Thursday, June 14, 2012

Dynamic inferior MI: STEMI or Non-STEMI? Does it matter?

A 63 year old with no cardiac history developed substernal chest burning while exercising, relieved with rest.  It later woke him from sleep and was constant.  He walked into the ED and had this ECG recorded at 0140:
There is subtle ST elevation (STE) in leads II, III, and aVF, with reciprocal ST depression in lead aVL (this must be present in inferior MI, or you should think of something else, like early repolarization or pericarditis).  There is thus injury, but there is not 1 mm of ST elevation in 2 consecutive leads.  (V2 also suggests posterior ischemia.)
This ECG is diagnostic of inferior MI

He was given aspirin, clopidogrel, sublingual nitro x 3 and IV nitro, and his pain improved but did not entirely resolve.  This ECG was recorded at 0157:
Most STE and ST depression is resolved.  There is now T-wave inversion in III, suggesitive of some reperfusion.  The artery is probably open.

The patient began having more pain again, and this was recorded at 0220: 
There is even more STE than on ECG #1, maybe 1 mm in 2 consecutive leads (in case it matters to you).  The T-wave is upright again.  This is called pseudonormalization because the T-wave is normally upright, but when T-wave inversion due to reperfusion reverts to upright, then it is "pseudo-" and implies re-occlusion.  (V2 again suggests posterior ischemia.)

He was taken for PCI of a distal RCA, found to have a 95% thrombotic occlusion.  Peak troponin I was less than 5 ng/ml.  Whether the artery was 100% occluded at the time of the 3rd ECG is not known.


This was called a Non-STEMI because there was not (depending on the person doing the measuring) 1 mm of STE in 2 consecutive leads.  But there was injury, and it was due to coronary occlusion or subtotal occlusion, and the pain was refractory to medical therapy.  So no matter what you call it, the patient needs immediate reperfusion therapy. 

Nature does not follow the metric ruler system nor does it adhere to graph paper.  That was invented by engineers and doctors and there is no magic to these numbers.

So where does the "magic" of 1 mm in 2 consecutive leads come from?  The randomized trials of thrombolytics vs. placebo enrolled patients with suspected MI and 1 mm of STE in 2 consecutive limb leads and found that the patients who received the drug had lower mortality than those receiving placebo.  The enrollment criteria were based on previous studies of MI, as diagnosed by CK-MB, that found that 1mm in limb leads had the best sensitivity, but at only 46%.

Thus, this non-angiographic data does not mean that some patients with less ST elevation would not benefit.  (In fact, in none of these thrombolytic trials did the authors specify the method of measurement of the ST segment!)

Schmitt et al. found that only 77% of RCA occlusions have at least 1 mm in 2 consecutive leads.  I recently showed that millimeter criteria are nearly worthless in differentiating subtle anterior STEMI from normal variant ST elevation.

Likewise, there are no randomized trials of therapy for refractory ischemia (definite ACS with ECG ischemia with medically uncontrolled symptoms).  In fact, since these patients should go immediately, they were excluded from all trials of emergent angiography for NonSTEMI.

The consensus, as documented in the ACC/AHA AND the Eurpean Soc of Cardiology Guidelines is that these patients should undergo immediate angiography [but thrombolytics only in the case of injury (STE) on the ECG].

Learning point: STEMI or Non-STEMI is an arbitrary definition, and doesn't always help direct therapy.


  1. Great ECG and logic as always.Thank you.My understanding is that in the pre cathlab era,the 2mm/1 mm criteria existed to assist with the significant side effects of thrombolytic therapy.Unfortunately cardiologists are still clinging on to the old evidence.

  2. Sir, i could not noticed ST elevation in lead II but yes ST elevations in Leads III and aVF with reciprocal changes in leads I and aVL. there is subtle ST elevation in leads V1 and and subtle ST depression in V3 and also marked ST elevation in aVR. So ECG showing both ST elevation and Depression in chest leads, these changes are of any importance? If at all my interpretation is correct.

    1. I do see STE in II, and zero STE in aVR. So STE in II, III, aVF, but NOT 1 mm. And minimal STD in V2. All consistent with inferior MI


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