ECG Blog #350 — Severe CP; Not Much on ECG

The patient whose ECG is shown in Figure-1 — was seen in a rural office (not near to any hospital) — for chest pain.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• Is this tracing benign?

Figure-1: The initial ECG in today's case — which was obtained during severe chest pain! (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The rhythm in ECG #1 is sinus at ~70/minute. All intervals (PR, QRS, QTc) and the axis are normal. There is no clear evidence for chamber enlargement. 

Regarding Q-R-S-T Changes:

• Considering the small size of the QRS complex in lead III — the Q wave in this lead is wide and relatively large. No other Q waves are seen. 
• R wave progression — is normal, with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.

The most remarkable findings in Figure-1 relate to ST-T wave Changes:

• In the Limb Leads — there is nonspecific ST-T wave flattening in high-lateral leads I and aVL.
• Although there may be a tiny amount of ST elevation in lead III — the T wave is upright, and the ST-T waves in leads II and aVF look normal. Overall — ST-T wave changes in the limb leads do not look to be acute.

In the Chest Leads:

• There is slight, upward-sloping ST elevation in lead V2 and V3 — which of itself is not an abnormal finding (ie, Slight, upward-sloping ST elevation in these 2 anterior leads is a common and normal finding).
• That said — there is more than the minimal amount of ST elevation that may normally be seen in lead V1. Raising suspicion that the ST-T wave in lead V1 is significant — are the findings in lead V6 of: i) ST depression; and, ii) T wave "imbalance", with the positive T wave in lead V6 beings smaller than the upright T wave in lead V1 (as highlighted within the dotted BLUE rectangles in Figure-2 — discussed in detail below).
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• Finally — Although there is no ST segment elevation in leads V3 and V4 — the T waves in these leads are biphasic (initially positive — then terminally negative, as per the double RED arrows in Figure-2).

Figure-2: I've labeled KEY findings in the initial ECG (See text).

PEARL #1: When T waves in each of the chest leads are upright (as they are in Figure-2) — the T wave in lead V1 is usually not taller than the T wave in lead V6. This "Imbalance" of precordial T-waves is not seen very often — and in the “right” clinical setting, has been associated with recent OMI (Occlusion-based MI) from a LCx culprit artery (See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM).

• NOTE: This is not to say that tall, upright T waves in lead V1 might not sometimes be the result of a repolarization variant or a mirror-image reflection of LV “stain” that can sometimes be seen in anterior leads. Instead — it is simply to say that on occasion — I have found recognition of a tall, upright T wave in lead V1 that is clearly taller than the T wave in lead V6 to be a tip-off to an acute coronary syndrome that I might not otherwise have recognized (See ECG Blog #182 and My Comment at the bottom of the page in the June 1, 2022 post in Dr. Smith's ECG Blog — for an additional examples of this finding).
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• To Emphasize: As an isolated finding — I would not be certain of the significance of the ST-T wave appearance in lead V1. BUT in the clinical setting of this patient presenting to the office for chest pain with: i) ST depression and the smaller upright T wave in lead V6 — and — ii) Terminal negativity of the T waves in leads V3,V4 — my index of suspicion for a recent event was raised.

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The CASE Continues:

Given the patient's chest pain — and the above ECG findings in Figure-2 — the patient was immediately referred to cardiology. But because all symptoms soon resolved, and the patient lived far away — he decided to return home.

• The patient returned to the office the next day feeling "absolutely fine" — and requesting another ECG in hope of being given "a clean bill of health".

The repeat ECG (which was recorded ~17 hours after ECG #1) — is shown together with the initial ECG in Figure-3.

QUESTIONS:

• Given the above clinical context — How would YOU interpret the repeat ECG #2 that is shown in Figure-3?
• Can you explain WHY the ST-T wave findings in ECG #1 were so subtle — despite the presence of 8/10 chest pain?

Figure-3: Comparison between the initial ECG — and the repeat ECG obtained when the patient was pain-free. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECGs in Figure-3:

There has been a dramatic change in the appearance of ECG #2 — compared to ECG #1 that was obtained the day before!

