A 31 year old with Diabetes and HTN complains of bilateral arm tingling and headache

This ECG was texted to me with the message "A 31 year old with Diabetes and HTN complains of bilateral arm tingling and headache."

There is high lateral ST Elevation and inferior reciprocal ST depression.
There is also STE in V2.

The computer calls it a STEMI.

What do you think?

STE in I, aVL and V2 is a pattern associated with "Mid-anterolateral OMI," which is seen with OMI of the first Diagonal.  See more of Mid-anterolateral OMI













I wrote back: "I think this is a false positive due to LVH.  PseudoSTEMI.  I can't tell you exactly why.  It just looks like it.  ECGs are often like faces to me.  I recognize them." 

More explanation: It does not meet any criteria for LVH, but just has the "look."  As I think about it now, it is the STE and upright T-wave in V2, with T-wave inversions in V5 and V6.

Furthermore, one should always be suspicious when the symptoms are so non-specific, especially when the patient is so young.

I sent the ECG to Pendell and he answered: "It seems like very high chance of false positive for LVH. The history would allow me to proceed with that assumption until I do some more investigation.  If it was chest pain it would be more difficult to go with my gut on that."  So we had exactly the same interpretation.


Then my friend wrote back with more clinical info:

He had a persistent bad headache and his BP actually went up to 220/120. Negative head CT and negative troponin x 2. I tried metoprolol and oral hydralazine with no luck and finally nicardipine at 10 mg/hr got him to about 170/90 and pretty comfortable which I was happy with. Never chest pain but had to treat as hypertensive emergency. EKG exactly the same on repeat.

Comment: the fact of the very high BP is very supportive of LVH.  If he had texted me that, I would have been more certain of a false positive.  And then 2 "negative" troponins, although that wording allows for many different troponin patterns. 

In fact, severe hypertension by itself can lead to greatly increased oxygen demand and type 2 acute MI, sometimes with ST Elevation.  See this case of Type 2 STEMI due to severe hypertension.  Here are more Type II STEMI.

Follow up:

"Some follow-up on my scary EKG from last week - no change on next day EKG, significant LV hypertrophy on echo, equivocal abnormal stress test vs artifact so he got sent to cardiology and had a clean cath. All for want of a prior EKG. At least I got the definitive answer. Amazing how scary an EKG can seem in isolation."

One more comment, and this is a difficult concept to comprehend: Even if the troponins had returned with an acute MI profile, the absence of any evolution on the ECG from one day to the next would prove that these ECG findings are not a result of that MI.  Any ECG finding that is a manifestation of ischemia will change over time.  One would have to say that the MI did not manifest on the ECG at all.

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MY Comment by KEN GRAUER, MD (8/30/2020):

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The 12-lead ECG in today’s case was texted to Dr. Smith for his opinion. For clarity — I’ve reproduced this tracing in Figure-1. The patient was a 31-year old man with a history of diabetes and hypertension — who presented with “bilateral arm tingling and headache”. His BP in the ED was 220/120 mm Hg. No prior tracing was initially available.

• HOW did YOU interpret ECG #1?
• WHAT features about this case support Dr. Smith’s impression that ECG #1 is not indicative of an acute MI?
• That said — WHAT features about this case are worrisome?

Figure-1: The initial ECG in this case (See text).

My THOUGHTS about ECG #1: The rhythm is sinus at 75-80/minute. Regarding intervals — the PR interval is normal and the QRS complex is narrow. The QTc may be of borderline duration. The frontal plane axis is normal (about +40 degrees). Voltage criteria for LVH are not satisfied. Regarding Q-R-S-T Changes:

• There appears to be a narrow (albeit fairly deep) Q wave in lead aVL. (I thought this was most likely to be a normal septal Q wave).
• R wave progression is normal — with transition (where the R wave becomes taller than the S wave is deep) occurring normally, here between leads V3-to-V4 (albeit the upper portion of the R wave in lead V4 appears to be cut off).
• The most remarkable findings on this tracing relate to the appearance of ST segments and T waves. There is definite ST elevation in high-lateral leads I and aVL. There is also 1-2 mm of J-point ST elevation in lead V2.
• There is coving of the ST segment in each of the inferior leads, and in leads V3-thru-V6. This is followed by fairly deep and symmetric T wave inversion in the inferior leads, and in leads V5 and V6 (with a suggestion of T inversion also in lead V4).

