The ECG in Figure-1 was obtained from a patient who presented to the ED (Emergency Department) with typical CP (Chest Pain).
QUESTIONS:
- Given this brief history — How would you interpret this ECG?
- What is in your differential diagnosis?
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| Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
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MY Thoughts on this CASE:
The history in this patient who presented to the ED with typical CP is clearly worrisome — and immediately places this patient in a higher-risk group for having an acute cardiac event. This places the "burden of proof" on us as providers to rule out an acute event — rather than the other way around (ie, We need to assume the abnormal findings on this ECG represent an acute MI until we can prove otherwise!).
Looking at today’s initial ECG in Figure-1:
- The rhythm in ECG #1 is sinus at ~80/minute. All intervals (PR,QRS,QTc) and the axis are normal.
- There are deep S waves in anterior leads V2 and V3. This may represent LVH (Left Ventricular Hypertrophy).
- The principal concern in this patient with new CP are the tall T waves with ST elevation in leads V2 and V3.
- PEARL #1: When LVH is manifest on ECG by the presence of deep anterior S waves — then LV "strain" from LVH with resultant anterior ST elevation (and not from acute infarction) may be seen in these same anterior leads!
Consider the ECG in Figure-2 — which I’ve taken from ECG Blog #461:
- The BLUE arrows in Figure-2 clearly highlight significant ST elevation. However, this ST elevation is not the result of acute infarction. Instead — this patient turned out to have marked LVH without any evidence for acute ischemia or infarction (Note the very deep S waves in leads V2,V3).
- Note within the RED insert in Figure-2 how the mirror-image of the ST-T elevation in these anterior leads — looks exactly like the typical ECG picture that we are used to seeing when LV “strain” is present in the lateral chest leads, as it most commonly is.
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| Figure-2: Tracing from my ECG Blog #461 — in which anterior ST elevation was not because of acute MI, but instead was solely the result of LV "strain" in a patient with marked LVH! |
Take another LOOK at today’s initial ECG — that I’ve reproduced in Figure-3. Keep in mind that this patient presented to the ED for new CP.
- As noted earlier — there are deep S waves in leads V2,V3.
QUESTIONS:
- Is the ST elevation and the tall T waves that we see in these anterior leads the result of LV “strain” — or — Does it seem like these ST-T wave changes may be more than what we might expect from simple LVH?
- In view of this patient’s CP — Is there anything we can do? (ie, to help distinguish if the anterior lead ST-T wave changes in Figure-1 are the result of LV “strain? — or acute ischemia? — or, of both LV “strain” + acute ischemia?).
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| Figure-3: Today’s initial ECG — that I’ve reproduced from Figure-1. |
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Confession: When I first saw today’s case — I was not at all certain regarding my impression for distinguishing between LV “strain” vs acute ischemia.
- Instead — I saw features consistent with LVH (ie, the deep S waves in leads V2,V3) — and — features consistent with acute ischemic ST elevation.
For clarity in Figure-4 — I’ve labeled ECG findings prompting my concern:
- PEARL #2: The concept of “proportionality” is KEY. While fully aware from clinical examples such as the case I illustrate above in Figure-2 — T wave amplitude in leads V2,V3 in Figure-3 "looks" disproportionately increased (both of these T waves rising ~10 mm above the baseline). The base of these T waves also “looks” wider-than-I-would-expect from simple LVH.
- To Emphasize: I have no numerical numbers for telling me the “accepted size” of T waves that would be consistent with LV “strain” from LVH. Instead — I rely on “pattern recognition” that my “eye” instantly recognizes from the experience of seeing countless cases. Even then — I was not certain of my suspicion from pattern recognition alone.
- That said — In support of my suspicion that the T waves in leads V2,V3 are hyperacute (and potentially indicative of acute ongoing infarction) — was the following: i) The clinical setting (Today’s patient presented with new CP); — ii) Neighboring leads V1 and V4 show subtle-but-real ST segment straighteing (slanted RED lines in these leads in Figure-4); — and, iii) Subtle ST segment flattening (if not slight ST depression) is seen in lateral lead V6 (BLUE arrow in this lead) — potentially consistent with an early Precordial "Swirl" pattern (See ECG Blog #380 — for review of Precordial Swirl).
