Wednesday, December 19, 2018

A woman in her 70s with chest pain

Written by Alex Bracey, with edits by Pendell Meyers and Steve Smith

The Case:

A woman in her 70s who does not routinely seek medical care and does not carry medical diagnoses presented to our ED with central chest pain.

Here is the initial EKG taken at triage:

There is ST depression in leads I, II, aVF, V4-6. There is an arguably large amount of area underneath the ST segment and T-wave of lead V1, concerning for hyperacute T-wave. There is the combination of abnormal STE in V1-V2 with abnormal STD in V4-6, which we have described many times as concerning for LAD occlusion (usually involving the septum; proximal to the septal perforator), as well as ST elevation in aVR and V2-3. There is poor R-wave progression and low R wave voltage in V2-V4. This ECG does not meet STEMI criteria.

There was no baseline ECG for comparison. There is clearly concern for ischemia, though it is not diagnostic for OMI at this time. Using the subtle STEMI calculator app would point out the following contraindications:

The ECG was shown to Dr. Smith with with zero clinical information, and he responded: “Looks like it is probably an LAD occlusion.” He explained further that this was due to the combination of STE in V1, with a very prominent T-wave, and STD in V5-6 as well as inferior leads, all suggesting a septal STEMI.

A reader asked this question: 
"Isn't there an ST elevation in aVR indicating proximal lad occlusion?"
Smith answer: "That may be seen in diffuse subendocardial ischemia (which may be LAD ischemia, but not occlusion, and which is reciprocal to widespread ST depression).  In this case, there is ST elevation in right precordial leads V1-V3, which is typical of occlusion.  The ST elevation appears to be a normal amount, but normal ST elevation is never associated with ST depression in other precordial leads (in this case, V5 and V6)."

The clinical team correctly recognized that the ECG was concerning, but did not feel that emergent cath lab activation was indicated initially.

The Case Continues:
Additional history revealed that the patient had been experiencing chest pain off and on for one month. She described the pain as “pressure like,” transient, non-radiating, and not associated with nausea, diaphoresis, shortness of breath, and not brought on by exertion. The reason that she had presented today is that the pain had been present for hours rather than minutes. She had been experiencing this chest pain when she arrived and when the initial ECG was taken; however, it had resolved by the time of initial examination.

The patient appeared well and had no acute findings on exam. Labs and CXR were ordered. Just before the labs resulted, the patient again reported chest pain. An ECG at that time was recorded, but the pain had apparently resolved again seconds-minutes before the time of the ECG:

There is much more profound STE in V1-V3, now formally meeting STEMI criteria. V2-3 have biphasic T waves with terminal T wave inversion with is possibly indicative of reperfusion. The change from initial to this ECG is unequivocal proof of a process that involves dynamic full thickness ischemia of the anterior wall, therefore anterior OMI until proven otherwise. However the artery may technically be slightly open at the time of this ECG.

Let’s take a closer look at the change between the two ECGs:

Closer comparison of the original ECG and the repeat, which was captured moments after the resolution of chest pain.

Recall that the ECG will undergo predictable changes depending on blood flow through the coronaries, exquisitely responsive to reperfusion and reocclusion, as above. On the original ECG, the cardiac myocytes were acutely deprived on blood flow and oxygen and began down the ischemic pathway, starting with hyperacute T waves. On the repeat ECG, blood flow and oxygen had just returned to the cardiac myocytes and therefore produced a reperfusion or pattern.

Another ECG was taken prior to cath:
Similar to the last ECG, ongoing ischemia

Based on this ECG, the cath lab was emergently activated. The initial labs resulted around the time of this activation, notably the first troponin T was 0.09 ng/mL (elevated).

The patient was taken to cath where she was found to have 100% proximal LAD occlusion, as well as significant non-culprit lesions elsewhere including distal LCX occlusion.
Spider view, showing proximal LAD prior to DES placement, TIMI 0

The occlusion shown in another view

LAD with wire through lesion prior to stent placement

LAD after DES placement with return of flow, TIMI 3

The troponin T continued to trend upwards, peaking at 2.3 ng/mL (very high, consistent with OMI).

Daily ECGs were recorded that continued to display the progression of reperfusion:
ECG recorded 2 hours post PCI with DES placement

ECG record 1 day post PCI with DES placement

Comparison of this patient's reperfusion progression to an example progression (on either side of the image) of Wellens/reperfusion from Smith et al, Acute Coronary Syndromes, EM Clinics of North America 2006.

The patient had an uncomplicated course after PCI and was discharged two days after the procedure.

Teaching Points:
In the presence of a normal QRS (in particular, in the absence of QRS abnormalities such as LBBB or LVH, the combination of STE in V1 and STD in V5 and V6 is very specific for septal transmural ischemia.

The value of repeat ECGs cannot be overstated. While the initial ECG in this case could have been identified as highly concerning by expert interpretation, repeat ECG solidified the diagnosis and was the reason for emergent PCI in this case. It is our opinion through many case reviews that repeat ECGs allow non-experts to achieve very good care for patients.

It is controversial whether a reperfused Occlusion MI should be emergently cathed, or whether they can be maximally medicated and carefully observed for the first hint of reocclusion. In our experience these patients have a significant rate of very short-term reocclusion, and therefore we believe on a population level that the overall outcomes would be better with emergent cath for this very high risk group. Many of these patients can “get away” with a few hours delay for an “urgent” cath, but some will reocclude and die in those few hours which may have been prevented by emergent cath.

Here is another LAD occlusion that had STE in V1 and STD in V5, V6:

A Very Subtle LAD Occlusion....T-wave in V1??

See our recent post regarding a recent randomized trial for transient STEMI:

Timing of revascularization in patients with transient STEMI: a randomized clinical trial

A Very Subtle LAD Occlusion....T-wave in V1??


  1. Wasn't there an ST elevation in avr in the first ecg indicating proximal lad occlusion?

    1. That may be seen in diffuse subendocardial ischemia (which may be LAD ischemia, but not occlusion, and which is reciprocal to widespread ST depression). In this case, there is ST elevation in right precordial leads V1-V3, which is typical of occlusion. The ST elevation appears to be a normal amount, but normal ST elevation is never associated with ST depression in other precordial leads (in this case, V5 and V6)

  2. Wellens syndrome?

    1. Indeed, but in this case, the occlusion EKG was recorded (the EKG during pain, with upright Ts).


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