• Other than minimal shallow T wave inversion in lead aVL of ECG #2 — there has been essentially no change in the limb leads. The relatively large Q wave in lead III is unchanged.
• In contrast — ST segments are now coved in all Chest Leads — with persistent ST elevation in leads V1,V2 — increased J-point ST depression in leads V4,V5,V6 — and new deep, symmetric T wave inversion in all chest leads.
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• In addition — it is important to NOTE: i) Lead V2 shows slight ST elevation with sharp descent of an initially upright T wave that evolves into terminal negativity; and, ii) Anterior R waves are preserved! — and, iii) The patient was without chest pain at the time ECG #2 was recorded!
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• IMPRESSION: The clinical picture and serial ECGs of this patient are diagnostic of Wellens' Syndrome! The deep T wave inversion across the chest leads represent reperfusion T waves from spontaneous reopening of a proximal LAD occlusion. That the LAD is now most probably still "open" — is supported by the fact that this patient's chest pain has not returned since the previous day. The additional fact that chest lead R wave amplitude has been preserved — is encouraging, and suggests that the amount of myocardial damage may be limited!

What is Wellens' Syndrome?

The clinical significance of Wellens' Syndrome — is that its recognition tells you that the patient has a high-grade LAD (Left Anterior Descending) coronary artery narrowing with presumably "hot" thrombus having high propensity to propagate and/or totally occlude the LAD at any point in time (including immediately). That said — Wellens' Syndrome remains a misunderstood and often misdiagnosed clinical entity. For clarity — Consider the KEY clinical and ECG features that establish the diagnosis of Wellens' Syndrome:

• There should be a history of prior chest pain that has resolved at the time the defining ECG is obtained.
• There should be no more than minimal (if any) troponin elevation. 
• There are no new infarction Q waves.
• There may be slight (but not marked) ST elevation in one or more of the chest leads.
• There is a characteristic biphasic T wave, with rapid T wave descent into terminal negativity in one or more of the chest leads (most often in lead V2 and/or V3 and/or V4). NOTE: This characteristic T wave picture is seen in lead V2 of ECG #2 (in Figure-3).

What Wellens' Syndrome is NOT:

Greatest misunderstanding relates to what Wellens' Syndrome is not! Avoidance of this misunderstanding is best accomplished by appreciating the pathophysiology of this syndrome. In essence — the characteristic biphasic T wave appearance with terminal negativity reflects a reperfusion T wave! The patient has recently had total LAD occlusion for a brief period of time — but has now spontaneously reperfused.

• The chest pain required for the definition of Wellens' Syndrome occurred at the time of coronary occlusion. But the reason the definition of Wellens' Syndrome requires the patient to be pain-free at the time the defining ECG is done — is that the "culprit" LAD lesion is now open. IF the "culprit" LAD lesion was still occluded — then rather than a warning of impending infarction (which is the purpose of promptly recognizing Wellens' Syndrome) — there would be ongoing acute infarction.
• There is no more than minimal (if any) troponin elevation — because the duration of coronary occlusion was so brief that no more than minimal myocardial damage resulted. IF there is greater troponin elevation — this implies that significant myocardial damage has already occurred (which by definition means that you are dealing with a completed infarction — and not with Wellens' Syndrome).
• For this same reason — there should not be new infarction Q (or QS) waves.
• There is no more than slight ST elevation — because Wellens' Syndrome is not a STEMI (ie, it is not an "ST Elevation" MI).
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• Instead — the characteristic biphasic T wave with rapid T wave descent into terminal negativity is an indication that there was brief total occlusion of the LAD, which has now reperfused. This ECG finding is a reperfusion T wave. It may look identical to the ST-T wave appearance after a STEMI with marked troponin elevation that has now reperfused (be this reperfusion spontaneous — or by treatment with PCI or thrombolytics).
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• Clinically — the risk posed by Wellens' Syndrome — is that it is proof that there has already been acute thrombotic occlusion of the LAD, albeit brief in duration and followed by spontaneous reopening of the vessel. But what spontaneously occluded and then reopened — is at high-risk of spontaneously occluding again (with no guarantee that there will again be spontaneous reopening the next time the vessel occludes).
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• CAVEAT: The diagnosis of Wellens' Syndrome should be made with caution (if at all) in a patient with marked LVH and ST-T wave changes of LV "strain". This is because the ECG finding of increased QRS amplitude that occurs in association with abrupt precordial transition from predominantly negative to predominantly positive QRS complexes — may result in an ST-T wave appearance identical to the biphasic T wave with terminal negativity characteristic of Wellens' changes (See ECG Blog #209 and Blog #254 and Blog #309 — for several examples of this "false positive" Wellens' appearance).
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• Please see the Audio Pearl and Figures-5 and -6 below in the ADDENDUM for more on Wellens' Syndrome

WHY then Were ST-T Findings so Subtle in ECG #1?