- P.S.: Limb lead findings in ECG #1 did show some ST segment flattening — but I interpreted this as nondiagnostic. However, the above noted chest lead findings were enough to raise my index of suspicion.
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| Figure-4: I've labeled the initial ECG. |
PEARL #3: The clinical reality is that we will not always be able to confirm our clinical suspicion as to whether or not a patient's symptoms are indicative of acute ongoing infarction from a single initial ECG. Fortunately — there are some simple, routine actions that will often very quickly provide a definitive answer. Among these actions are the following:
- i) Check Troponin. In 2026 — Patients presenting to an emergency facility for new CP will almost automatically have a serum Troponin assay immediately drawn. Initial results are often forthcoming within 1 hour in an active ED. Any degree of Troponin elevation in a patient with new worrisome symptoms is significant (and may of itself be indication for prompt cath — even with a nondiagnostic ECG).
- KEY Point: Although any elevation of Troponin is significant in a patient with new worrisome CP — Keep in mind that an initial normal hs-Troponin does not rule out acute infarction! (See Pearls #3,4,5 in ECG Blog #392 — for more on the fine points regarding use of serum Troponin levels).
- ii) Look for a prior ECG on your patient. Perhaps the fastest and easiest way to determine if seemingly nondiagnostic ECG findings are "new" (therefore indicative of a new acute change until proven otherwise) — is to compare the initial ECG with a baseline tracing on the patient.
- iii) Do bedside Echo — looking for a localized wall motion abnormality. Interpreting bedside Echo for a wall motion abnormality can be tricky — and requires a skilled operator. But if your patient with new CP manifests a localized wall motion abnormality — this is highly suggestive of acute ongoing infarction. (NOTE: If the Echo is normal — but your patient was not have CP at the time the Echo was done — this does not rule out acute infarction).
- iv) Repeat the ECG within a short period of time (I favor repeating the ECG in a patient like the one in today's case within 10-to-20 minutes!). It is often surprising how quickly (and dramaticallly) a non-diagnostic initial ECG may change within a very few minutes!
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The Repeat ECG ...
Providers on the case "read my mind". They were suspicious of an ongoing acute event from the history and initial ECG — but could not at that point convince the interventionist.
- A prior tracing was not readily available for comparison.
- Providers repeated the ECG within 15 minutes.
To facilitate comparison in Figure-5 — I've put the initial ECG next to the repeat ECG done just 15 minutes later.
- To no one's surprise — Cardiac catheterization was immediately arranged on seeing the repeat ECG.
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| Figure-5: Comparison between today's 2 ECGs. |
PEARL #4: Clinicians sometimes wait much longer than is needed to repeat an initial non-diagnostic ECG. Especially when CP is ongoing — the dynamic ST-T wave changes that are obvious in Figure-5 occurred within 15 minutes!
- There is no need to wait longer than this to repeat the initial ECG.
- And if you are still concerned by the history — but the 1st repeat ECG remains non-diagnostic — Have a low threshold to continue repeating frequent ECGs until such time that you can feel comfortable with a definitive diagnosis.
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CASE Conclusion:
- Unfortunately — I do not have further follow-up on this case.
- That said — the cause of the serial ECGs in Figure-5 is virtually certain to be acute proximal LAD occlusion.
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Acknowledgment: My appreciation to Tayfun Anil Demir (from Antalya, Turkey) for the case and this tracing.
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ECG Blog #380 - Precordial "Swirl"
ECG Blog #380 — What is "Swirl"?
https://ecg-interpretation.blogspot.com/2023/05/ecg-380-what-is-swirl-metodo.html
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The ECG in Figure-1 — was obtained from an older woman with persistent CP (Chest Pain) over the previous day. Her symptoms lessened after Nitroglycerin — so the decision was made not to activate the cath lab. Do YOU agree with this decision?
