillation

22. LVH
QRS changes:
Increased QRS amplitude with prolonged duration,
LAD
Notching or slurring of R wave
Intra ventricular conduction defects.

23. ST –T changes
ST segment normal or elevated in leads with tall R waves.
ST segment depression [flat/ down slope] and T wave is asymmetriacally inverted.
Volume overload conditions:
Tall upright T wave, narrow (<25msec), deep Q waves (0.2mv) in leads I, Avl, V 4-6.
Mechanism: ST-T changes are secondary to LVH they occur due to primary disorder of
repolariastion that accompany the cellular processes of hypertrophy and myocardial
ischemia.

25. LEFT BUNDLE BRANCH BLOCK
The ST –T wave changes with LBBB are discordant with QRS complex.
Thus ST segment is depressed and T wave is inverted in leads with positive
QRS waves [ leads I Avl, V5, V6] and
The ST segment is elevated and the T wave is upright in leads with
predominantly negative QRS complexes.
The discordant ST-T wave pattern is reflection of the altered pattern of
ventricular activation.
With LBBB, the right ventricle is activated and recovers earlier than the left ,
so recovery vectors are directed toward the right and away from the left
ventricle.

27. Pulmonary embolism
Causing right ventricular pressure overload
Ecg changes are
1. QR or qR pattern in the right ventricular leads
2. S1Q3T3 pattern
3. ST segment deviations and T wave inversion in leads V1-V3
4. Incomplete or complete RBBB.
5. In massive pulmonary embolism ST segment elevations may be seen in the right
midprecordial leads.

30. BRUGADA SYNDROME
Ecg changes
Coved type ST segment elevation [>2mm] followed by a negative T wave in the right
precordial leads V1-V3.
Episodes of polymorphic ventricular tachyarrhythmia and SCD.
Mechanism: mutations in the SCN5A encoded cardiac sodium channels, decreases inward
sodium or calcium currents or increases outward ‘K’v 4.3 potassium currents.

32. HYPOTHERMIA
The J wave in hypothermia is referred TO as OSBORN WAVE.
A J wave is a dome or hump shaped wave that appears at the end of QRS complex
and that has same polarity as the preceding QRS complex.
The J wave is normal variant or seen in J wave syndromes [ brugada pattern, early
repolarization pattern]
Mechanism: augmented net outward current ‘I’to in phase 1 of action potentials
on the epicardium but not on the endocardium, creating a transmural potential
gradient leading to QRS notching and ST elevation.

34. HYPERKALEMIA
Earliest changes: narrowing and peaking of T waves . QT interval is shortened so
action potential duration decreases.
Moderate to severe: ST elevations V1-3 Simulating ischemic current of injury or
brugada pattern.
Asystole or non diagnostic findings preceded by sine wave ventricular flutter like
pattern.
In later: Sinus rhythm persists with conduction between sino atrial and atrio
ventricular nodes without producing ‘P’ waves
Mechanism: hyperkalemia reduces atrial and ventricular RMP there by inactivating
sodium channels , decreases Vmax and conduction velocity

36. HYPERCALCEMIA
Ecg changes
1.Abbreviation of QT interval [ ST segment portion]
2.Decreased T wave amplitude , sometimes with T wave notching or inversion.
Produces a high takeoff of the J point/ ST segment In leads V1 V2 simulating acute
ischemia.
Mechanism: an increased extracellular calcium concentration shortens the
ventricular action potential duration by shortening phase 2.

39. wpw syndrome type A
Ecg changes
1. Q wave
2. QT vector discordance in inferior leads can simulate inferior infarction
3. Delta waves simulate inferior M.I by pseudo infarct Q wave in leads II, III, aVF,
Goldberger suggested discordant T waves are normal finding in Type A
WPWS.
4. Mechanism: delta vector oppose and obliterate initial vector of infarction
producing a normal looking ECG.

41. How WPW syndrome mask M.I
Left accessory pathway with no overt ST changes associated with infarction
1.Fragmented QRS complexes
2Q/T vector concordance
definition of fQRS: QRS complexes with presence of an additional R wave R’ or
notching in the nadir of the R wave or S wave, or the presence >1R’
(fragmentation) in 2 contiguous leads corresponding to a major coronary territory.
Mechanism: distortion of intraventricular conduction secondary to myocardial
scarring/ fibrosis.

42. LBBB IN M.I
SGARBOSA criteria:
1.ST segment elevation > 1mm concordance with QRS complexes
2.ST segment depression > 1mm in V1-3
3.ST segment elevation> 5mm discordant with QRS complex.
Mechanism: delayed LV activation
Iinitial septal activation from right to left side so absent septal Q wave.
Secondary ST –T changes in LBBB obscure the injury currents.

44. RBBB IN M.I
Ecg changes at mid inter ventricular septum
1.R wave disappears in V1-2 with onset of QR or qR,
2.No Q waves in V5-6
At inferior inter ventricular septum
1.Vector that run through mid and low septum disappears
2.QR or QS complex in V3-4
M.I at left free wall
1.qrS or QrS in V5,V6 with notching q or Q and S always.

45. Posterior wall M.I without RBBB.
Ecg changes
Broad R wave
ST segment depression
T wave inversions in V1
Posterior M.I with RBBB
Excessive discordant (depression) ST segment in V1-2
ST segment elevation > 5mm in posterior leads
Restoration of ST segment depression after reperfusion.

47. M.I with V-P rhythm
SGARBOSA criteria
1.ST segment elevation>1mm in leads with predominantly positive QRS
2.ST segment depression >1mm in V1-3
3.ST segment elevation >5mm in leads with negative QRS complexes.

48. Acute M.I in CRT/ Biventricular pacing
1.Fusion beats form pseudoinfarct pattern with qR/ QR complexes
2.ST segment elevation >5mm in negative QRS leads
3.New ST segment elevation 1-3mm in anterolateral leads V3-6 and leads I, II, aVL,
with reciprocal ST depression and reduced ‘R’ wave progression.