The ECG in Figure-1 — was obtained from a 65-year old man who was admitted to the hospital for unilateral weakness that began a number of days earlier. No chest pain. Hemodynamically stable. His stroke symptoms had stabilized at the time this ECG was recorded.
- In view of this clinical history — How would YOU interpret the ECG in Figure-1?
- Beyond-the-Core: What is T-QRS-D?
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| Figure-1: The initial ECG in today's case. (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 bradycardia at a rate just under 60/minute. All intervals (PR, QRS, QTc) are normal. The frontal plane axis is normal at +10 degrees. There is no chamber enlargement.
Regarding Q-R-S-T Changes:
- There are no significant Q waves. In leads III and aVF — we see the interesting phenomenon that a large and wide Q wave is present for the 3rd beat in these leads — but there is no Q wave for the 1st, 2nd and 4th beats in these leads. Instead — we see a multiphasic (ie, fragmented) complex with an initial positive deflection (r wave).
- Leads III and aVF "look up" at the heart from the perspective of the diaphragm — and are therefore subject on occasion to this type of variation in QRS morphology as a result of diaphragmatic motion. Clinically — I interpret this variation of QRS morphology that we see in these 2 leads of Figure-1 as indicative of no significant Q waves.
- Regarding R wave progression — Transition occurs early, with abrupt development of and all positive QRS complex as early as in lead V2.
- The most remarkable finding in ECG #1 — relates to the very tall and peaked T waves in the chest leads. These T waves tower over their respective R waves in leads V2 and V3. T waves remain disproportionately peaked in multiple other leads. For example — the T waves in limb leads II and aVF are almost twice the amplitude of the tiny R wave in these leads.
- In addition to T wave peaking — there is significant J-point ST elevation in multiple leads. This is most marked in leads V2 and V3 (attaining 3 mm!) — but is also considerable in leads V1 and V4, and present to a lesser extent in lead V5. Considering how tiny the QRS complex is in lead V1 — the ST segment is markedly elevated.
- Finally — U waves of uncertain significance are present in leads V2-thru-V5.
IMPRESSION:
Despite the absence of chest pain — the obvious concern regarding interpretation of ECG #1 — is whether these ST-T wave findings indicate a recent (and possibly still acutely ongoing) cardiac event:
- T waves in the chest leads resemble deWinter T waves in terms of their chest lead location — and the truly giant size that some of these T waves attain. In the original deWinter et al. NEJM description of this ECG finding (See ECG Blog #183 for details) — the tall, peaked T waves represented a "static pattern" indicative of high-grade LAD narrowing or occlusion that persisted until reperfusion was achieved. This might explain persistence of the ST-T wave changes seen in ECG #1, that was recorded almost a week after the onset of stroke symptoms.
- That said — the T wave picture in Figure-1 differed from that typically seen with deWinter T waves, in that there was no J-point ST depression in any of the leads with tall, peaked T waves. Instead — there was frank ST elevation in several of these leads.
- While serum K+ clearly needs to be checked — the ST-T wave appearance in Figure-1 was not particularly suggestive of hyperkalemia because of the ST elevation and the fact that the base of many of the peaked T waves was wider-than-expected for pure hyperkalemia.
- BOTTOM Line: Given the history of stroke symptoms beginning days before the ECG in Figure-1 was recorded — I found it difficult to know how to interpret this tracing (especially given the absence of chest pain). My best assessment was that the remarkable ST-T wave changes in ECG #1 represented deWinter-like T waves — with need to assume a recent (or still ongoing) acute cardiac event until proven otherwise.
A Final ECG Finding to Consider = T-QRS-D!
The concept of Terminal QRS Distortion (T-QRS-D) was unknown to me prior to my active participation as an Associate Editor in Dr. Smith's ECG Blog. Since then I've seen many patient cases that validate the clinical utility of this ECG finding promoted by Dr. Stephen Smith. When present — T-QRS-D may provide invaluable assistance for distinguishing between a repolarization variant vs acute OMI (ie, When true T-QRS-D is present in a patient with new symptoms — it is virtually diagnostic of acute OMI = Occlusion-based Myocardial Infarction). I illustrate the ECG finding of T-QRS-D below in Figure-2, which I've excerpted from My Comment in the November 14, 2019 post in Dr. Smith's ECG Blog. To review:
- T-QRS-D — is defined as the absence of both a J-wave and an S-wave in either lead V2 or lead V3. Although simple to define — this finding may be subtle! I fully acknowledge that it has taken me a while to become comfortable and confident in its recognition.