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| Figure-1: The initial ECG in today's case. |
MY Thoughts on the ECG in Figure-1:
In a patient with CP that had been persistent over the previous day (until Nitroglycerin was given) — the initial ECG shown in Figure-1 is extremely worrisome. - The rhythm is sinus. Intervals (PR, QRS and the QTc) and the frontal plane axis are normal.
- Voltage for LVH is satisfied — at least by Peguero Criteria (Sum of deepest S in any chest lead + S in V4 ≥23 mm in a woman — as discussed in ECG Blog #73).
Regarding Q-R-S-T Wave Changes:
- Q Waves — None are seen.
- R Wave Progression — Transition (where the R wave becomes taller than the S wave is deep) is slightly delayed, occurring between leads V4-to-V5. That said — R wave amplitude is of reasonable size in all anterior leads (with slight reduction in R wave size from V2-to-V3 probably the result of lead placement).
The most significant abnormalities relate to ST-T Wave Changes:
- In the Limb Leads — There is nonspecific ST-T wave flattening, with slight ST depression in multiple leads (ie, in leads I,II,III,aVF).
- In the Chest Leads — Assessment for ST elevation in the anterior leads is especially challenging in ECG #1. This is because there is normally a small amount of upward-sloping ST elevation in leads V2 and V3. That said — in a patient with CP, the amount of ST elevation in leads V2 and V3 looks excessive to me, in association with ST-T waves that look potentially hyperacute. Thus, despite satisfying voltage criteria for LVH — considering the depth of the S waves in leads V2,V3 — the ST-T waves in these leads still look a little bit taller, fatter-at-their-peak and wider-at-their-base than I would expect them to be.
- Support that the ST-T waves in leads V2,V3 are likely to be abnormal — is forthcoming from the appearance of the ST-T wave in lead V1. In the absence of a deep S wave in lead V1 — it is uncommon to see ST elevation in this lead. It is simply not normal to see a full 1 mm of ST elevation in lead V1 (as we do in Figure-1) — especially in view of the ST segment straightening that is present in this lead.
- PEARL #1: The above noted findings in leads V1,V2,V3 are subtle! It is for this reason that I'll emphasize that the one lead in ECG #1 that indisputably manifests an abnormal ST-T wave is lead V6. In a patient with new and persistent CP — it is never normal to see the amount of flat ST depression that is present in lead V6. Abnormal ST segment flattening and depression is also seen in neighboring lead V5, but not nearly as marked as in lead V6.
- KEY Point: It is the fact that I know the flat ST depression in lead V6 is abnormal in a patient with persistent CP — that tells me the ST-T waves in leads V1,2,3 also have to be assumed abnormal until proven otherwise!
BOTTOM Line: The patient in today's case is an older woman who presents with a 1-day history of new and persistent CP. Her initial ECG should be interpreted as highly suggestive of acute proximal LAD occlusion until proven otherwise.
- NEW Concept: In a patient with CP — the ECG findings of anterior lead ST elevation, in association with lateral chest lead ST depression — is consistent with the pattern of Precordial "Swirl" (that I discuss below).
Continuation of Today's CASE:
A prior ECG on today's patient (done ~5 years earlier) was found — and is shown in comparison with the initial ECG in Figure-2. - Does this previous tracing strengthen our impression about this patient's initial ECG?
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| Figure-2: Comparison of the initial ECG in today's case — with a prior ECG done ~5 years earlier. What do we learn from reviewing this previous ECG? |
Comparison of ECG #1 and ECG #2:
IF there was any doubt about whether the ECG findings in today's tracing (ie, in ECG #1) are acute — it should have vanished the moment the prior ECG in Figure-2 was found!
