1. ST Segment Elevation in Conditions Other Than Acute Myocardial Infarction
Bobby Dery MD
Department of Emergency Medicine
St. Mary’s Hospital
Grand Junction, CO
Intro: Glad to be introduced as the new guy, because it brings up several important points:
I want to be sure you understand what is going on here- publicly shaft the new guy.
I am new. Most of you have far more experience than I do. My goal is to cover the basics- I hope there is something of value here for each of you. Be gentle.

2. Goals • Review several general principles of EKG interpretation.
• Cover the common causes of ST elevation other than ischemia.
• Briefly review a few of the less common, perhaps esoteric, causes of ST elevation.
• Leave you more comfortable differentiating the various causes of ST elevation.
• Avoid putting you to sleep.
Confession_ I am not a cardiologist. Lecture designed for non-cards: EDP’s; PMD’s; other interested parties. But I am biased towards EM!
Big part of EKG reading is short lists of DDx: tall R V1, PRWP,

3. Significance
• AMI is often represented on the EKG by ST-segment elevation.
• Reperfusion therapy has proven beneficial in these infarctions.
• The earlier the reperfusion, the greater the benefit.
• In fact, time to reperfusion is now a closely monitored measure of quality of care.
• However, AMI is not the only source of ST-segment elevation on the EKG…
Granted I have an ED bias.

4. Significance
• J Emerg Med 1998: 171/202 (85%) ED pts. with CP and ST elevation with dx other than MI.
• Ann Emerg Med 1994: 63/123 (51%) with CP and ST elevation with dx other than MI.
• Am J Cardiol 1994: 10/93 (11%) of pts. receiving thrombolytics did not have AMI.
• Ann Emerg Med 1996: 35/609 (6%) of pts. receiving thrombolytics did not have AMI.
Granted I have an ED bias.

5. Diagnosis: Left Bundle Branch Block Early Repolarization
Acute Myocardial Infarction

6. Diagnosis: Early Reoplarization Early repol 1 v1 v2 v3 v4 v5 v6
Early repolarization, a misnomer, describes a pattern of localized or diffuse ST segment elevation. This is especially seen in leads with prominent R waves. In this example leads I, II, V5 and V6 illustrate the early repolarization pattern. ST segments usually have a "concave upwards" pattern and take off after a small S-wave is inscribed.

7. “Early Repolarization”
• A misnomer.
• A normal variant; seen mostly in young, healthy.
• Typical Features:
- 1-4mm in mid-precordial leads
- greatest elevation at V4
- J-point notching common
- tall T waves without inversion
- concave up ST segment (“smiley”)
- PR depressionearly repol of atrial tissue
Referred to as early repol; but clinical studies fail to demonstrate earlier-than-normal onset of ventricular recovery
Young, healthy people. Esp black men.
1-4 mm in mid-precordial leads. NORMAL VARIANT
Greatest in V4, c notching of J point.
Concave up ST segment
Tall T waves without inversion.
Also can see early repolarization of atrial tissue with PR depression
LIMB LEADS: ST elev II > III (vs inf. MI)
Reciprocal ST depression in aVR but NOT aVL (again vs inf MI- which is big ddx)

8. Early Reoplarization Early repol again
Now notice: ST ^ I and II but NOT III c reciprocal ST v aVR but not aVL. This is classic early repol in the limb leads!!!

9. Diagnosis:
Male Pattern
v v v3 v v5 v6

10. J Am Coll Cardiol 2002;40:1870-76 Surawicz et al
Female
Male
St. Vincents Hospital, Indianapolis, IN
I show this just so you don’t think I am making this stuff up.
V3. 60 msecs p j-point. Line from j-point through 60 msec line. Measure angle of line.
FEMALE: j-point at Q-Q line. Angle flat (19 degrees).
MALE: j-point above Q-Q, angle of ST segment 36 degrees

