Conclusion: 53 YOF with AMS: STEMI or Secondary ST-T changes?

This is the conclusion to the previous case:

53 YOF with AMS: STEMI or Secondary ST-T changes?

This female presented to the ED with Altered Mental Status (AMS), via ambulance, as STEMI ALERT, after completing approximately 3 hours of her usual dialysis.

This was the 12 lead ECG provided by EMS…

lvh osceola final


We have a sinus rhythm with Bi-atrial Enlargement or Abnormality and Left Ventricular Hypertrophy with Secondary ST-T changes.

We can categorize ST-T changes as Primary or Secondary.

  1. Primary ST-T changes refer to changes due ischemia
  2. Secondary ST-T changes refer to non-ischemic repolarization abnormalities (i.e. LVH, Bundle Branch Blocks, ect…)

What does this mean?

This is not a STEMI, but rather ST segment elevation due to altered ventricular repolarization. A prior ECG from a previous visit was significantly similar, but we were unable to obtain a hard copy.

So remember the main reason the dialysis center called EMS? AMS. The patient was found to be hypoglycemic and was treated with 25 g of Dextrose 50% with improved mental status and GCS.

The following 12 lead ECG was obtained:

lvh ed

Both computerized ECG interpretation recognized Secondary ST-T changes, as well as Atrial abnormality, with no STEMI recognized. Although the computerized interpretation is accurate in most case, our ability to interpret ECGs is one of the most important skills as healthcare providers and clinicians, which is why we will break down our findings in this case.

What do we see?

  • Sinus rhythm, regular with PRI within normal range
  • Physiologic leftward axis
  • Prolonged QTc
  • Biatrial Enlargement or Abnormality: (as discussed before, many clinicians have adopted the term abnormality over enlargement due to the possibility of atrial dilation or hypertrophy, not confirmed by ECG)

biatrial enlargement


  • Right Atrial Enlargement/Abnormality (P Pulmonale): P wave > 2.5 mm in lead II

This is usually present in cases of chronic Pulmonary HTN and increased Right Ventricular (RV) workload

Click HERE for further on Pulmonary pressures and ECG changes

  • Left Atrial Enlargement/Abnormality: in this case, deep P wave > 40ms between downslope and upslope in V1

This is usually present in cases of Mitral or Aortic Valve stenosis, chronic systemic HTN and increased Left Ventricular (LV) workload

  • LV Strain pattern: Slight downsloped ST segment depression with asymmetric T wave inversion, suggesting increased LV workload (secondary ST-T change, not ischemia)
The increase in LV pressures will affect the repolarization from epicardium to endocardium, altering its vector, leading to the Strain pattern seen in these leads which look at the LV.

lead i lvh


  • Left Ventricular Hypertrophy (LVH):  Many criterias exist to determine LVH, but we will focus on some of the most commonly used:

Sokolow Lyon Criteria

    • S wave in V1 + R wave in V5 or V6 > 35mm

Cornell Criteria

    • S wave in V3 + R wave in aVL > 28 mm in men

Other common criterias included:

  • R wave  in aVL > 11 mm
  • R wave in Lead I + S wave in lead III > 20 mm
  • R wave in V4-6 > 25 mm

v1-3 lvh


Notice how the highest ST segment elevation is present in the leads with the deepest S waves, V1-3. This means that the elevation is proportional to the depth of the S wave. In simple terms:

The deeper the S wave, the higher the ST segment. The taller the R wave, the deeper the St segment.

This is why LVH is known to be an Anterior STEMI mimic

Although the ST segments in V2-3 are not the common concaved elevation seen in these precordial leads, there are no other signs of MI, with normal R wave progression and no changes over time.

The presence of Atrial abnormality and history of  HTN supports the diagnosis of LVH, although, the confirmation of hypertrophy is best obtained with Echocardiogram, revealing the true LV muscle mass and index.

Troponin I was .08 ng/dL during this event, while the last two ED visits, one month apart, were .16 ng/dL and .21 ng/dL, secondary to renal failure and HTN. No occluded arteries were found during previous angiogram with no ECG changes. Serum Potassium of 4.7 mEq/L. The patient was admitted for further observation with no cardiac complications, and overall improvement.



  • I agree completely that LVH may indeed be a “stemi-mimic” – and that in this case, the overall ECG picture of this 53yo female dialysis patient clearly suggests this answer given biatrial abnormality, dramatically increased QRS amplitude and the nature of her ST-T wave abnormalities. I like using the “Mirror Test” not only when I look for posterior infarction – but also in case of marked LVH like this. Inverting those ST-T waves in V1,V2,V3 – and holding them up to the light will show some J-point depression and an ST-T wave segment that looks like strain (ie, the “mirror test” on the ST segment in V3 will look identical to what we see in aVL; that in V1,V2 will be a bit scooped, though still very suggestive of strain). KEY POINT: It is possible to have BOTH chest pain from ischemia/infarction + LVH and strain in the same patient – so rather than saying, “there is LVH and strain so there cannot be a stemi” – one should assess each case on its own merits. In this case – the history (not to mention that long QT) suggest a CNS or metabolic event. It will sometimes be less evident from the ECG that LVH and ischemia/infarction are not both taking place … Nice case Ivan!

  • Mike says:

    Hi Ivan
    Thanks for this interesting case. I know this is a bit off track with regards to what is being discussed, but I was interested in your reiteration that LA enlargement is now being referred to as LA “abnormality”. Do you mean that this is due to the ECG not being able to distinguish BETWEEN atrial dilatation and hypertrophy. Or do you mean that LA “abnormality” is used because the ECG is unable to reliably diagnose LA enlargement/hypertrophy? i.e. the terms “enlargement” and “hypertrophy” are used synonymously.

    As a cardiac sonographer I’ve hardly EVER seen atrial hypertrophy (i.e. thickening of the atrial walls). I’m also wondering if the terms LVH and RVH are inadvertently applied to an ECG when in actual fact the patient turns out to have a dilated LV/RV? Maybe I’m just confused – Being constantly stuck in the echo lab I try to keep up with my ECG skills when I can. Thanks!

    • Ivan Rios says:

      Hi Mike, the reason abnormality is being used over enlargement, as you asked, is due to the ECG not being able to differentiate between true enlargement/hypertrophy or dilatation. We suspect there would be enlargement due to the width and height of that abnormal P wave, which suggest delayed conduction from a suspected “enlargement”, but could well be conduction delay due to abnormal depolarization for another reason.

      Similar principals apply to LVH and RVH, however, with a history of HTN, valvular malfunctions, COPD or Pulmonary Disease, and these ECG changes, these suspicions of LVH/enlargement fit a bit better. Ultimately, I would love to confirm with ECHO but the reality is that many cases don’t get it.

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