Wednesday, October 14, 2020

Dynamic ST Elevation

A 70-something male with 3 CAD risk factors developed intermittent left sided chest discomfort 29 hours prior.  It began again 2 hours prior to first ECG.  Pain was 7/10 radiating to left arm with SOB and diaphoresis.

Here was the prehospital ECG

Sinus rhythm. Slight ST depression in I, aVL, and V4-V6, consistent with ischemia.

These medics were smart and well trained, and so they recorded another several minutes later due to persistent symptoms:
New ST Elevation in V4-V6, with obliteration of the S-waves.
There is also new subtle STE in inferior leads

They arrived in the ED and another ECG was recorded:

Chest pain still 7/10
Now there remains the STE in inferior leads and STD in I and aVL.  This alone would be enough to call inferior OMI even without the previous diagnostic prehospital ECG.
STD in V2
Hyperacute T-waves remain in V4-V6 but the STE is resolved.

This is diagnostic of an infero-postero-lateral OMI (that is also a STEMI, or STEMI (+) OMI).  It is reperfusing and re-occluding.  Thus, it can be called a "Transient STEMI"

The cath lab was activated.

The BP was 194/83. A nitro drip started at 50 mcg/min.  BP then 140/67 and pain improved from 7 to 3/10.

The interventionalist was happy to take the patient to the cath lab, but he mysteriously commented that "there is going to be nothing there."

The initial high sensitivity troponin I returned at 83 ng/L (99th %-ile URL = 34 ng/L for men; LoD = 4 ng/L).  Depending on the population, this level by itself (without any clinical or ECG data), has a PPV for Acute MI of anywhere from 30-80%.  With this patient's presentation (pretest probability), the PPV of the troponin alone is at least 80%.


The LAD has 70% disease in the mid segment of the vessel, involving the LADD2 origin

RCA: RCA has Normal take off.

The Mid segment of the RCA has 90% disease.

Culprit is 90% occlusion of the LCX-OM1 (1st Obtuse Marginal).

They put a stent in the OM1, and left the other disease to be treated later.

Here is the post PCI ECG:


Technically difficult study

The estimated left ventricular ejection fraction is 60%.

Normal estimated left ventricular ejection fraction .

No wall motion abnormality probable.

Peak troponin = 6240 ng/L.  This is not a terribly high troponin and the peak troponin of STEMI using contemporary troponin is usually above 10 ng/mL (roughly equivalent to 10,000 ng/L in the high sensitivity assay).

Because it was a transient STEMI, the infarct size was small, leaving no discernable wall motion abnormality.

Later, the patient went back to have the other arteries stented.  (There is new data showing that for some patients, stenting all the arteries at the initial angiography results in outcomes at least as good as delayed stenting.  In this case, stenting was only delayed by a couple days.)

Learning Points

1. Should a transient STEMI go to the cath lab emergently?  I would argue yes. See this post: Timing of revascularization in patients with transient STEMI: a randomized clinical trial

2. Rapid reperfusion may leave no wall motion abnormality. (Although in this case it was a technically limited study)

3. STEMI frequently has open artery at angiography.  At least 16% of patients with STEMI at presentation have TIMI-3 flow just minutes later at emergent angiography (many more have an open artery with less than TIMI-3 flow). 

Stone GW et al. Normal flow (TIMI-3) before mechanical reperfusion therapy is an independent determinant of survival in acute myocardial infarction. Circulation 2001;104(6):636–41.

4. Most (70%) STEMI have peak Abbott contemporary troponin I > 10 ng/mL, but we don't have data on high sensitivity troponin (ng/L)


MY Comment by KEN GRAUER, MD (10/14/2020):


Insightful case showing 4 serial tracings during evolution of a STEMI in which the “culprit” artery was reperfusing and re-occluding. Although I limit my comments below to the initial EMS ECG that was done in the field ( = ECG #1) — I wanted to first reemphasize some important points brought out by Dr. Smith’s discussion above.

  • The History is essential! The patient in this case was an older man with risk factors who described, “intermittent left-sided chest discomfort” over more than 1 day — with recurrence of this chest discomfort 2 hours prior to ECG #1. Awareness of this history greatly enhanced my insight at the time I interpreted this 1st ECG.
  • Not uncommonly — the “culprit” artery may suddenly occlude — then spontaneously reopen (sometimes prior to the patient seeking medical attention) — and on occasion (such as in today’s case) — continue to open and close spontaneously a number of times. Interpreting the serial ECGs in today’s case, in association with this patient’s History  tells us this is what was happening.
  • Even a “recent” STEMI may fail to show ST elevation at the time the ECG you are looking at was done IF — prior to this, there has been an ongoing process of intermittent occlusion, followed by spontaneous reopening.
  • Depending on WHEN the cath was done during the course of a “transient” STEMI — the “culprit” artery may not always still be occluded at the time of cardiac catheterization.
  • It may be difficult to determine the “culprit artery” from the initial ECG if the patient has multi-vessel disease (as did the patient in today’s case). In such instances when ECG findings may not be localized — the indication for cath may be cardiac chest pain with ischemic findings on ECG, even if no specific “culprit artery” is suggested on the ECG.

With this as introduction — Please TAKE another LOOK at the initial ECG that was done in today’s case ( = ECG #1 in Figure-1).

  • Given the history in today's case — WHY is this initial ECG so concerning?
  • HOW MANY leads in ECG #1 show abnormalities?