- NOTE: It's important to correlate ongoing circumstances at the time that a prior tracing was done (ie, Was the patient stable and asymptomatic — or were they having chest pain, an exacerbation of heart failure, or some other ongoing process at the time the prior ECG was recorded?). This point is particularly relevant regarding ECG #2 — because sinus tachycardia is seen on this earlier ECG. In addition — there were more prominent anteroseptal forces on this earlier tracing (ie, in the form of an R wave = S wave in lead V1, with similar-looking equiphasic QRS complexes in leads V2-thru-V5).
- The above said — there previously was no indication of any ST elevation, or of any potentially hyperacute ST-T waves in the anterior leads of ECG #2 — nor was the distinct, flat ST depression in lead V6 present in this prior ECG! These differences between the 2 tracings in Figure-1 strongly support our suspicion that the ST-T wave changes in ECG #1 have to be interpreted as acute until proven otherwise!
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What is Precordial Swirl?
In the October 15, 2022 post of Dr. Smith's ECG Blog — Drs. Smith and Meyers introduce the colorfully descriptive term known as Precordial Swirl — as an intriguing ECG sign that facilitates recognition of a unique ECG pattern strongly suggestive of a very proximal site of acute LAD occlusion (usually proximal to the 1st septal perforator) — with resultant septal ischemia, in addition to anterior wall and apical involvement.
PEARL #2: In the setting of acute LAD OMI (Occlusion-based MI ) — the pattern of Precordial Swirl is recognized by the finding of ST elevation in leads V1 and aVR — and — reciprocal ST depression in leads V5 and V6.
- When considering Precordial Swirl — I like to focus on the ST-T wave appearance in leads V1 and V6.
- Although 1-2 mm of upsloping ST elevation is commonly (and normally) seen in anterior leads V2 and V3 — most of the time we do not see ST elevation in lead V1 (or if we do — it is minimal!). Therefore — I become immediately suspicious of "Precordial Swirl" whenever there is suggestion of LAD OMI — and — in addition, lead V1 looks different than expected!
- NOTE: Sometimes recognition that lead V1 looks "different-than-expected" — is only forthcoming after realizing that lead V2 is clearly abnormal.
In Figure-3 — I've selected 6 sets of V1,V2 leads from the series of tracings shown by Drs. Smith and Meyers in their October 15, 2022 post on Precordial Swirl.
- Although admittedly subtle — the ST segment coving with slight but disproportionate ST elevation in lead V1 of A, B and C in Figure-3 is clearly an abnormal appearance for the ST segment in lead V1. In association with neighboring chest leads suggestive of acute LAD OMI — this picture should raise suspicion of Precordial Swirl.
- Example F in Figure-3 is more subtle — because the S wave in lead V1 is deeper. That said — this coved shape of ST elevation in lead V1 of F should still raise suspicion in a patient with new symptoms.
- The ST-T wave segment in lead V1 of example D — closely resembles the "shape" of LV strain in an anterior lead from a patient with LVH. However, the S wave in example D — is not at all deep in either lead V1 or V2 — which in a patient with chest pain should strongly suggest the possibility of Precordial Swirl.
- The ST-T wave shape in lead V1 of example E also appears to be subtly abnormal. Support that this finding is real — is forthcoming from our impression that the T wave in neighboring lead V2 looks more peaked than expected — which in a patient with new symptoms, should strengthen our suspicion of a disproportionately positive T wave in lead V1.
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| Figure-3: Selected sets of V1,V2 leads from the examples of Precordial Swirl provided in the October 15, 2022 post in Dr. Smith's ECG Blog. |
NOTE: It's EASY to get fooled by LVH! This is because LV "strain" with LVH is sometimes more manifest in anterior rather than lateral chest leads — in which case there may be anterior lead ST elevation (ie, the reciprocal of lateral lead ST-T wave depression). The history and associated deep anterior S waves (ie, the reciprocal of tall lateral lead R waves) will suggest LVH rather than Precordial Swirl (See ECG Blog #254 and My Comment at the bottom of the page in the February 6, 2020 and June 20, 2020 posts in Dr. Smith's ECG Blog).
