STEMI MIMICS

STEMI mimics(1) are important to understand, because in taking the time to investigate the mimic, we can miss opportunity for early treatment of the real disease. Unlike STEMI equivalents, which have been covered previously, some of the mimics are not as serious.
​Here are some examples.

This can be in 2 forms, where in both the ST segment is concave:

1. Male pattern: 1-3 mm STE in V1-V4
2. Female pattern: 1mm STE in V1-V4

The formal definition of a STEMI as per AHA/ACC(2) is:

• Men
  • < 40 yo: >2.5 mm ST-elevation in V2 or V3, 1 mm in any other lead
  • ​> 40 yo: >2.0 mm ST-elevation in V2 or V3, 1 mm in any other lead
• Women: >1.5 mm ST-elevation in V2 or V3, 1 mm in any other lead

​The ECG below is from a male who presents with chest pain. It is normal.

This condition is present in a younger population group and amongst athletes. There are three types:

1. Type 1: Pattern occurs in the lateral leads
2. Type 2: Pattern occurs in the inferior/inferolateral leads
3. Type 3: Pattern occurs throughout the whole ECG.

BER Pattern:
Point notch with elevation
STE with concave up morphology V2-V6, II, III, avF usually < 2mm
No reciprocal changes
​Symmetrical Concordant T wave
​STE/T-wave height <0.25 in V6

Benign Early Repolarisation may not be that benign, being associated with serious arrhythmias in some studies.

Diffuse STE
ST/T-wave >0.25
There are 4 stages in pericarditis:

• Stage I: ST and PR changes
  • Diffuse concave up ST segment elevation,
  • Reciprocal ST depression in  aVR. 
  • PR elevation in lead AVR + V1
• Stage II: Normalisation of ST segments
• Stage III: T wave inversions.
• Stage IV: Normalisation of T waves

ST-T and QRS discordant.
​STE is concave and <5mm

Peaked T waves
​Downsloping ST segment.

Type I: Coved Pattern

• Leads V1-V2
• High take-off > 2mm and concave downscoping ST segment

Type II: Saddle-back

• Leads V1-V2
• Minimum ST elevation

Can present with STE in Precordial leads
A more common presentation of right ventricular injury is STE in V1-V3 and/or ST depression of V4-V6.
Theories for why STE occurs in the precordial leads include:

1. Paradoxical Embolism via atrial-septal defect or patent foramen ovale (5)
2. Myocardial ischaemia caused by a sudden pressure load on the right ventricle, which is unable to compensate.(5)
3. Hyperaemia from PE induces a catecholamine surge, increasing myocardial workload and ischaemia.(6)

1. Wang K, et al.  ST- segment elevation in conditions other than acute myocardial infarction. N Engl J Med. 2003 Nov 27; 349(22): 2128- 35. 
2. O’gara PT,  et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127(4):e362-425.
3. ​Kayanı WT et al. ST Elevation: Telling Pathology from the Benign Patterns. Global Journal of Health Science. May 2012, ​4(3):51-63
4. Mirijello A et al. Brugada electrocardiographic findings in an 80-year-old man. BMJ Case Reports. July 2013.​
5. Cheng TO. Mechanism of ST-elevation in acute pulmonary embolism. Int J Cardiol. 2005;103:221-223
6. Falterman TJ, et al. Pulmonary embolism with ST segment elevation in leads V1 to V4: case report and review of the literature regarding electrocardiographic changes in acute pulmonary embolism. J Emerg Med. 2001;21:255-261.
7. ​Wilson G T et al. Pulmonary Embolism Mimicking Anteroseptal Acute Myocardial Infarction. JAOA • Vol 108 • No 7 • July 2008