Wednesday, August 26, 2009

Persistent ST elevation after previous MI, otherwise known as "LV aneurysm" morphology

Case 1. Classic anterior LV aneurysm morphology (Persistent ST elevation after previous MI).

This 46 yo male presented with chest pain. There is 1 mm of ST elevation in V1-V3, but there are large QS-waves preceding the STE. Such QS waves are highly suggestive of old transmural MI, with subsequent akinesis or dyskinesis of the anterior wall. Acute MI, if early in its course (first 6 hours, at least), always has tall T-waves in addition to ST elevation.

There is one retrospective study (Smith SW. American Journal of Emergency Medicine 23(3):279-287, May 2005) showing that the T/QRS ratio is significantly greater in acute anterior STEMI than in old anterior MI with persistent ST Elevation.  We have since validated this and are writing the manuscript as of November 2014.

The best criterion for differentiating was the sum of STE in V1-V4 divided by the sum of the QRS's in V1-V4 (TV1+TV2+TV3+TV4 divided by QRSV1+QRSV2+QRSV3+QRSV4). If this value was greater than 0.22 vs. less than 0.22, then it is likely to be acute STEMI. 

Another rule that was almost as good: if any one of the leads had a ratio of T to QRS greater than, vs. less than, 0.36, it was very likely to be STEMI.

T-waves in aneurysm may be upright or inverted, but in neither case should they have high voltage. [Deep inversions suggest very recent NSTEMI (e.g., Wellens'). Tall T-waves suggest acute STEMI.]

The above ECG has a summed ratio of 0.05 and is clearly NOT an acute STEMI. It is important to know that only about 70%-80% of patients with the ECG morphology of "LV aneurysm" actually have an LV aneurysm, as defined by echocardiographic dyskinesis. "LV aneurysm" is far less common in this era of reperfusion, in which STEMI is not allowed to progress to full infarction (also known as "transmural" infarction, an old but useful term). The patient above had akinesis and had formerly had a mural thrombus, which is a common complication of an immobile wall which also may have post-infarction inflammation.

This patient ruled out for MI with negative troponins.

Case 2. Exaggeration of persistent STE after old MI by tachycardia

This 65 yo male presented with dyspnea but no CP. The lungs sound wet. The ECG is shown.
There is quite a bit of ST elevation in the anterior leads, but it is preceded by very deep QS waves suggestive of old MI. Previous MI can have persistent ST elevation, and just like in Left Bundle Branch block and other entities, ST elevation may be exaggerated in states of tachycardia. Therefore, the T-wave to QRS ratio may also be exaggerated. Here the formula TV1+TV2+TV3+TV4 divided by QRSV1+QRSV2+QRSV3+QRSV4 = 0.27, substantially greater than 0.22, and would indicate acute STEMI. But one must be suspicous of a false positive in the presence of extreme tachycardia such as this. Also arguing against STEMI is the fact that there is no single T/QRS ratio (V1-V4) greater than 0.36.

The difficult decision is this: is this an old MI with exaggerated persistent STE due to tachycardia, or is it an old MI with a new STEMI superimposed? Given that the BNP was greater than 5000 and the patient had no chest pain, and the high likelihood that such a morphology represented the former (not the latter) diagnosis, the patient was not set up for angiogram and reperfusion.

A previous ECG was found and is shown:

It is evident that there previously was classic LV aneurysm morphology, but with much less ST elevation and shorter T-waves. The ratio here is low.
For rule 1: (4.5 + 7.5 + 4 + 0) divided by (14.5 + 31 + 20 + 19) = 0.19 (less than 0.22)
For rule 2: the lead with the highest ratio is V1: 4.5 divided by 14.5 = 0.31 (less than 0.36)

A previous echo had shown severe decreased LVF with an akinetic anterior wall.

Clinicians correctly interpreted the first ECG as exaggeration of ST elevation of old MI due to tachycardia, stress, and exacerbation of CHF. Treatment of CHF resulted in a slowing heart rate. Follow up confirmed all troponins negative and resolution of ST elevation when the heart rate came down.


  1. Hello,

    We are medical students and were hoping that you could explain what causes the ST elevation seen in ECG during MI?

    Many thanks

    Amy, Sam, Emily and Mark

  2. Amy, Sam, Emily, and Mark,

    Good question. Unfortunately, the topic is both very complex and not well understood. If you read the first chapter of my text "The ECG in Acute MI", there is an attempt at explanation.

    Fortunately, it is not important in managing patients to know why there is ST elevation.

    Steve Smith

  3. Hi,
    Persistant ST elevation of more than 4mm infer. leads (DII, DIII, AVf) associated with the typical reciprocal ischemic changes in anteroseptal territory.
    This ST elevation is persistant for about 8 days.
    Any comment about this condition (patient was not in severe pain, not known for DM, stable clinically)

  4. Case 2:

    A think the patient has LVH (according to Estes criteria: deep S wave in V3, left atrial abnormality, strain pattern, left frontal axis deviation; VAT in I and aVL also seem to be high).
    If yes, this can also contribute to (or be the cause of) low anterior forces and ST elevation.

    1. How do we know if it is because of LVH or wall motion abnormality (aneurysm, hypo-, dis-, akinesis)?

    2. If LVH, can we use the T/QRS rule? Or should we use the rule of too much discordance as in LBBB?



    1. there was a recent article on ST elevation in LVH which I have yet to mention in my blog because a) in my first reading, it did not seem to have the best methodology and b) I have not read it thoroughly. In that paper, they found that a ratio of ST elevation to S-wave of 25% or more was consistent with MI. So there is some similarity between LVH, LV aneurysym, and LBBB.

  5. Dr Smith, lets presume that I have forgotten on the formula and the calculation and I was presented with this patient. And no previous ECG was given to make comparison

    Based on QS pattern in lead V1-V2, T wave inversion in high lateral leads and more importantly presence of small Q waves there, could I safely presume this as a LV aneurysm before i proceed with my bedside echo? In addition to that, there seems to be LVH criteria satisfied in lead I and avL, however, Im curious, shouldnt a post MI patient has a dilated myocardium rather than a hypertrophied one? If so how could u explain the voltage ( which for me is quite high ) in this patient? And the T wave inversion signifies that this patient has reperfusion or LVH strain ( if it really presents )?


    1. Ryan,
      I would immediately recognize this as LV aneurysm without using my equation. The equation helps those who cannot recognize it.
      The voltage you see is the S-wave which represents the voltage going away from the lead due to depolarization of the posterior wall, which is indeed hypertrophied. The loss of R-wave is because of anterior aneurysm.
      STeve Smith

  6. Dr Smith, I have seen a number of EKG'S over the years with chronic persistent low level St elevation in the inferior leads after prior inferior STEMI but i can't find anything in the literature, can you comment on this.

    1. Steven,
      Yes, persistent ST elevation after previous MI is a well known ECG morphology, also known as "LV aneurysm" because about 80% of the time there is diastolic dysfunction (the definition of anatomic aneurysm). In anterior LV aneurysm, it is not hard to differentiate old MI vs. acute STEMI (see link below). However, for inferior STEMI vs. inferior aneurysm, it is much more difficult to differentiate. If there is shallow T-wave inversion, or small T-waves, the Q-waves and STE are more likely old. If there is a large upright T-wave, more likely acute STEMI.
      Steve Smith


Recommended Resources