This document discusses myocardial infarction (MI) and myocardial ischemia. It begins by defining MIs that result from total coronary occlusion (Q-wave MI) versus subtotal occlusion (non-Q-wave MI). It then describes the blood supply territories of the main coronary arteries and shows examples of ECG patterns for different types of MIs, including anterior, inferior, and lateral MIs. It also discusses non-ST elevation acute coronary syndrome (NSTEACS), describing the ECG patterns of ST depression and T-wave changes seen in myocardial ischemia, including Wellens' syndrome. Throughout, it localizes arterial territories and compares ECG findings to understand the likely location and extent of ischemia/infarction.

1. Myocardial Infarction
Dr. Mohmmed AL jaberi
6/05/2014

2. Introductions
 When myocardial blood supply is abruptly reduced or cut off to
a region of the heart, a sequence of injurious events …
ischemia >>> necrosis >>>> fibrosis (scarring) .
 Rupture of an Atherosclerotic Plaque followed by Acute
Coronary Thrombosis is the usual mechanism .
 MI's resulting from total coronary occlusion ( Q-wave MI ) .
 MI's resulting from subtotal occlusion ( non Q-wave MI ) .
 2/3 of MI's presenting to ER evolve to non-Q wave MI's .

3. Myocardial Blood Supply

4. Myocardial Blood Supply
 The left anterior descending coronary artery ( LAD ) :
– it's branches usually supply the anterior and anterolateral walls of the
left ventricle and the anterior 2/3 of the septum
 The left circumflex coronary artery ( LCX ) :
– its branches usually supply the posterolateral wall of the left ventricle
 The right coronary artery ( RCA ) :
– its branches supplies the right ventricle, the inferior and true posterior
walls of the left ventricle, and the posterior 1/3 of the septum. The
RCA also gives off the AV nodal coronary artery in 85-90% of
individuals; in the remaining 10-15%, this artery is a branch of the LCX

5. Inferior
II, III, aVF
Lateral
I, AVL,
V5-V6
Anterior /
Septal
V1-V4
Localising The Arterial Territory

6. Acute Anterior STEMI
• ST elevation and Q wave formation in V2-5, I and aVL.
• Reciprocal ST depression in lead III

8. Hyperacute anteroseptal STEMI
• ST elevation is maximal in the anteroseptal leads (V1-4).
• Q waves are present in the septal leads (V1-2).
• There is also some subtle STE in I, aVL and V5, with
reciprocal ST depression in lead III.
• There are hyperacute (peaked ) T waves in V2-4

9. Extensive Anterolateral STEMI
• ST elevation in V2-6, I and aVL .
• Reciprocal ST depression in III and AVF

10. Anterior-inferior STEMI
• ST elevation in the precordial and inferior leads.
• Hyperacute T waves, most prominent in V1-3
• Q waves in V1-3, as well as leads III and aVF

11. High lateral STEMI
• ST elevation primarily localised to leads I and aVL
• It is usually associated with reciprocal ST depression and T wave
inversion in the inferior leads .

12. Anterolateral STEMI
• ST elevation in the anterior (V2-4) and lateral leads (I, aVL, V5-6).
• Q waves waves are present in both the anterior and lateral leads,
most prominently in V2-4
• Reciprocal ST depression in inferior leads III and AVF

13. Inferior STEMI

14. Inferior STEMI
• Inferior MIs account for 40-50% of all myocardial infarctions
• Generally have a more favourable prognosis than ant. MI (in-
hospital mortality only 2-9%) .
• Up to 40% of patients with an inferior STEMI will have a
concomitant right ventricular infarction .
• Up to 20% of patients with inferior STEMI will develop significant
bradycardia due to second or third-degree AV block.
• Inferior STEMI may also be associated with posterior infarction ,
which confers a worse prognosis .
• Both RCA and circumflex occlusion may cause infarction of the
inferior wall

15. Inferior STEMI
 RCA occlusion is suggested by :
* ST elevation in lead III > lead II
* Presence of reciprocal ST depression in lead I
* Signs of ventricular infarction : STE in V1 & V4R
 Circumflex occlusion is suggested by :
* ST elevation in lead II = lead III
* Absence of reciprocal ST depression in lead I
* Signs of lateral infarction: ST elevation in the lateral
leads I and aVL or V5-6

16. Inferior STEMI / LCX occlusion
• ST elevation in the inferior (II, III, aVF)
• ST depression & T wave inversion in aVL
• Q-wave formation in III and aVF
• ST elevation in lead II = lead III and absent reciprocal change in
lead I suggest a circumflex artery occlusion

17. Inferior STEMI / RCA occlusion
• ST elevation in the inferior II, III and aVF with
• Early Q-wave formation in II, III and aVF
• ST depression & T wave inversion in aVL
• ST elevation in lead III > II with reciprocal change present in lead
I and ST elevation in V1-2 suggests RCA occlusion with associated
RV infarction .

