Is this hyperacute anterior STEMI or something else?

A 41 year old male is pulled over during morning rush-hour by sheriff’s deputies.

He states that he is on his way to the hospital because he is having chest pain. EMS is called to the scene.

The patient is awake, alert, and oriented to person, place, time, and event.

His skin is pink, warm, and moist.

He appears acutely ill and anxious.

He states that he has a history of high blood pressure and renal insufficiency. He takes several medications, but he can only recall that one of them is a beta blocker.

  • Onset: 1 hour ago while sleeping.
  • Provoke: Nothing makes the pain better or worse.
  • Quality: Patient describes the pain as a poorly localized “fullness” or “pressure”.
  • Radiate: The patient cannot tell whether or not the pain radiates.
  • Severity: The patient reluctantly gives the pain a 7/10.
  • Time: The patient states he has had the pain on several occasions over the past few months but did not seek medical treatment.

Vital signs are assessed.

  • RR: 20
  • HR: 76
  • NIBP: 138/78
  • SpO2: 99% on room air

The cardiac monitor is attached.


A 12-lead ECG is obtained.


The treating paramedic was concerned that the T-waves in leads V1-V3 might represent hyperacute anterior STEMI.

However, this was not a STEMI. It was left ventricular hypertrophy with a strain pattern and mild hyperkalemia.

First, let’s look at the 12-lead ECG and make the case for LVH.

This ECG has the general pattern of “T-wave discordance”. In other words, the T-waves are deflected opposite the majority of the QRS complex, which is suggestive of a secondary ST-T wave abnormality.

In this case the most likely cause is left ventricular hypertrophy with a so-called “strain pattern”.

I say “general pattern” because it’s not true in every lead. When I look for T-wave discordance I mentally remove isoelectric or equiphasic leads, particularly in the transition zone (the point at which a QRS goes from mostly negative to mostly positive in the precordial leads).

Let’s circle the leads I would mentally remove from this 12-lead ECG to decide whether or not “T-wave discordance” is present.


With those leads removed, are the T-wave deflected opposite the QRS complexes?


Could that be a coincidence?

Highly unlikely!

The high lateral leads in particular are showing a very typical looking strain pattern.

This can be a problem because it could easily be mistaken for “lateral ischemia” or reciprocal changes secondary to acute STEMI!

Does this ECG meet the voltage criteria for LVH?

Not exactly, but I believe we can make the case using the Romhilt-Estes point scoring system. This ECG would get at least a 4 (probable LVH), and it’s right on the borderline for left atrial enlargement and delayed intrinsicoid deflection in leads V5 and V6 which would give it a score of 5 or 6.

But I don’t think that’s important.

The next question we want to ask is, is the degree of the secondary ST-T wave abnormality proportional to the amplitude of the QRS complex in the opposite direction?

The answer is yes.

Remember, we’re looking at the ST-segments and the T-waves together.

At first glance it looks like there might be more ST-elevation in lead V1 than lead V2. However, I believe this is an optical illusion created by the biphasic P-waves in lead V1, as well as the more defined (less diffuse) J-points in lead V1.

Let’s blow this up a little bit.


When we use the TP-segments as a baseline, we can see that it’s debatable as to whether or not lead V1 shows more ST-elevation, but it’s obvious that lead V2 shows a more pronounced ST-T wave abnormality.

The T-waves seem a little bit narrower than we might have expected with LVH, perhaps with a slightly later take-off. Also, the QTc is well within “normal” at 419 ms.

I don’t have the exact lab value, but the feedback I received on this case was that the patient had a potassium level that moderately high.

Consider the following graphic that compares the T-waves of hyperkalemia to the T-waves of acute anterior STEMI.


There isn’t much documentation out there as to what hyperkalemia is supposed to look like in the presence of a secondary ST-T wave abnormality, but you’ll notice that with hyperkalemia, the T-waves are narrow and have a late take-off, while with acute anterior STEMI, the T-waves are more “broad-based”.

The take-home point is that T-wave discordance strongly suggests the possibility of a secondary ST-T wave abnormality. That being the case, I would wait for changes on serially obtained ECGs before calling a Code STEMI.