11. Male
J Am Coll Cardiol

12. The Male Pattern
• So prevalent it is a normal finding, not a normal variant.
Am J Cardiol: 6014 healthy males (USAF). 91% with 1-3 mm elevation; greatest in V2.
J Am Coll Cardiol: 529 males. 91% with
>1 mm elevation V1-V4 among y/o.
• Incidence of ST elevation declines with age. Only 30% of men 76 years or older display this pattern.
• Elevation of 1-3 mm. Most marked in V2. Concave up.
Who cares? Repol differences among genders may explain higher rate of Torsades in females.
Also: Hormonal hypothesis- pattern changes in males over life time. Increases at puberty, peak yrs, declines with age as testosterone declines.
Females have no such decline. Fewer females have female pattern, but it persists throughout life and ?leads to higher Torsades???
Virilized females follow same pattern as males also.
Cardiologists give a shit about this stuff.

13. Male Pattern
v v v3 v v5 v6

14. Normal Variant!! Diagnosis: • Some young men.
v v v3 v v5 v6
Also: QT tends to be short; not so in AMI
Also: coved (rounded, not peaked) ST segments (scary).
Echo to know what is going on
• Some young men.
• Combination of early repol and juvenile T-wave?
• “Very suggestive of AMI”.

15. 8 m/o with juvenile T wave pattern
Persistent juvenile pattern — The T wave vector may be directed posteriorly in children, resulting in an inverted T wave in the right precordial leads V1-V3. The vector usually becomes anterior with age, resulting in upright T waves in these leads; however, the T waves may remain inverted in V1-V3 in a minority of adults, a finding known as a persistent juvenile pattern. (Uptodate.com)

16. Juvenile T Waves
• The T wave vector may be directed posteriorly in young children, resulting in an inverted T wave over right precordium.
• This vector usually becomes anterior with age. By age 10 most with upright T wave axis in V1-3.
• T waves may remain inverted in a minority of adultscalled the Persistent T Wave Pattern.
• Combine this with some ST elevation from early repolarization and you get a concerning shape!

17. Normal and normal variants
Nl variants summary
v1 v2 v3 v4 v5 v6
Male
Pattern
Early
Repol.
Persistent
T wave
1) Notice, all of these meet criteria of AHA/ACC for thrombolytics. So ACEP (EDP’s) Clinical Policies Subcommittee added qualifier “ ST ^ not c/w early repol, pericard, LVH, or BBB”. Even this does not address nl ST elevation present in R precordials in many healthy persons!
2) Notice, in all of these “normal” patterns, the QRS and the ST are concordant…both up. Often this finding is scary…lead into the lvh/lbb discordant theme.

18. Diagnosis:
LBBB
The rhythm is sinus, with first degree A-V block and left bundle branch block (LBBB).
Notice the SECONDARY ST elevations and depressions- simulating or masking infarction.

19. LBBB
• Understand the EKG concept of “primary” and “secondary” ST changes.
• In general, the deeper the S wave, the greater the ST segment elevation. (i.e. secondary ST change.)
• LBBB classically has deep S waves in right sided pre-cordial leads ST elevations in these leads.
• This phenomena makes diagnosing antero-septal ischemia difficult in the presence of a LBBB.

20. Diagnosis:
LBBB
Atrial fibrillation with pre-existing left bundle branch block
Sometimes this can be confused with ventricular tachycardia but closer inspection can identify the irregularity.
Irregularly irregular rhythm - suggesting AF.
Features of typical left bundle branch block
wide QRS >120 ms (3 small squares)
no secondary R wave in lead V1
no lateral Q waves

21. Diagnosis:
Left Ventricular Hypertrophy
Hyperkalemia
Pericarditis

22. Diagnosis:
LVH

23. LVH
• Again we see the deeper the S wave the greater the ST elevation…similar concept as with LBBB.
• LVH is one of the most common conditions mistaken for AMI.
• Elevated ST segments with LVH tend to be in V1 and V2 only.
• Elevated ST segments with LVH tend to be concave up; in distinction to the ST segments in AMI.