Putting the Findings in ECG #1 Together — IF this patient had presented with new-onset, worrisome chest pain — I would clearly be concerned about an acute evolving STEMI. After all, there is significant ST elevation in both high-lateral leads (leads I and aVL) — and, there is J-point ST depression with a near mirror-image reciprocal picture between leads III and aVL. ST coving with fairly deep T wave inversion is seen in each of the inferior leads, and in leads V5,V6 (with ST coving also in V3,V4).

• BUT — the patient is a younger adult, and there is no mention of any chest pain.
• That said — we should assume that the high-lateral ST elevation with potential reciprocal ST depression in the inferior leads is acute until we can demonstrate otherwise.

NOTE: There are some reasons to suspect that the findings in ECG #1 are not acute (Figure-2).

Figure-2: I’ve labeled some findings from Figure-1 (See text).

Among the reasons I thought ECG #1 might not reflect an acute MI were:

• In addition to not having any chest pain — the clinical presentation in this case was malignant hypertension in a diabetic patient with longstanding hypertension. Many of these patients have marked LVH associated with ST segment coving and significant T wave inversion (not unlike what we see in ECG #1).
• As noted earlier — voltage criteria for the ECG diagnosis of LVH in this 31-year old man are not seen in ECG #1. That said — sensitivity of the ECG for detecting LVH is imperfect at best (generally under 60%). False negatives are common. Moreover, despite not satisfying textbook criteria for LVH voltage — one gets the distinct impression that there is “extra QRS amplitude” in the form of surprisingly deep inferior lead S waves (given substantial height of the R waves in these leads). And clinically — many (if not most) patients with diabetes and longstanding hypertension who present to the ED with a BP = 220/120 mm Hg will have LVH.
• As I’ve often emphasized in Dr. Smith’s ECG Blog — the finding of ST-T wave changes consistent with LV “strain” in a patient with “the right disease” (ie, longstanding hypertension, now presenting as malignant hypertension) — dramatically increases the likelihood of true LVH. This is true even when voltage criteria for LVH are not seen on ECG.
• ST-T wave changes of LV “strain” most often manifest in one or more of the lateral leads (For more on LVH — See My Comment at the bottom of the page in the June 20, 2020 post). But instead of seeing ST-T wave changes of LV “strain” in lateral leads — some patients manifest a “mirror-image” of strain in anterior leads. I believe the unusual shape of the elevated ST-T wave in lead V2 in Figure-2 (within the BLUE rectangle) reflects LV “strain” in this patient with marked LVH. Doesn’t the mirror-image of this ST elevation in lead V2 (within the RED rectangle in Figure-2) look exactly like LV “strain” usually looks in lateral leads?
• Finally — the small RED arrow in lead I of Figure-2 points to a most distinct J-point notch. While it clearly is possible for patients with acute infarction to manifest J-point notching — this notching, together with the shape of the gently upsloping, elevated ST segment we see in lead I resembles the picture commonly seen in repolarization variants.
• BOTTOM Line: The patient in today’s case has malignant hypertension. He did not have chest pain. While fully acknowledging that I was not certain he was not having an acute event — I thought the above considerations could clearly explain the ST elevation in leads I, aVL and V2 — as well as the ST coving and T wave inversion in multiple other leads. Had this been acute lateral infarction — rather than the same ST coving with deep T wave inversion that we see in the inferior leads — I would have expected a different shape for the ST-T waves in lateral chest leads V5 and V6 (if not some ST elevation in these leads). I was pleased to learn that Echo confirmed significant LVH — and, that cardiac cath confirmed normal coronary arteries.
• P.S. — In addition to malignant hypertension, the “bilateral arm tingling” this patient experienced suggested the possibility of hyperventilation (superimposed on his malignant hypertension). It is good to remember that hyperventilation itself is a cause of ST depression and/or T wave inversion! It turned out that this was not the case for this patient — because apparently, his ECG the next day was unchanged (whereas the T wave inversions should have resolved if hyperventilation was the cause).