That’s important because according to some studies LVH is the most common cause of ST-segment elevation amongst chest pain patients, so we need a solid strategy to deal with this frequently-encountered STEMI mimic!


Romhilt D, Bove K, Norris R et al. A Critical Appraisal of the Electrocardiographic Criteria for the Diagnosis of Left Ventricular Hypertrophy. Circulation. 1969;40(2):185-196. doi:10.1161/01.cir.40.2.185.

Van Mieghem C, Sabbe M, Knockaert D. The Clinical Value of the ECG in Noncardiac Conditions. Chest. 2004;125(4):1561-1576. doi:10.1378/chest.125.4.1561.

Further reading

Should you activate the cardaic cath lab?

Usefulness of the QRS/T angle when diagnosing acute STEMI

Updated 03/16/2016


  • Max says:

    In terms of STEMI/NotAStemi, it certainly does meet the criteria for a STEMI activation. I'm trying to figure out how I'd tell the receiving ED doctor "I know I was looking at this, but I didn't want to activate the lab because. . ." and I just don't see that conversation going well for me. So I'd probably call, and have Cardiology meet me downstairs.ST elevation in the septal-antero region, with reciprocal in the lateral leads. That's what I think the receiving ED would hone in on, and hang me out by my ankles if I didn't call it in as such; especially given this guys "look".That said; he's definitely not communicating adequately based on the story. He seems either altered, or recalcitrant, to tell us the whole story. So I wouldn't be surprised to hear it fall out that there's some sort of recreational drug component – which he's likely not going to tell me on the scene as there are officers around. Hopefully that may fall out in the truck on the way. Cocaine induced MI would be high on my list of suspects given the patient's history, presentation, and behaviour. But until (unless) he confesses, I would play it in his best interests.

  • I'd agree with Max—I'd call a STEMI alert, even though in my mind it is borderline. But given his presentation, history, and this 12-lead, I'd much rather be safe than sorry.Max; where are you getting the recreational drug component? I'm not sure I saw anything to suggest that; however, my experience is very limited when it comes to cocaine induced MI.

  • Max says:

    There's nothing in the 12-lead making me say that, unfortunately. Given the patient's history of this having happened a few times over the past month or two, I'm just leaning towards mimics.The way the patient is being described just strikes me as evasive. Like he's hiding something, or just isn't quite all there. And of the mimics I can think of, the only one that I can see a patient acting evasive/strung-out over, is the cocaine use.

  • Hillis says:

    The 12 lead ECG shows HYPERACUTE T wave in the anterior leads V1-3 with contralateral changes with ST depression in the lateral leads I, aVL and V6 .. YES, it is anteroseptal STEMI -> Rush the patient to cath lab.

  • Mike says:

    I think I would hold off on the STEMI notification. Not that I wouldn't transport the pt emergently or perform serial EKG's. The peaked, hyperacute T waves concern me for hyperkalemia, which goes along with the renal insufficiency hx. Though they could represent an early stage of MI. The T wave inversions look "strainish," and there are some pretty high voltages (though) none seem to meet specific voltage criteria. This goes along with the HTN hx.So, close monitoring along with secure IV access. Rapid transport because between the presentation and the EKG's there seems to be some badness occuring. And the key, serial EKG's watching for progression of hyperkalemia, changes which firm up a STEMI dx, or new findings. The monitor didn't identify it as an "Acute MI," correct? Okay Tom, smack me down with the next EKG!Mike S.

  • Craig UK says:

    Hi. I agree that this chap has hyperacute T waves on the anterior leads, which may be normal variant, but as far as ST elevation, i see very little, especially as this can be normal on the two leads where there is minimal elevation. I would like to see the same patients ECG after opiates and nitrates. However, from the ECG shown i would say this is a high lateral NSTEMI unless the elevation develops in which a STEMI could be diagnosed. I dont know what your protocols are in the US but here in the UK he would not be taken straight to the lab unless a STEMI is thought.