- For additional examples that illustrate this concept of "proportionality" (regarding relative size of ST-T wave deviations compared to QRS amplitude in the respective lead) — Check out the additional examples of LVH that mimic Precordial Swirl which are provided in the October 15, 2022 post in Dr. Smith's ECG Blog.
Precordial Swirl Appearance in Lead V6:
The final component for diagnosing Precordial Swirl — is to see reciprocal ST depression at least in lead V6 (if not also in lead V5):
- Once I've decided that the tracing I am looking at is not an example of LVH that mimics Precordial Swirl — I focus my attention on the shape of the ST-T wave in lead V6.
- I've reviewed my approach to the ECG diagnosis of LVH often (See ECG Blog #245 — among many other posts). In Figure-4 — I've reproduced from the above cited June 20, 2020 post my schematic illustration of the ST-T wave appearance that may be seen in one or more lateral leads for demonstrating LV "strain".
PEARL #3: In general, the shape of ST-T wave depression in lead V6 with Precordial Swirl does not look like either C or D in Figure-4. Instead — the depressed ST segment tends to be flatter. Therefore — THINK Precordial Swirl in a patient with new symptoms IF you see:
- Other signs suggestive of acute LAD OMI.
- The ST-T wave in lead V1 looking "different-than-expected".
- A relatively flattened appearance to the depressed ST segment in at least lead V6 (if not also in lead V5).
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| Figure-4: Schematic illustration and description of LV "strain" on ECG. |
CASE Follow-Up:
Cardiac cath was performed on today's patient — and complete proximal LAD occlusion was found.
- In Figure-5 — I compare the post-PCI ECG with the initial tracing in today's case.
FINAL QUESTION:
- How would YOU interpret the post-PCI tracing?
- Based on the ECGs in Figure-5 — Did PCI succeed in opening the "culprit" artery?
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| Figure-5: Comparison of the initial ECG in today's case — with a post-PCI tracing. Was PCI successful? |
Interpretation of the Post-PCI ECG:
There is significant baseline artifact in the limb leads of ECG #3. Despite this artifact — this tracing is still interpretable.
- The frontal plane axis in both of the ECGs in Figure-5 is similar — which means that lead-to-lead comparison will be valid. There are no acute changes in Limb Lead ST-T wave appearance.
In contrast — the Chest Leads show that there has been marked evolution of this patient’s anterior MI:
- There has been significant loss of anterior R wave forces in ECG #3 since the initial ECG. Specifically — the R wave in lead V2 is now smaller — with further loss of R wave from V2-to-V3 — and disappearance of the initial R wave in lead V4 (to form a QS complex in this lead). This loss of anterior forces is consistent with myocardial injury from the large infarction.
- PEARL #4: Note change (deepening) of the S waves in leads V3,V4 of ECG #3. This is not indicative of LVH — but instead results from the loss of anterior forces, that now leaves posterior forces “unopposed” (with resultant deeper anterior S waves).
- KEY POINT: It’s good to be aware that QRS amplitudes may undergo hard-to-predict amplitude changes over the course of acute MI evolution.
Chest Leads also show marked changes in ST-T wave appearance:
- Compared to ECG #1 — there is clearly more ST elevation in leads V2,V3 of ECG #3 — with new ST elevation now present in lead V4.
- That said — an even more striking change in ST-T wave appearance — is the very steep decline of the descending limb of the T wave in leads V2,V3,V4!
- PEARL #5: It's important to appreciate that although this steep T wave decline appearance looks like the anterior T waves seen in Wellens' Syndrome — this is not Wellens' Syndrome, because infarction has already taken place (whereas Wellens' Syndrome occurs in the absence of CP — and serves as an ECG warning sign that appears before a large infarction with QS waves has taken place — as discussed in ECG Blog #254).
- Finally — The ST-T wave appearance in leads V5,V6 of the post-PCI tracing ( = ECG #3) — is very different than it was in the initial ECG. Instead of ST segment flattening and depression (that was seen in ECG #1 ) — there is now ST segment coving in lead V5 (a continuation of the ST coving seen in neighboring lead V4, albeit without any ST elevation) — and, there is no longer ST depression in lead V6.