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

MY Thoughts on ECG #1: The rhythm is sinus bradycardia at ~55/minute. All intervals (PR, QRS, QTc) are normal. The axis is leftward at about -20 degrees. There is no chamber enlargement. Regarding Q-R-S-T Changes:

  • There is a small, narrow Q wave of uncertain significance in lead aVL. There are QS complexes in leads V1 and V2.
  • R Wave Progression  R waves develop appropriately after the QS complexes in leads V1,V2 — with transition (where R wave height surpasses S wave depth) occurring normally, seen here between leads V3-to-V4.
  • NOTE: The finding of a QS complex in lead V1, or even in both leads V1 and V2 does not by itself necessarily mean that there have been anterior (or anteroseptal) infarction. A majority of patients with this finding will not have had anterior infarction. It is only when patients with a narrow QRS and no LVH have a QS complex in leads V1, V2 and V3 — that prior anterior (or anteroseptal) infarction becomes very likely.

Assessment of ST-T Wave Morphology in ECG #1: In the context of today’s patient (who presents with chest pain) — lots of leads show ST-T wave abnormalities in ECG #1. These ST-T wave abnormalities include:

  • ST straightening in multiple leads (horizontal RED lines in Figure-2).
  • ST segment coving, with slight elevation in lead V1.
  • Abrupt angulation between the straight ST segments and the ascent of T waves in leads V3V4V5 and V6 (RED lines).
  • T waves that look more voluminous than they should be, compared to R wave amplitude in the same lead. This is especially true for the T waves in leads II, V2 and V3 — and probably also for the T waves in leads V4V5V6.

My Impression of ECG #1: Many of the ST-T wave changes described above are subtle. That said — ST-T wave abnormalities highlighted by the RED lines in Figure-2 are seen in no less than 11 of 12 leads!

  • In isolation — the ST-T wave changes in leads I, III, aVL, aVF and V1 in a patient without acute symptoms would probably not prompt concern.
  • And, ST segment straightening with angulation at the onset of the T wave is often a nonspecific finding that does not necessarily reflect acute ischemia.
  • But, in the context of an older patient with risk factors who develops new chest pain — I interpreted the above-described T waves as hyperacute until proven otherwise.

BOTTOM Line: Frank ST elevation that confirmed the diagnosis of acute STEMI was seen in the 2nd EMS ECG (shown above) in today’s case. But the point to emphasize is that even without this 2nd ECG — the acute ischemic (hyperacute) ECG findings I describe for ECG #1, in conjunction with the history of ongoing chest pain and ST-T wave abnormalities that are seen in no less than 11/12 leads — should prompt suspicion of recent OMIand provide clear indication for prompt cath.

Figure-2: I’ve labeled abnormal ST-T wave findings in ECG #1 (See text).


  1. I beg to differ with Ken when he says that the first ecg represents OMI and even without the 2nd ecg showing at elevation, is enough indication for emergency cath. The changes on the first ecg are compatible with Nsteacs and can be managed medically in my opinion. If patient symptoms do not improve or he has arrhythmia, hemodynamics instability or grace risk score>140,he may be subjected to emergency cath study.

    1. Hi Subhasish. I am happy to respectfully agree to disagree with you. Let me respond by reproducing the specific wording that I used for my BOTTOM Line in My Comment above = “Frank ST elevation that confirmed the diagnosis of acute STEMI was seen in the 2nd EMS ECG (shown above) in today’s case. But the point to emphasize is that even without this 2nd ECG — the acute ischemic (hyperacute) ECG findings I describe for ECG #1, in conjunction with the history of ongoing chest pain and ST-T wave abnormalities that are seen in no less than 11/12 leads — should PROMPT SUSPICION of recent OMI, and provide clear indication for prompt cath.”

      So — this 1st ECG by itself is of course not a STEMI — since there is no ST elevation. But as we’ve repeatedly stated (and demonstrated) on Dr. Smith’s ECG Blog — dependence on strict “STEMI-criteria” will miss over 25% of OMIs (and many of those events labeled as “NSTEMIs” turn out to also be OMIs). The history is KEY to today’s case — the ST-T wave picture in lead V3 of ECG #1 instantly tells us that these may be hyperacute changes — and in that context RED lines in my Figure-2 show no less than 11/12 leads with abnormalities — which in a patient with worrisome new and ongoing chest pain, I think has to be interpreted as suspicious for recent (perhaps very recent) OMI — in which case prompt cath with reperfusion may save significant myocardium (and sometimes, as per other cases we’ve shown) may be lifesaving.

  2. agree with you Ken. but i certainly can see what Dr Singh is saying. ecg 1 might be a quite difficult sell to many cardiologists. but yes there are subtle abnormalities in multiple leads(11 of the 12), in a 70-y.o. with CP, dyspnea, pain down the left arm, and diaphortic.
    but as the bible (or other good books) say, one ecg begets another, so that even the cardiologist might be convinced by ecg 2.
    thank all three of you, including our friend and colleague in Pondicherry, India.

    tom fiero, ED doc, merced, california.

    1. THANKS Tom. I agree that there will be times in which a 2nd (and/or 3rd or 4th) ECG will needed in order to convince the cardiology team you are working with that prompt cath is needed. As always, do what needs to be done (ie, stat Echo, serial troponins, frequent repeat ECGs, more than 1 phone call … ) to get the right treatment for your patient. That said — we should continue to strive for optimal treatment — which in a patient with ONGOING new and severe chest pain AND ST-T wave changes in multiple leads including some hyperacute changes means that “this should be enough” to justify prompt cath.


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