Male in early 40's with 1.5 hours of chest pain

A third year medical student sent me this ECG and asked for my interpretation:

Recorded 0625

Here is what I wrote back: 
"Tough one.  Probably is acute LAD occlusion, needs serial ECGs/echo."

Standard ST elevation criteria

Note there is not enough ST elevation to meet the standard criteria, which require at least 2 mm ST elevation at the J-point, relative to the PQ jct., in leads V2 and V3 for a male over 40 years old.  In this case, there is 1 mm in V2 and 2 mm in V3.

1. Standardization and Interpretation of the Electrocardiogram, full text
2. MacFarlane 2004 (47% sensitive and 98% specific for MI as diagnosed by biomarkers.)


I had used my formula:

STEV350 = 2.5 mm (but it might be 3 mm)
QTc = 410
R amplitude in V4 = 14 mm

The value I obtained was 22.6 (23.2 if 3.0 mm is used for STE V3).

At a cutoff of 23.4 (my typically recommended cutoff), the sensitivity for LAD occlusion among subtle cases is 86% (much higher if all LAD occlusions are used as the denominator), with a specificity of 91%.

At a cutoff of 22.0, the sensitivity was 96% but with decreased specificity of 81%.

To me, the T-waves looked too fat to be normal.  And even though the formula was not greater than 23.4, at 22.6 or 23.2, it is close enough to be worried.

Outcome:

The pain had started at 5 AM, so that initial ECG above was at 1.5 hours after pain onset.

It was not recognized as possible LAD occlusion.  Initial troponin T was negative at less than 0.01 ng/mL (99% is less than 0.10 ng/mL).

2.5 hours later, the patient was seen by a cardiologist and the ECG interpretation was: "ECG - NSR without any ST-T changes.  No STEMI.  Will cycle markers and admit to Observation unit for rule out and stress test."

Comment: this is a patient who needs intensive evaluation in order to rule in, not rule out, MI

At 11:14, almost 5 hours after presentation and first ECG, the troponin T returned at 0.37 (this is pretty high for Trop T).   CK was 368.

A 2nd ECG was recorded:

All ST elevation has resolved, proving that the first ECG was indeed STEMI.  Fortunately for the patient, the LAD appears to have spontaneously reperfused.  There are persistent R-waves, suggesting that not too much damage was done.  But these can be misleading.

At 12:21 another ECG was recorded:

Now there is recurrent ST elevation.  The LAD is re-occluding.

The patient was taken for Cath at 1414 and was found to have a 100% proximal LAD occlusion after a large D1 (the D1 had a 90% stenosis).  So, mid-LAD occlusion.

Trop T at 1752 was 2.11 ng/mL (this is really quite high and indicates a large infarct and significant myocardial loss).

Learning points:

1.  Beware large fat T-waves.  Use the formula for differentiating normal variant ST elevation from subtle LAD occlusion.  A value less than 22.0 will only miss 4% of subtle LAD occlusion.  If the value is higher than 22.0, serial ECGs are essential.

2.  Cardiologists are not generally trained to find these subtle signs of coronary occlusion.

3.  This is a NonSTEMI due to coronary occlusion.  Many NonSTEMI are due to occlusion and do not get rapid reperfusion,  They are not diagnosed until late, when biomarkers return,  They usually do not go to the cath lab until the next day (because they are "NonSTEMI") and they thus have worse outcomes, higher biomarkers, and higher mortality than NonSTEMI who have an open artery at cath.