  • Terry says:

    This looks alot like the strain pattern in the power point 12-lead interpretation–garcia. Strain pattern in Leads I and AVL. No cath lab this is an STE mimic. Still follow your c/p protocols though and fax the 12-lead.

  • Hve to agree, gonna call the ED with ?STEMI. I too have the a bit of hesistant skepticism. Being pu;lled over "rushing to the hospital for chest" tends to have the favor of acute onset POLice-itis, the only thing lacking is the smell of 2 carbon particles hydroxides and being in a cell at 3AM. But he has the contributory medical disorders, the right recent history answers and even a more than suggestive PE and 12 Lead with the backing of a not always but well recognized algorithm. The longer I'm in this business the more cynical I become, but I've also become a very conservative clincian, with the attitude that, I'd rather argue with an ER doc or triage nurse rather than an attorney or state regulator,

  • Christopher says:

    Does not meet STEMI criteria, however, I see STD I/aVL/V6 and STE in aVR. There is also septal STE, with what could be hyperacute T waves. It also could be normal STE for V1-V3 in men.Transport to a PCI capable facility with a call-in detailing ACS w/ elevation not quite meeting STEMI criteria. Transmit ECG if possible.

  • Anonymous says:

    Not a stemi…. sorry guys not enough elevation in anatomically continuous leads and i dont think those are reciprocal changes just general ischemia possibly. Plus the pt is boarderline for LVH and incomplete BBB. Think those are whats causing your "elevation". Bu before i made th decision to or not to call a cath lab i wld like right sided and posterior 12 leads.

  • Brown Frown says:

    Borderline criteria for LVH, the axis is starting to turn leftward, he's Beta-blocked, I'm going with a strain pattern w/ lateral ischemia.

  • akroeze says:

    The only thing I can add to the already excellent posts is that the ST segments seem to be concave. I gather from the recent teaching posts here that this tends to put things more towards the "mimic" side of things.

  • Anonymous says:

    I agree with Mike S. and view the strip shows more of a LV strain vs. STEMI.

  • Geoff says:

    Another good one. I also am stuck between the STEMI, Hyperkalemia & Strain Pattern. I wouldn't be able to call a STEMI alert because the computer didn't interpret STEMI. I would try to go towards a PCI center though.The T waves are very concerning to me especially based on his presentation. I was under the impression that hyperkalemia and peaked T waves first start in V3-V4, anybody have anything on this? Obviously, this could be a while in though if that is his problem. They do appear peaked though.The ST Depression in I & aVL look like a strain pattern, even though the LVH is just below the millivolt requirement. Also, the STE seems between 1 & 2 mm in V1 & V2. The S Wave in V1 is 18mm & V2 is at 23mm, the ST segment doesn't seem to change, but the T wave is definitely taller in V2. I thought the ST segment was supposed to elevate more in the leads with the deeper S Wave. The ST Depression does seem to be deeper in I to go with the taller R wave compared to aVL (something an ER Doc told me once, but I haven't researched yet). Oh, also, the transition seems a bit late and V5 & V6 seem like small complexes compared to I & aVL (does this mean anything w/ LVH?).Treat O2, IV, ASA, NTG, MS (based on time), serial ECGs. In terms of the ambulance running…baseline seems good…transport, fortunately my closest is also a PCI center, so I guess I'm cheating my way out on this one. Looking forward to more!

  • LVH with LAE. LV strain. T-waves are big with big QRS complexes. Normal varient.

  • Hillis says:

    Am still insisting for Acute Anterolateral STEMI.Hyperkalemia is unlikely becouse hyperkalemia will show tall tented DIFFUSE T wave in all leads not only confined to V1-V3 !!..WHY Strain pattern ??It is unlikely too becouse it does not fit the sokolow criteria for LVH (S in V1 + R in V5 or V6 ≥ 35 mm ) so count it firstly before saying the patient is having or not LVH..And please don't ignore the contralateral changes in the lateral leads even if minimal it has a significant clue for STEMI.

  • Lead 1 meets LVH limb lead criteria. With LAE, I am more convinced of LVH. I see the ST depression, looks like strain. I'm not always right, but it is my guess. The elevation in precordial leads looks normal with T wave discordance.

