Acute anterior STEMI from LAD occlusion, or Benign Early Repolarization (BER)???

For another fascinating related ECG, click here: 
Acute MI from LAD occlusion, or early repolarization? 

Case:

This is a 46 yo male with acute onset of chest pain, in distress, who called the ambulance. He arrived and had this ECG recorded at 0118 AM. 

A followup ECG and the answer is below.

There is 1 mm of ST elevation in V2 and V3, so this meets the criteria for reperfusion by the ACC/AHA guidelines. Unfortunately, the majority of patients who meet such "criteria" do not have MI. The most common reason for ST elevation is early repolarization.

(In this case, the limb leads are suggestive of ischemia as well, with some subtle ST depression inferiorly, suggesting pending ST elevation in aVL due to lateral MI from proximal LAD occlusion.)

I have developed a decision rule to differentiate Anterior STEMI from BER in patients who present to the ED with chest pain. These rules only apply when the DDx is Anterior MI vs. BER. A simple rule is the R-wave rule, which depends on the fact that, in BER, the R-wave is always well developed:

If the mean R-wave amplitude from V2-V4 is less than 5 mm, then it is almost certainly MI. If greater than 5 mm, it is probably BER. A cutoff of 5 mm gives a sensitivity for MI of about 70%, but a specificity of greater than 95%.

There are a couple other more complex rules, one of which uses QTc-B, R-wave amplitude in lead V4, and ST elevation at 60 ms after the J-point in lead V3.

Another equally accurate one, also derived using logistic regression, uses QTc and 2 averages: mean ST elevation at the J point (STEJ) from V2-V4 and mean R-wave amplitude from V2-V4.

Both rely on the findings that the mean ST elevation was higher in the MI group, and the mean QTc in BER is shorter (mean = 390 ms), and mean R-wave amplitude is lower.

If the formula: (1.553 x mean STEJ in mm) + (.0546 x QTc in ms) - (0.3813 x mean RA in mm, not mV) is > 21, vs. less than or equal to 21, then it represents MI with high sensitivity and specificity.

In this case, the values are (1.553 x 1.0) + (.0546 x 420) - (.3813 x 1.17) = 1.553 + 22.93 - 0.3813 = 24.1

Thus, the rule predicts that this is anterior MI.

The clinicians were suspicious of MI, so they were smart to obtain serial ECGs. They obtained the second ECG at 0143:

This shows unequivocal straightening of the ST segments, compared to the first ECG. This ST straightening results in T waves which are fattened and "hyperacute". This is diagnostic of anterior STEMI.

In case you can't see this difference in the straightening of the ST segment, here they are side-by-side:

He had a 100% proximal thrombotic LAD occlusion with TIMI-0 flow. It was opened and stented.

The followup ECG might give an idea of what this patient's T-waves looked like before his occlusion:

ST elevation on prehospital ECG is gone upon arrival to the ED

This is a 55 yo male with chest pain. The medics recorded the first ECG, which shows unequivocal ST elevation in leads V4-V6.


Our medics have the authority to activate the cath lab from the field, and they did so. After arrival in the ED, the second ECG was recorded.

There is no significant ST elevation here. It has resolved spontaneously. There is ST depression with hyperacute T waves, best seen in lead V3. This has been associated with 3% of LAD occlusion (http://content.nejm.org/cgi/content/extract/359/19/2071).

The patient had LAD occlusion; because of the prehospital ECG, and the authority to activate the cath lab, his door to balloon time was 36 minutes. Had there been no prehospital ECG, there may have been no coronary intervention at all because of the absence of ST elevation in the ED.

Atrial fibrillation with rapid ventricular response with ECG injury pattern

This elderly woman presented hypotensive, pale, and tachycardic.  Here is the initial ECG. 

There is an irregularly irregular rhythm (atrial fibrillation) with a very fast ventricular response.  There is an injury pattern, with ST elevation in II, III, aVF, reciprocal ST depression in I and aVL, and ST depression of posterior injury in precordial leads.

Did we activate the cath lab?  No. We looked at the whole patient, not just the ECG.  We suspected GI bleed and this was confirmed with blood on rectal exam.  An ultrasound of the inferior vena cava confirmed that it was flat (low central venous pressure).  Had this been a primary cardiac event, the CVP would be high and the IVC distended, and the patient might have also been in pulmonary edema.

She was given blood and fluids until the bedside ultrasound showed good central venous pressure (distended inferior vena cava), but she remained hypotensive, tachycardic, and the ST elevation did not resolve. Thus, we electrically cardioverted her at 200J biphasic, but this was unsuccessful x 3. We infused amiodarone 300 mg IV, but with no improvement, and a subsequent cardioversion was again unsuccessful.  We then loaded her with 500 mcg/kg of esmolol and started her on a 50 mcg/kg/min drip, after which a fifth cardioversion was successful, and resulted in the second ECG shown here:

The rhythm is sinus, rate normal, and all ST elevation and depression is now resolved.

Troponin peaked at 19, and there was a subsequent inferior wall motion abnormality. A stress sestamibi showed no inducible ischemia, so no cath was done. Whether there was thrombus in the infarct-related artery, or whether this was only demand ischemia (Type II MI) is uncertain. Nevertheless, it is wise to convert atrial fibrillation with a rapid response when the patient is unstable; any injury pattern on the ECG constitutes instability.

Though demand ischemia usually shows as ST depression (or nonspecific findings) on the ECG, it may occasionally present with injury (ST elevation).