I initially found it surprising that despite the history of severe new chest pain (subjective severity score by the patient = 8/10) — the ECG findings in the initial tracing were relatively modest.

• The probable reason for the relatively modest ST-T wave findings in the initial tracing — is that ECG #1 presumably reflects a state of "pseudo-normalization". It is likely that minutes before ECG #1 was recorded — there was marked precordial lead ST elevation. IF the stenotic LAD had just spontaneously reopened near the time that ECG #1 was recorded — then elevated ST segments "on their way" toward developing deep T wave inversion might be nearly isoelectric, as they are in ECG #1.
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• PEARL #2: Development of subtle-but-real biphasic (up-down) T waves, as are seen in leads V4,V5 in ECG #1 (double RED arrows in Figure-2) — in a patient whose severe chest pain is rapidly resolving, may be the earliest sign of the characteristic T wave appearance seen in Wellens' Syndrome.
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• PEARL #3: As emphasized above — an essential criterion for the diagnosis of Wellens' Syndrome, is that the patient must be pain-free at the time that the defining ECG is recorded. But catching this "pain-free" state on ECG depends on when and how many ECGs are obtained! Although the patient in today's case was still having severe chest pain at the time ECG #1 was recorded — by the history provided above, this patient's chest pain resolved soon after ECG #1 was obtained — and the patient remained pain-free (at least until the time he returned to the office the next day to record ECG #2).
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• PEARL #4: The importance of promptly recognizing Wellens' Syndrome — is that this identifies a high-grade proximal LAD stenosis that has already undergone brief occlusion (with fortunate spontaneous reopening of the "culprit" LAD lesion). The problem is that the LAD may spontaneously reocclude — with no guarantee that it will spontaneously reopen again. Therefore — recognition of Wellens' Syndrome is indication for timely cath in the hope of preventing a longer-lasting occlusion that causes significant myocardial damage.

What did this Patient's Baseline ECG Show?

Support that the subtle ECG findings in the initial tracing were truly acute — was forthcoming once this patient's prior ECG became available.

• Compare the patient's baseline ECG (obtained several years earlier — at a time when he was asymptomatic) — with the initial ECG in today's case (Figure-4). WHAT do you see?

Figure-4: Comparison between the initial ECG — and the patient's baseline ECG obtained several years earlier. (To improve visualization — I've digitized the original ECG using PMcardio).

Comparison of the Baseline ECG with ECG #1:

• The inferior leads in the baseline ECG are virtually identical to the inferior leads in today's initial tracing. Note in Figure-4 — that the relatively large and wide Q wave in lead III is essentially unchanged. This confirms that this Q wave is not a new finding. Whether this Q wave in lead III represents an old inferior infarction vs an incidental insignificant finding is uncertain (ie, an isolated Q wave in lead III or lead aVF is not necessarily an abnormal finding).
• In high-lateral leads I and aVL — there is nonspecific ST-T wave flattening in ECG #1 that was not seen in the baseline tracing. 
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• In the Chest Leads — the T waves in leads V1-thru-V6 are all upright and normal in appearance. Note especially that the amplitude of the upright T wave in lead V6 of ECG #3 is clearly greater than that of the T wave in lead V1 (ie, There is no precordial lead T wave "imbalance" in the baseline tracing). 
• The amount of J-point ST elevation in lead V1 is more in ECG #1 — than it was in the baseline tracing.
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• BOTTOM Line: Availability of this patient's baseline ECG confirms that the above described subtle ECG findings in leads I,aVL; V1; V3,V4; and V6 in today's initial tracing — are all acute findings!

FINAL Follow-Up:

I unfortunately do not know details of the longterm course for today's patient. But the final diagnosis from this patient's hospital admission was "NSTEMI" (ie, Non-ST Elevation Myocardial Infarction) — so it is clear that recognition of Wellens' Syndrome was missed.

• Even without troponin confirmation — the clinical history in today's case, when correlated to this patient's serial ECGs is diagnostic of OMI (ie, of brief coronary occlusion from Wellens' Syndrome — followed by spontaneous reopening of the "culprit" LAD lesion).
• Optimal therapy would have included cardiac cath with PCI.

