Thursday, March 9, 2023

A man in his 50s with chest pain

 Sent by anonymous, written by Pendell Meyers

A man in his 50s with no prior known medical history presented to the Emergency Department with severe intermittent chest pain. He had episodes of chest pain off and on all night, until about 1 hour prior to arrival when the pain became constant, crushing, 10/10 chest pain that radiated to both arms. He denied any lightheadedness, shortness of breath, vomiting, or abdominal pain. Vitals were within normal limits.

Here is his triage ECG at 0343:

What do you think?

Meyers interpretation: Diagnostic of LAD OMI, with hyperacute T waves in a large LAD distribution including precordial leads, high lateral leads, and inferior leads. Barely any STE, and thus not meeting STEMI criteria. Yet completely diagnostic of acute LAD occlusion.

Here is the response from PM Cardio's Queen of Hearts AI model:

Trained with many cases of hyperacute T waves, the AI confidently diagnoses them in this case.

Read our recent editorial: Hyperacute T-waves Can Be a Useful Sign of Occlusion Myocardial Infarction if Appropriately Defined. Annals of Emergency Medicine

Cardiology was called to evaluate the patient immediately for emergent cath, but they stated that the ECG did not meet STEMI criteria and elected to wait for further information before proceeding with cath.

He was given 6mg IV morphine for ongoing pain. 

His initial troponin T returned at 0.03 ng/L (abnormal for this assay is anything greater than 0.01, which is also the limit of detection, because this is an older troponin assay).

Bedside echo performed by cardiology fellow at 0407:

"Hypokinesis to akinesis of apical septal, apical lateral, apical anterior, apical inferior, and mid anteroseptal segments based on very limited views."

Isn't it amazing?? Active crushing chest pain requiring morphine, positive troponin, echo showing wall motion abnormalities, and a diagnostic ECG, and still the patient is not taken to the cath lab or given lytics, all seemingly because the ECG does not meet STEMI criteria. And yet this is normal behavior in many places around the world under the STEMI paradigm in my experience and the experience of our readers and contributors. 

Finally, his second ECG was performed at 0507 and thankfully showed STEMI criteria (but this is 84 minutes later than our OMI diagnosis!):

Obviously LAD OMI. But take a second to make sure you see that this LAD produces STE in anterior, low lateral, high lateral, AND inferior leads! Many providers will object that this is "diffuse" STE, that there are "no reciprocal changes", etc. This is a completely false and dangerous misconception. This is focal STE/HATW of a large area. The STD in aVR is reciprocal to large STE vectors in those opposite directions.

Only now that the patient has STEMI criteria is he allowed to go to the cath lab, at around 0530. It showed a mid LAD culprit with 95% with no pre intervention timi flow listed. PCI was performed, with TIMI 3 flow after the intervention.  

Note that this obvious STEMI does not have 100% stenosis at the time of cath. This is in part because the state of the artery during the ECG is frequently different than the state of the artery at the time of the angiogram. A significant portion of obvious STEMIs have TIMI 3 flow upon rapid angiogram. See the excerpt at bottom of post, taken from our 

OMI Facts and References page.

Several hours after cath:

Acute LAD reperfusion. 

24 hours after presentation:

Further evolution of reperfusion.

Troponins (ng/L):

(This is tropoinin T, which has much lower values than troponin I)











Formal echo (few hours after cath):

EF 49%

mid anterior septum moderately hypokinetic

anterior apex dyskinetic

inferior apex dyskinetic

septal apex akinetic

apical cap dyskinetic

apex dilated and dyskinetic, consistent with an aneurysm

moderate apical left ventricular thrombus

He survived to discharge. Do you think his long term outcome will be as good as if his OMI were recognized appropriately on arrival, 1.5 hours earlier? 

Learning Points:

Patients with OMI can be diagnosed faster and more accurately by ECG interpretation that is more advanced than just STEMI criteria.

NSTEMI patients with active refractory ischemic symptoms despite medical management, even in absence of a diagnostic ECG, are recommended for emergent cath by all guidelines.