  • And it's S in v1 or v2, which ever is deeper.

  • Mark says:

    I agree that lead I does awfully close to meeting voltage criteria for LVH and the HTN hx and possible LAE are also suggestive. However, I think there are some subtle reasons to think the ST changes on this ECG suggest otherwise. I think the strongest evidence to the contrary is the fact that V1 appears to have somewhat more STE than V2 despite the fact that V2 clearly has a larger S wave. That would definitely not be consistent with LVH induced STE. Also, call me crazy, but is there slight STE in lead III? Between that and largest amount of STE being in V1 I would definitely want a right sided look. There is also evidence of lateral ischemia. V6 has obvious flattened, ischemic looking STD. That raises the possibility in my mind that the STD and flipped T's in I and aVL may be ischemic changes as well. They do look more "staininsh" than anything as someone already said but are you completely sure those T's aren't symmetric? I've never been great at eyeballing that but even if they aren't I think they are still suspicious for reciprocal changes to lead III in this context. It's not an overwhelming argument but I would definitely get a right sided ECG, obtain serial ECG's and strongly push for this guy to go to a STEMI receiving hospital.

  • Geoff says:

    Okay, reviewing the earlier LVH posts now, I do see you also said that the depression should be in proportion to the QRS height. So it appears the QRS height in I is proportional to the ST depression compared to aVL, but the ST elevation in V1 & V2 doesn't seem to correlate…I still wonder about the QRS in V6 not being very tall and the morphology of the STD in V5 & 6 is different than I & aVL.

  • Mark,The septal wall (v1/v2) are fed by the LAD, and the inferior wall(II, III, aVF) is fed by the RCA. This is true in almost everyone. This is why STE in both these areas would be very suspicious. Anything is possible. I am with you, if V1 STE is > V2 STE with a smaller amplitude S-wave in V1, this is significant.

  • Christopher says:

    Also the STE in aVR is suggestive of LCA occlusion and seems odd in the face of LVH. I went browsing through a few libraries of LVH ECGs and could not find one w/ elevation in aVR.

  • Christopher,Also the STE in aVR is suggestive of LCA occlusion and seems odd in the face of LVH. I went browsing through a few libraries of LVH ECGs and could not find one w/ elevation in aVR.I am so happy to see that someone else is examining aVR. STE in aVR > than STE in V1 is suggestive of Left Main coronary stenosis. Dr. Smith has sited this as a reciprocal change, while Dr. Amal Mattu states this is a representation of infarct in itself. It is may be a very significant finding. The findings indicative of LMCA stenosis:• ST-segment elevation in aVR > ST-Elevation in V1The findings indicative of increased morbidity and/or mortality:• ST-segment elevation in aVR & aVL• Reciprocal ST depression in inferior leads• Presence of right bundle branch block (RBBB) and/or left anterior fascicular block (LAFB) I noticed it on this 12-lead, but LVH is much more likely. I am unsure as well what both would look like together. So I follow the odds, and clinical picture… I'm not a good gambler.

  • Troy says:

    My guess is cardiac hypertrophy. I notice a strain pattern through the chest leads and with the I and aVL leads. The thing that concerns me is the STE in aVR. I would take him to a PCI capable center because I’m spoiled and have them close by and treat it like a CP. The thing I’m thinking is that they guy also has renal insufficiency so maybe he has some cardiomyopathy goin.

  • Ren says:

    The anterior-septal leads look very concerning for presence of hyperacute appearing Twaves-quick sharp steep take off. In addition, he has high lateral T wave inversions with ST elevation in aVR. This would be concerning for a left main lesion>LAD. Hyper K should also be considered given his renal hx.

  • Saleh Awdaly says:

    The hyperacute T waves for diagnosis of IHD is the buzzle of the ECG, however, more wider base and tip and with long QT could be considered as an early manifestation of IHD. But the question remaining if the hyperkalemic state is associated with real findings of T waves of IHD (Hyprid manifestation )).nevertheless, waiting and using more additive aids to increase the sensitivity for diagnosis.

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