PEARL #5: A KEY "Take-Home" Point from today's case — is appreciation of the importance of correlating the specific timing of serial ECGs to symptom severity. It is because the course of an acute evolving cardiac event may be stuttering (ie, with spontaneous reperfusion — and then reclosure of the "culprit" artery — sometimes repeated multiple times until the eventual "final state" of the culprit vessel is reached) — that the true story may only be learned by this detailed correlation. For example:

• The relatively modest ST-T wave changes that are seen in ECG #1 of today's case (despite the presence of severe chest pain at that time) — make sense when this initial tracing is interpreted in light of the completely normal ST-T wave appearance in the baseline tracing — and — the subsequent deep, symmetric T wave inversion seen in ECG #2 at a time when the patient was pain-free. It is this correlation of symptoms and serial ECGs that allows definitive diagnosis of Wellens' Syndrome (with the occurrence of a transient OMI — instead of the "default" diagnosis of NSTEMI that was made by the hospital team).
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• For another example of this step-by-step correlation of serial ECGs with symptom severity — Check out ECG Blog #337.

PEARL #6: I close today's case with brief reference to a new concept known as "Precordial Swirl". This unique ECG pattern strongly suggests a very proximal site of LAD occlusion (usually proximal to the 1st septal perforator branch) — with resultant septal ischemia, in addition to anterior wall and apical involvement (Details in the October 15, 2022 post in Dr. Smith's ECG Blog).

• In the setting of acute LAD OMI — the finding of Precordial "Swirl" is recognized by ST elevation in leads V1 and aVR — and reciprocal ST depression in leads V5 and V6. 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!
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• NOTE: Sometimes recognition that lead V1 looks "different-than-expected" — is only forthcoming after realizing that lead V2 is clearly abnormal.

Rather than "precordial swirl" — today's initial tracing represents part of the evolution of Wellens' Syndrome. But note that there is abnormal ST elevation in lead V1 (which is clearly new compared to baseline ECG #3) — and — there is ST depression in lead V6 of ECG #1 (which also was not present in the baseline tracing) — and — we know from the history in today's case that transient LAD occlusion did occur.

• I suspect that IF we could have obtained an ECG a little bit before ECG #1 — that we would have seen anterior ST elevation with definitive ST-T wave findings consistent with "precordial swirl". 

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ADDENDUM (10/1/2021): In the following 2 Figures — I post written summary from my ECG-2014-ePub regarding Wellens’ Syndrome. 

• CLICK HERE — for a PDF of this 3-page file on Wellens’ Syndrome that appears in Figure-5 and Figure-6.

 

 

Figure-: Regarding Wellens’ Syndrome (from my ECG-2014-ePub).

Figure-6: Wellens’ Syndrome (Continued). 

—  — 

Today's ECG Media PEARL #26a (7:40 minutes Audio) — Reviews what Wellens' Syndrome is — and what it is not.

 

 

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Acknowledgment: My appreciation to Kianseng Ng and Chris Chow (from Malaysia) for the case and this tracing. 

• Credit to Kianseng Ng for coining the following quote: If the history is classical and the ECG is "normal" — then you probably missed something in the ECG.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).
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• ECG Blog #209 and ECG Blog #254 and ECG Blog #309 — Review cases of marked LVH that result in similar ST-T wave changes as may be seen with Wellens' Syndrome. 
• ECG Blog #245 — Reviews my approach to the ECG diagnosis of LVH (outlined in Figures-3 and -4, and the subject of Audio Pearl MP-59 in Blog #245).
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• ECG Blog #320 — Reviews acute OMI of the 1st or 2nd Diagonal (presenting as Wellens' Syndrome).
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• ECG Blog #326 — Reviews a case of Wellens' Syndrome that was missed.
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• ECG Blog #182 — and My Comment at the bottom of the page in the June 1, 2022 post in Dr. Smith's ECG Blog — show examples of T Wave Imbalance (ie, When the upright T in lead V1 is taller than the T in lead V6).
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• ECG Blog #337 — for Review of a case illustrating step-by-step clinical correlation between serial ECGs with symptom severity.
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• See the October 15, 2022 post (including My Comment at the bottom of the page) — for review and illustration of the concept of "Precordial Swirl" (due to proximal LAD OMI).