Monday, July 15, 2019

A female in her 60s with sudden chest pressure

Written by Pendell Meyers


A female in her mid 60s with history of SVT and HTN presented with sudden onset 3/10 chest tightness while lying in bed in the early morning. She had nausea and diaphoresis with this event, as well as tightness between her scapula, and a loose bowel movement.

Here is her initial ECG at presentation to the ED at time zero (no prior available):

What do you think?









Sinus rhythm with significant downsloping STD in V1-V3, maximal in V1-V2. There is also subtle STE in V6 with large-area T-wave with straight/convex ST segment morphology. The T-waves in the inferior leads could be large if a prior ECG were available for comparison.

This ECG is diagnostic of acute MI of the posterior and lateral walls. The most common etiology of this condition is Occlusion MI (OMI) affecting these walls, most likely LCX or other artery in this territory including a diagonal or obtuse marginal, or RCA in some cases.

Because the current STEMI vs. NSTEMI paradigm greatly undermines the understanding and recognition of the STD of posterior OMI, this finding was not initially recognized.

Initial troponin returned slightly elevated at 0.02 ng/mL. This triggered a repeat ECG at t = 50 minutes:



The findings above are still present but slightly improved, however there is still active ischemia on this ECG. OMI is ongoing until proven otherwise.

It is unclear whether the patient still had symptoms at this time.

The patient was admitted to cardiology for NSTEMI. There was no bed in the cardiology unit, so the patient was boarding in the ED.

The second troponin returned at 0.13 ng/mL, prompting another repeat ECG at t = 2 hrs:
Further improvement but still not back to baseline.



CT aorta was negative for dissection.

She was started on heparin.

Trop #3 at t = 6 hrs 30 min = 0.41 ng/mL
Trop #4 at 9 hrs = 1.13 ng/mL
Trop #5 at 12 hrs = 1.17 ng/mL

Finally, a note from the admitting team states that she will be taken to cath for ongoing chest pain and rising troponins at t = 15 hrs.


Cath at t = 16 hrs:

Mid LCX 100% occlusion with TIMI 0 flow. TIMI 3 after PCI. Also noted triple vessel disease with RCA 70% and LAD mid 90%.







ECG the next day:




First five measurements were before cath, then you can see the spike as sequestered troponin in non-perfused myocardium is released after reperfusion.

Learning Points:

STD maximal in V1-V4 with a normal QRS complex (not explained by RBBB, etc) is worrisome for posterior OMI until proven otherwise. Posterior leads may be helpful, but lack of clear elevation in the posterior leads does not obviate concern for posterior OMI when the STD on the anterior leads is diagnostic.

Ongoing ischemia (by symptoms, troponin, or ECG) despite medical management is an indication for emergent cardiac catheterization.



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Comment by KEN GRAUER, MD (7/15/2019):
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SUPERB case discussion by Dr. Meyers regarding a tracing that I feel manifests a number of unique and important features. The patient is a woman in her 60s, who presented with new-onset chest discomfort.
  • I focus my attention on the interpretation of the initial ED tracing ( = ECG #1 in Figure-1). I've added ECG #3 to Figure-1 for comparison purposes.
Figure-1: The 1st and 3rd ECGs shown in this case (See text).

My THOUGHTS on ECG #1 The ECG findings in this initial ED tracing are subtle and easy to overlook. I've labeled some of the key findings.