24. Diagnosis:
LVH
LVH with secondary ST-T change

25. Diagnosis: Pericarditis
pericarditis (2) : (note : diffuse ST elevation pattern)

26. Pericarditis
• Diffuse ST elevation in pre-cordial and limb leads: it would be rare for MI to do this.
• Typically a diffuse process, which affects the atria as well PR depression = atrial current of injury.
• Notice: aVR is a contrarian! (ST ; PR)
• ST segments usually “smiley”; < 5mm of elevation.
• These EKG findings are variably present, as pericarditis has several stages.

27. Diagnosis:
Pericarditis

28. Diagnosis:
Septal Myocardial Infaction
Hyperkalemia
Brugada Syndrome

29. Diagnosis: Brugada Syndrome
The rhythm is sinus. There is a right bundle branch type pattern with “funny” ST elevation in leads V1 and V2.
This pattern is classic for Brugada Syndrome. Brugada Syndrome was initially described in 1992, in patients with syncope or sudden cardiac death and this characteristic ECG pattern. About half of cases are familial. Brugada Syndrome appears to be more common in males than females, and seems to be more prevalent in Southeast Asia than other parts of the world. Interestingly, Brugada Syndrome has been linked to mutations in the sodium channel gene SCN5A, the same gene implicated in the congenital long QT syndrome type 3 (LQTS3). The mutation in LQTS3 appears to cause augmentation of the late sodium current (INa), whereas in Brugada Syndrome the effect seems to be early inactivation of this sodium channel or loss of function altogether.

30. Brugada Syndrome
• First described in 1992 by Josep and Pedro Brugada. (see AJEM 3/03)
• Believed due to a Na channel defect in epicardium, but not in endocardium of RV.
• Structurally normal heart.
• Predisposes to VT and VF. (think syncope).
• Believed to account for 40-60% of cases of idiopathic V-fib!
EKG
• Complete or incomplete RBBB pattern.
• ST segment elevation in V1 and V2.
• ST segment begins from top of R’ wave, is downsloping, and ends with an inverted T wave.
Mutations in cardiac Na channel gene. Loss or depression of action potential in R ventricular epicardium but not endocardium. Result: transmural voltage gradient responsible for ST ^ V1 and V2 and genesis of VT.
Me: no antiarrhythmics helpful- pt needs prompt cards f/u for EPS/ICD placement
V1 Brugada
V1 Hyper K
V1 PE

31. Diagnosis: Brugada Syndrome
Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation, and sudden cardiac death: A distinct clinical and electrocardiographic syndrome. J Am Coll Cardiol 1992; 20:

32. Diagnosis:
Hyperkalemia
hyperkalemia : (note : tall, peaked T waves)

33. Hyperkalemia • Tall, symmetric, peaked T waves (K  5’s)
• QRS prolongation (K  6’s)
• Loss of P wave amplitude
The scaffold I use to remember these changes is that they begin at the T wave and progress backwards through the EKG complex as serum K rises.
• “Dialysible current of injury”, aka pseudo-infarction pattern
• Sine wavedeath.

34. Diagnosis: Hyperkalemia v1 v1 v2 v2 v3 v3
hyperkalemia, very severe : (note : widen QRS merging into ST segment (on the verge of sine wave)) v3 v3

35. Anterior Septal MI
Diagnosis:

36. Diagnosis: Anterior Septal MI Acute anterior myocardial infarction
ST elevation in the anterior leads V1 - 6, I and aVL
reciprocal ST depression in the inferior leads

37. Diagnosis: Inferior MI Acute inferior myocardial infarction
ST elevation in the inferior leads II, III and aVF
reciprocal ST depression in the anterior leads

38. Diagnosis: Ventricular Aneurysm
-Persistent STE approximately seven weeks after extensive AMI indicates left ventricular aneurysm
-Complications of Acute Myocardial Infarction Quick Reference    Left ventricular aneurysm Cause: fibrosis of necrotic myocardium after transmural myocardial infarction Symptoms: heart failure, arrhythmias, mural thrombus formation Physical findings: heart failure; ventricular arrhythmias; peripheral embolization Laboratory evaluation: chest x-ray, echocardiogram, electrocardiogram (persistent ST-segment elevation at site of previous myocardial infarction) Treatment: treat heart failure; control ventricular arrhythmias; anticoagulation; aneurysectomy

39. Ventricular Aneurysm • Complication of AMI.
• Persistent ST elevation weeks to months after extensive MI indicates ventricular aneurysm.
• Caused by fibrosis of necrotic myocardium following transmural infarction.
• Can present as HF, arrhythmia, embolus.
• Aneurysectomy.

