A 50-something with cocaine chest pain and ST Elevation in V1 - V3

This case was expertly managed by Aaron Robinson (https://twitter.com/ARobinsonMD), one of our Hennepin EMS fellows, and by Danika Evans, a superb Hennepin G3 resident. 

This ECG was texted to me with the words "Cocaine" and "Chest pain."

There were no previous ECGs available for review.

There are QS-waves in V1 and V2.  There is ST Elevation in V1-V3, with large T-waves.  This looks scary and looks a lot like an LAD OMI.  However, there is also T-wave inversion in V5 and V6.  

There is also high voltage.  

I don't think this meets any of the many different voltage criteria for LVH, all of which are relatively insensitive and nonspecific, but it does look like LVH because of:

 1) the relatively high voltage, especially in V5 and V6 

2) slight ST depression with T-wave inversion in V5 and V6. 

3) STE in V1 and V2 primarily

4) QS-waves in V1 and V2 (QR-waves would be unusual in LVH)

Such morphology is usually LVH and not OMI.

STE in V1 and V2 may be septal OMI, but usually not with T-wave inversion in V5 and V6 (see many examples below)

He also sent this one, recorded 41 minutes later: 

There is a slight change in leads V3 and V4, but probably due to lead placement, with these 2 leads slightly farther around the chest on ECG 2 than ECG 1.

I wrote: "Wow. That is a really tough one. V2 and V3 look exactly like anterior LAD OMI. But then V5 and V6 make it look like it is LVH."

"What does the echo look like? An anterior wall motion abnormality should be pretty obvious. So if you do not see one, then this is probably an LVH mimic. It would not be a bad idea to do a pathway B"

But he beat me to it and was already in the process of obtaining a bedside echo. 

Here is one representative parasternal short axis view of the LV:  

The anterior wall is at the top, closest to the probe

This clearly shows excellent anterior wall motion and very thick LV wall.

Therefore, it is very unlikely that V1 and V2 represent anterior OMI.

This ECG was recorded at 82 minutes:

No Evolution; this supports absence of OMI

Troponin I (hs) were: 0 hour: 7 ng/L, 2 hour: 9 ng/L, 4 hour: 8 ng/L (Rules out Acute MI)

Thus, the chest pain was non-ischemic.

Formal echo the next day showed:

CONCLUSIONS -- SUMMARY

 

Moderately increased left ventricular wall thickness.

Normal left ventricular size and systolic function with an estimated EF of 68%.

No regional wall motion abnormality.

Dynamic intracavitary gradient, peak 34 mmHg at rest and mmHg with Valsalva.

Indeterminate left-sided diastolic parameters.

  

The hypertrophy is somewhat more prominent at the apex. This, in conjunction with the dynamic intracavitary gradient, raises concern for hypertrophic cardiomyopathy. 

Learning Points

Right precordial ST Elevation: Septal OMI vs. LVH:

Here is a typical case of massive LVH, with secondary ST Elevation in V1 and V2.  Note that there is a QS-wave in V1, STE is in V1 and V2, there is ST depression in V5 and V6, with negative T-waves in V5 and V6.

Notice the T-waves are negative in V5 and V6

Examples of Septal OMI. Note that, even though there is ST depression in V5 and V6 (reciprocal to the STE in right precordial leads), there is no T-wave inversion in V5-V6!)

A man in his 50s with "gas pain"

Developed into this:

A woman in her 70s with chest pain

Chest Pain and RBBB. What do you think?

Chest pain in a patient with previous inferior STEMI. Scrutinize both the ECG and the history!

Septal STEMI with lateral ST depression, then has collateral reperfusion resulting in Wellens' waves

Septal STEMI with ST elevation in V1 and V4R, and reciprocal ST depression in V5, V6

This is a Septal OMI.  

Full LAD Occlusion with STE in V1-V3, STD in V5 and V6, but does not have the elements of LVH described above.

This was missed, ruled in by serial troponins, found to have LAD OMI next day.  Peak troponin I of 80 ng/mL (very large MI)