Descriptive Analysis of ECG #1:
  • The rhythm is sinus at ~80/minute. The PR interval is normal. The QRS complex is not wide. Assessment of the QTc interval is a bit tricky because of the RED arrows in leads V2 and V3 (See below) — but I believe the QTc is normal. The frontal plane axis is leftward — but not enough to qualify as LAHB (left anterior hemiblock), because the QRS is not predominantly negative in lead II. I estimate the axis to be about -20 degrees. There is no chamber enlargement.
Regarding Q-R-S-T Changes:
  • Other than lead aVR, the only Q wave is seen in lead aVL. This Q in aVL is of uncertain significance.
  • Determination of Transition (where the R wave becomes taller than the S wave is deep) is difficult to discern in ECG #1 — because QRS complexes in virtually all chest leads are approximately isoelectric!
The most remarkable finding in ECG #1 relates to the ST-T wave Changes:
  • initially did not see much in the way of ST-T wave changes in the limb leads.
  • The most “eye-catching” finding is the ST depression/T wave inversion in lead V(within the RED rectangle in ECG #1). Neighboring leads V2 and V3 show ST-T wave flattening, with a lesser degree of ST depression. The T wave in V4 is almost flat, but the ST segment in this lead is not depressed.
  • The most important finding (and perhaps the easiest to overlook) — is the Selevation in lead V(within the GREEN rectangle in ECG #1). The ST segment takeoff in lead V6 is straightened (parallel to the angled BLUE line) — and the J-point clearly starts above the dotted RED baseline in this lead.
  • Returning to the limb leads for a 2nd look — the ST segment takeoff in each of the inferior leads (relative to the R wave) looks a bit straightened, and possibly fatter-at-its-peak-than-it-should-be in leads II and aVF. As per Dr. Meyers — these inferior T waves might be hyperacute — but without access to additional tracings from this patient, I would not be at all sure about whether the inferior leads manifest anything acute.
COMMENT: The clinical history (a woman in her 60s with new chest discomfort) — clearly was worrisome for an acute cardiac event. That said, I was not initially certain about acute OMI from my 1st review of ECG #1. My thoughts regarding this tracing were the following:
  • IF it would not be for the ST elevation in lead V6 — the principal finding on ECG #1 would be the ST-T wave depression in anterior (as well as right-sided) leads V1,V2,V3. Anterior ST depression and/or T wave inversion is an ECG finding that should always prompt consideration of RV “strain”, as occurs in acute PE (For more on ECG recognition of Acute P— Please see My Comment at the bottom of Dr. Smith’s April 5, 2019 Blog post). Other findings in ECG #1 that are potentially consistent with acute RV “strain” are the presence of numerous S waves (in leads I, II, III; and across all chest leadswhat could be construed as an incomplete RBBB pattern in lead V1 (with narrow terminal S waves in leads I and V6). But AGAINST acute PE as the diagnosis are: ithe History, which sounds cardiac, without hint of acute dyspnea; andiithe unusual ECG finding of ST-T wave depression being by far most remarkable in lead V1, and no more than modest in leads V2 and V3. Typically, with acute RV “strain” — leads V2, V3 and often V4 show much more marked ST-T wave abnormalities than are seen here. The most marked ST-T changes are usually not seen in V1.
  • In my opinion — the shape and relative amount of ST-T wave depression in the anterior leads is also different than what is usually seen with acute posterior involvement. Whereas the majority of acute posterior MIs are associated with acute inferior MI (which is not seen in ECG #1) — it is possible to see isolated posterior infarction with certain LCx lesions. That said, most of the time there is not that unusual ECG finding of ST-T wave depression being so much more remarkable in lead V1, than in leads V2 and V3. (For more on the ECG diagnosis of Acute Posterior M— CLICK HERE).
  • On the other hand — close inspection of the ST-T wave in lead V(within the GREEN rectanglereveals definiteacute-looking ST elevation in this lead. Rather than acute posterior MI — I believe the unusually-shaped ST-T wave depression we see in right-sided lead V1 of ECG #1 reflects a mirror-image reciprocal ST-wave change to the shape of the elevated ST segment in left-sided lead V6 (See mirror-images of leads V1 and V6 in Figure-1).
  • Many providers have been taught to obtain posterior leads” (ie, leads V7, V8 and sometimes V9when attempting to diagnose acute posterior MI. In my experience — posterior leads have never helped me, as use of the Mirror Test” (as I describe and illustrate HEREhas virtually always allowed me to recognize acute posterior MI without need to use posterior leads. That said, ECG #1 illustrates one instance in which I bet leads V7 and V8 (if they would have been done— would have further clarified the question of ST elevation in lead V6.
  • Fragmentation of the QRS complex is seen in several leads in ECG #1 (WHITE arrows in leads III, aVL and V1). The significance of recognizing fragmentation of the QRS complex — is that it suggests scar, which usually indicates prior infarction and/or cardiomyopathy. In retrospect — this fragmentation on the initial ECG provided a clue that this patient has severe multi-vessel coronary disease, as was later confirmed on cath.
  • ECG #1 also manifests U wave inversion (RED arrows in leads V2 and V3). This is not a common finding. Even when present — it is difficult to recognize, and often goes overlooked. The clinical significance of U wave inversion, is that it is a marker of severe ischemia. Suggestion of a negative U wave deflection after the T wave is less marked in subsequent ECGs done as this case progressed, and absent on the following day’s ECG after reperfusion.
BOTTOM Line: In this 60+ year old woman with new chest discomfort — the acute-looking ST elevation in lead V6 with mirror-image reciprocal ST-T wave changes in lead V1 additional ischemic changes in leads V2 and V3 — should be enough to merit acute cath.
  • Knowledge that serial troponins were increasing persistence of chest pain further supported the need for acute cath.