40. Summary Thoughts
• This is an important differential, and some of the differences are subtle.
• The most common causes of ST elevation mistaken for ACS in multiple studies were: LVH, early repolarization, BBB and ventricular aneurysm.
• In developing a differential consider: shape of the ST segment, leads involved, other features of the EKG, and the general clinical picture.

41. Summary Thoughts...
• I put the diagnoses in groups to aid memorization:
1) Three Normal Variants:
male pattern, early repol, juvenile T wave pattern.
2) Two Secondary ST changes: LVH, LBBB
3) Two with weird, downsloping ST:
Brugada Syndrome, hyper K
4) Pericarditis: Diffuse- it’s own catagory
5) ACS and ventricular aneurysm:
6) Other: PE, cardioversion,

42. CME Quiz

43. Diagnosis: Left Ventricular Hypertrophy Early Repolarization
Acute Myocardial Infarction

44. Diagnosis:
Left Ventricular Hypertrophy
Hyperkalemia
Pericarditis

45. Diagnosis:
Septal Myocardial Infaction
Hyperkalemia
Brugada Syndrome

46. Suggested Reading • Wang et al. N Engl J Med 2003, 349:22
• J Am Coll Cardio 2002;40:1870-6
• Ann Emerg Med 1994; 23:17-24
• J Emerg Med 1998;16:797-8
• Am J Emerg Med; March, 2003
• Uptodate.com
• Am J Cardiol 1960; 6:200-31

47. No mas

48. CME Quiz

49. EKG Dreaming

50. B. Dery Colorado West Emergency Physicians Grand Junction, CO
ST Segment Elevation in Conditions Other Than Acute Myocardial Infarction
B. Dery
Colorado West Emergency Physicians
Grand Junction, CO
Big part of EKG reading is short lists of DDx: tall R V1, PRWP,

51. Lastly…
v1 v v v v v6 PE DC
Cardio-
version

52. NEJM tracings

53. nejm1

54. Nejm1.1

55. nejm2

56. Nejm2.1

57. Nejm3

58. N Engl J Med 2003;349:2128-2135. Wang K et al
nejm4 1 2 3 4 5 6 7 8 9 10 11 12

59. Lvh2-skip

60. Lbbb-skip

61. Lbbb2-skip

62. Pericard1-skip

63. Pericard2-skip

64. Pericrd3-skip

65. Ant mi1-skip
anterior MI : (under evolution, ST elevation in the anterior leads V1 - 6, I and aVL, reciprocal ST depression in the inferior leads)

66. Post mi3-skip Acute posterior myocardial infarction
(hyperacute) the mirror image of acute injury in leads V1 - 3
(fully evolved) tall R wave, tall upright T wave in leads V1 -3
usually associated with inferior and/or lateral wall MI

67. Aneurysm#1-skip
ECG obtained 2.5 hours after onset of chest pain showing STE in anterolateral distribution. Note the prominent Q wave with marked STE at this early stage of AMI. Giant R waves are seen in leads V3 and V4; STD (reciprocal change) is also seen in inferior leads.

68. Persistent juvenile pattern
Persistent juvenile pattern — The T wave vector may be directed posteriorly in children, resulting in an inverted T wave in the right precordial leads V1-V3. The vector usually becomes anterior with age, resulting in upright T waves in these leads; however, the T waves may remain inverted in V1-V3 in a minority of adults, a finding known as a persistent juvenile pattern. (Uptodate.com)