18. Inferolateral STEMI
• ST elevation in the inferior (II, III, aVF) & lateral leads (I, V5-6).
• ST depression in V1-3 is suggestive of associated posterior
infarction (the R/S ratio > 1 in V2 is consistent with this)

19. Inferoposterolateral STEMI
• ST elevation in the inferior (II, III, aVF) & lateral leads (I, V5-6)
• ST depression in V1-3 with tall, broad R waves and upright T waves
and a R/S ratio > 1 in V2 indicate concomitant posterior infarction
(this patient also had ST elevation in the posterior leads V7-9).

20. Posterior MI
• ST depression in V2-3
• Tall, broad R waves (> 30ms) in V2-3
• Dominant R wave (R/S ratio > 1) in V2
• Upright T waves in V2-3

21. Myocardial Ischemia

22. Introductions
 Non-ST-elevation acute coronary syndrome (NSTEACS) encompasses two
main entities :
– Non-ST-elevation myocardial infarction (NSTEMI).
– Unstable angina (UA)
 The differentiation between these two conditions based on the presence/absence of
raised cardiac enzymes at 8-12 hours after the onset of chest pain. Both produce the
same spectrum of ECG changes and symptoms and are managed identically in the ER
 There are two main ECG abnormalities seen with NSTEACS:
– ST segment depresion
– T wave flattening or inversion
 Other ECG patterns of ischaemia :
– Hyperacute T waves or pseudonormalisation of previously inverted T
waves (i.e. becoming upright) suggest hyperacute STEMI .
– U-waves inversion

23. Morphology Of ST Depression
• ST depression can be either upsloping, downsloping, or
horizontal .
• Horizontal or downsloping ST depression ≥ 0.5 mm at the J-
point in ≥ 2 contiguous leads indicates myocardial ischaemia
(according to the 2007 Task Force Criteria ).
• ST depression ≥ 1 mm is more specific and conveys a worse
prognosis.
• ST depression ≥ 2 mm in ≥ 3 leads is associated with a high
probability of NSTEMI and predicts significant mortality (35%
mortality at 30 days).
• Upsloping ST depression is non-specific for myocardial
ischaemia.

24. Morphology Of ST Depression
ST depression: upsloping (A), downsloping (B), horizontal (C)

25. Distribution of ST segment depression
• ST depression due to Subendocardial Ischaemia is usually
widespread — typically present in leads I, II, V4-6 and a variable
number of additional leads.
• A pattern of widespread ST depression plus ST elevation in aVR
> 1 mm is suggestive of left main coronary artery occlusion .

26. T wave inversion
• T wave inversion may be considered to be evidence of
myocardial ischemia if:
– At least 1 mm deep
– Present in ≥ 2 continuous leads that have dominant R waves
(R/S ratio > 1)
– Dynamic — not present on old ECG or changing over time

27. Wellens’ Syndrome
• Wellens’ syndrome is a pattern of inverted or biphasic T waves
in V2-4 (in patients presenting with ischaemic chest pain) that is
highly specific for Critical Stenosis Of The LAD Artery.
• Patients may be pain free by the time the ECG is taken and
have normally or minimally elevated cardiac enzymes; however,
they are at extremely high risk for extensive anterior wall
MI within the next 2-3 weeks.
 There are two patterns of T-wave abnormality in Wellens’
syndrome:
– Type 1 Wellens’ T-waves are deeply and symmetrically inverted
– Type 2 Wellens’ T-waves are biphasic, with the initial deflection positive
and the terminal deflection negative

28. Type 1 Wellens’
– Type 1 Wellens’ T-waves are deeply and symmetrically inverted

29. Type 2 Wellens’
– Type 2 Wellens’ T-waves are biphasic, with the initial deflection
positive and the terminal deflection negative

30. Non-specific ST segment and T wave changes
• The following changes may occur with myocardial
ischaemia but are relatively non-specific:
– ST depression < 0.5 mm
– T wave inversion < 1 mm
– T wave flattening
– Upsloping ST depression

31. Widespread Subendocardial Ischaemi
• Widespread ST depression, seen in leads I, II and V5-6
• There is also some subtle ST elevation in V1-2 and aVR with small Q
waves in V1-2, suggesting that the cause of the widespread
ischaemia is a proximal LAD occlusion

32. High lateral STEMI !/ Reciprocal change
• Horizontal ST depression in III and aVF
• Regional ST depression should prompt you to scrutinise the ECG for
signs of reciprocal ST elevation… In this case there is subtle ST
elevation in aVL , there is a high lateral STEMI

33. Type 2 Wellens’ syndrom
• T waves in V1-4 — biphasic in V1-3 and inverted in V4.
• It’s highly specific for a critical stenosis of the proximal LAD

34. Inverted U waves
• There are inverted U waves, most prominent in leads V5-6.
• This is an infrequently recognised but very specific sign of ischaemia
this patient had a 12-hour troponin of 4.0 ng/mL.

35. Dynamic ST depression in a patient with chest pain A
• Widespread ST depression(I, II, V5-6) indicates subendocardial
ischaemia.
• Q wave in lead III with slightly elevated ST segment suggests the
possibility of early inferior STEMI

36. Dynamic ST depression in a patient with chest pain B
• The ST changes have now resolved.
• Inferior ST segments and Q waves are stable — this patient had a
history of prior inferior MI
• Troponin was raised, confirming that the initial ST depression was due
to NSTEM

37. References

38. Thank You