PEARL #6: One of the KEY learning points of today’s case — is the importance of correlating ECG findings with the clinical situation. The more serial tracings recorded (and the better the notation of whether each serial tracing was associated with chest pain — and if so, relative severity of that CP) — the easier it becomes to correlate clinical events.
- For example — We would not normally expect to see more ST elevation after PCI (as we do in ECG #3) — unless reperfusion of the "culprit" artery with the procedure was not successful — or — unless additional ECGs done prior to PCI showed additional ST elevation occurred before angioplasty opened the occluded vessel. In today's case — presumably this latter possibility is what occurred — in which case (assuming no CP after PCI) — the steep T wave descent with deepening T wave inversion in the anterior chest leads of ECG #3 presumably reflects coronary reperfusion.
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Acknowledgment: My appreciation to Kim Jiwon (from Seoul, Korea) for the case and this tracing.
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Related ECG Blog Posts to Today’s Case:
- ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
- ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery — as well as the importance of the term, "OMI" ( = Occlusion-based MI) as an improvement from the outdated STEMI paradigm.
- ECG Blog #367 — for another example of acute LCx OMI.
- ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.
- ECG Blog #194 — AIVR as a sign that the "culprit" artery has reperfused.
- ECG Blog #260 and ECG Blog #292 — Reviews when a T wave is hyperacute — and the concept of "dynamic" ST-T wave changes.
- ECG Blog #230 — How to compare serial ECGs.
- ECG Blog #254 — What Wellens' Syndrome is and is not ...
- ECG Blog #337 — an OMI misdiagnosed as an NSTEMI ...
- ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
- ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
- ECG Blog #80 — reviews prediction of the "culprit" artery (with another case to illustrate the Mirror Test for diagnosis of acute Posterior MI).
- ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post).
- ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.
- ECG Blog #350 — regarding T Wave Imbalance in the Chest Leads.
- ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).
- ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
- The importance of the new OMI (vs the old STEMI) Paradigm — See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog.
- 20 Cases of Precordial Swirl (or "Look-Alikes" ) — Reviewed in the October 15, 2022 post of Dr. Smith's ECG Blog (including My Comment at the bottom of the page).
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ADDENDUM (5/24/2023):
Josep Serra Tarragon wrote me asking whether inverted U waves were present in the lateral chest leads of ECG #1. On taking another look — I have to agree with him that they are! (BLUE arrows in leads V4,V5,V6 — in Figure-6).
- There are 2 QRS complexes in simultaneously-recorded leads V4,V5,V6, in which we see the ST-T wave. I do not see inverted U waves clearly in the first QRS complex — but BLUE arrows that I have drawn into Figure-6 are certainly consistent with inverted U waves for the 2nd QRS complex.
- Inverted U waves are an uncommon, usually ignored phenomenon. That said — when present in the right clinical situation, they are an indicator of significant ischemia (Correale et al — Clin. Cardiol 27:674-677, 2004).
- Attention to negative U waves was first pointed out to me by Dr. Barney Marriott in the mid 1980s. Thereafter — I looked for negative U waves over a period of many years, but very rarely found them. Much of the time, there was simply too much "noise" on the tracing to be certain of their presence — or the heart rate was such that it was difficult to distinguish what was "real" inverted U wave vs terminal ST-T wave, baseline movement, or the next P wave.
- The mechanism for U wave inversion remains uncertain. Best theory is delayed repolarization of the His-Purkinje system.
- Bottom Line: The clinical setting in this Blog #380 is certainly consistent with ischemia. I believe Dr. Tarragon is correct that this is highlighted by the BLUE arrows in Figure-6.
- My THANKS to Dr. Tarragon for pointing this out!
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| Figure-6: I've added BLUE arrows to leads V4,V5,V6 of ECG #1 — to indicate inverted U waves. |
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