As I emphasized in the last Dr. Smith ECG Blog post (from July 11, 2019) — Among the best ways to enhance appreciation of subtle acute changes on an initial ECG — is by comparison with a later ECG. This should be evident from comparison of the initial ECG in this case ECG #1 in Figure-1) — with ECG #3 done 2 hours later.
  • Note in ECG #3 — that the ST elevation in lead V6 is now gone. The ST segment in this lead is also not as straight as it was in ECG #1.
  • ST-T wave changes in lead V1 do not look nearly as acute in ECG #3 as they did in ECG #1. ST-T wave changes in leads V2 and V3 are also less marked.
  • Finally — Compare T wave appearance in the inferior leads between the 2 tracings in Figure-1. The fact that the T wave in each of the inferior leads of ECG #3 is flatter supports our suspicion that early hyperacute T wave changes were present in the inferior leads of ECG #1.
  • Putting this all together — serial ECGs in this case show dynamic ST-T wave changes — which, in a patient with ongoing chest discomfort is indication for prompt cath.

Our THANKS to Dr. Meyers for presenting this case!



2 comments:

  1. Excellent case with discussion by Dr. Meyers and great commentary by Dr. Grauer.

    Basolateral MIs are among the worst for not showing typical signs of STE or even hyperacute T waves. Many times there is a transmural infarction with no signs on the ECG. I agree with Ken that, in the right setting, ST depression in V1 - V3 is sufficient for diagnosis and V7 - V9 are not necessary. Just be careful that you understand the difference between an ACUTE lateral (formerly "posterior") MI and a SUBACUTE or otherwise completed MI. In his groundbreaking paper that showed that we could indeed diagnose "posterior" MIs on a 12-lead ECG, Dr. Perloff described what a posterior MI should look like: "tall R wave in V1 with flat ST depression and an upright T wave." Unfortunately, what he described was a completed, post-reperfusion artery (turned "right-side up," it would actually represent a large Q wave, still some STE with inverted T waves). In the acute setting, a lateral (formerly posterior) MI will often begin with wide and deeply inverted T waves (upside-down hyperacute T's), then flat or downward sloping ST depression (STE) and inverted T waves (pre-reperfusion T waves).

    Why do we have no inferior wall involvement? Probably because 85 - 90% of the time the LCx is not the major supplier of circulation to the inferior wall (i.e., it is non-dominant). But make no mistake - even when it is non-dominant - the LCx supplies 15 - 25% of the inferior wall of the left ventricle! We usually don't see a problem with this during LCx occlusions (as in this patient) because the RCA is supplying blood and 80% of the time the LAD is also supplying blood to the inferior wall.

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    1. Thank you (as always!) Jerry for your insightful comments! — :)

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