A picture is worth 1,000 words. I’ve taken the lead V3 examples in Figure-2 from previous cases posted on Dr. Smith’s ECG Blog:
- TOP in Figure-2 — Despite marked ST elevation in this lead V3 — this is not T-QRS-D, because there is well-defined J-point notching (BLUE arrow). This patient had a repolarization variant as the reason for ST elevation.
- BOTTOM in Figure-2 — This is T-QRS-D, because in this V3 lead there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline).
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Is there T-QRS-D in Figure-1?
Return to the initial ECG in today's case that was shown in Figure-1. Take another look at the ST-T waves in leads V2 and V3.
- Is T-QRS-D present in either of these leads?
ANSWER:
For clarity in Figure-3 — I've enlarged and have labeled the QRST complexes in leads V2 and V3 from today's tracing.
- In Lead V2: The ST elevation is not consistent with T-QRS-D — because there is prominent J-point notching (BLUE arrow).
- In Lead V3: There is T-QRS-D — because there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline).
PEARL #1: Overall in my experience — T-QRS-D is not a common finding among patients with acute coronary occlusion. That said — the potential value of this finding when it is present, is indisputable (as was seen in today's case when this ECG finding provided strong support in favor of recent infarction).
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| Figure-3: Blow-up view of the QRST complexes from leads V2 and V3 of today's tracing (See text). |
Putting It All Together:
While the absence of chest pain makes it difficult to determine the timing of events in today's case — the dramatic deWinter-like T waves in the chest leads of ECG #1, that occur in association with the T-QRS-D seen in lead V3 — suggested to me the need to presume recent LAD occlusion with resultant infarction until proven otherwise.
- Whether the infarction occurred before the stroke (perhaps causing the stroke) — is uncertain from the limited information known.
- That said — Today's case presumably provides an insightful example of a "silent" MI (ie, no chest pain) — with this MI only being recognized because the patient had a stroke (See ECG Blog #228).
CASE Follow-Up:
Unfortunately — Follow-up of today's case is somewhat limited. What can be said is: i) Serum K+ at the time the initial ECG was recorded was not elevated; and, ii) The ECG abnormalities described above were promptly recognized — so Cardiac Cath was performed. This revealed 3-vessel disease with the following specific findings:
- LMain (Left Main coronary artery) — atheromatous, but no significant lesion.
- LAD (Left Anterior Descending) — 80-90% tandem lesion, extending from the proximal LAD to the mid-LAD. TIMI Flow = Grade 2-to-3 (ie, partial flow) — suggesting that there had been obstruction (and that the proximal LAD had been the "culprit" artery) — but that this vessel had spontaneously reperfused. This tandem lesion was successfully stented.
- PEARL #2: This case illustrates how to presume the occurrence of a recent infarction despite the absence of 100% coronary occlusion at the time cardiac cath is performed. Clinical correlation of the timing of symptoms with troponin values and serial ECGs — together with appreciation of how commonly spontaneous reperfusion occurs — are KEY for making this determination.
- LCx (Left Circumflex) — 70-80% tandem lesion, extending from the proximal LCx to the mid-part of this vessel. Coronary flow was normal (ie, TIMI Grade 3) — and the LCx was not felt to be a "culprit" vessel. PCI of the LCx was deferred to the near future.
- RCA (Right Coronary Artery) — 60-70% proximal stenosis — but normal ( = TIMI Grade 3) flow. No stenting was deemed necessary for this vessel.
- For brief review of TIMI Grade Flow —> Go To — Sarkar et al: Stat Pearls, NIH, 2022.
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Acknowledgment: This case was anonymously submitted to me for use in my ECG Blog.
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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 #183 — Reviews the concept of deWinter T-Waves (with reproduction of the illustrative Figure from the original deWinter NEM manuscript).
- ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute?
- ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?").
- ECG Blog #193 — Reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and — reviews the basics on how to predict the "culprit" artery.
- ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.
- ECG Blog #228 — Reviews the concept of "Silent" MI.
- ECG Blog #215 — Reviews a case with T-QRS-D.
- The November 14, 2019 post in Dr. Smith’s ECG Blog (Please scroll down to the BOTTOM of the page for My Comment and illustration of the phenomenon of T-QRS-D = Terminal QRS Distortion).