Hyperacute T waves do not yet have a formal research definition, but are likely defined best by an increased ratio of area under the curve compared to their QRS complex. 

ECG AI may soon alleviate the burden of humans needing to spend significant time and effort memorizing ECG patterns.

TIMI Flow at time of cath for STEMI(+) OMI:

Outcomes used to ascertain the presence of OMI on the ECG cannot be based solely on TIMI flow of the lesion at the time of the angiogram because the state of the artery frequently differs between the time of the ECG and the time of the angiogram. Proven STEMI has an open artery in 19% to 36% of cases, depending on whether it is TIMI −1, −2, or −3 flow. Karwowski et al showed that only 64% of 4581 STEMIs had TIMI 0 flow on angiogram. [25] Stone et al found that 72% have TIMI 0 or 1 flow. [26] Finally, Cox et al found that 80% had TIMI 0, 1, or 2.27 Thus, approximately 20% of true, obvious STEMIs have TIMI 3 flow at immediate angiogram. [27]

25. Karwowski J, Gierlotka M, Gasior M, Polonski L, Ciszewski J, Beckowski M, Kowalik I, Szwed H. Relationship between an in-farct related artery, acute total coronary occlusion, and mortality in patients with ST-segment and non-ST-segment myocardial infarction. Pol Arch Intern Med. 2017;127:401–411.

26. Stone GW, Cox D, Garcia E, Brodie BR, Morice MC, Griffin J, Mattos L, Lansky AJ, O’Neill WW, Grines CL. Normal flow (TIMI-3) before mechanical reperfusion therapy is an independent determinant of survival in acute myocardial infarction: analysis from the primary angioplasty in myocardial infarction trials. Circulation. 2001;104:636–641. doi: 10.1161/ hc3101.093701

27. Cox DA, Stone GW, Grines CL, Stuckey T, Zimetbaum PJ, Tcheng JE, Turco M, Garcia E, Guagliumi G, Iwaoka RS, et al. Comparative early and late outcomes after primary percutaneous coronary intervention in ST-segment elevation and non–ST-segment elevation acute myocardial infarction (from the CADILLAC Trial). Am J Cardiol. 2006;98:331–337. doi: 10.1016/j.amjcard.2006.01.102

Learning Points:

TIMI 3 flow at the time of cath does not mean a patient didn't have OMI or STEMI.

Many patient with obvious STEMI(+) OMI have TIMI 3 flow at the time of angiogram.

TIMI flow alone cannot be used as an outcome definition for OMI or STEMI.

My Comment by KEN GRAUER, MD (3/9/2023):

This was a difficult post for me to read … We have to learn from the errors of omission and commission that took place. Among the Lessons to be Learned include the following:

  • Respect the clinical setting. — The previously healthy 50-ish year old man in today’s case presented with a history of chest pain that initially was intermittent — but which then became “constant"  "crushing” and “10/10 in severity” — resulting in him coming to the ED in the middle of the night (ie, his initial ECG was obtained at 3:43 am). This type of clinical presentation instantly places this patient in a very high prevalence group for an acute cardiac event even before we look at his ECG and troponin results. By definition — this is the type of patient for whom we need to rule out an acute cardiac syndrome — rather than requiring millimeter-based STEMI criteria before we consider an acute event.

  • Forget the outdated “STEMI paradigm” when interpreting the ECG. — Details on those ECG findings that should have been recognized on the initial tracing in today's case follow below.

  • Realize that even slight Troponin elevation IS Significant in this Setting— The initial Troponin T was elevated! Although the amount of troponin elevation was modest (ie, an initial value of 0.03 — vs 0.01 for the upper limit of normal with the older troponin assay that was used) — in a high prevalence presentation in this patient with new "crushing 10/10 chest pain" — any troponin elevation on the initial blood draw is significant.

  • Don’t Ignore Bedside Echo Results! — In this patient with new "crushing 10/10 chest pain" and an initial troponin that already was elevated — a bedside Echo showing wall motion abnormalities in multiple cardiac segments was ignored.

  • IF in Doubt about the Diagnosis — REPEAT the ECG. Do so Soon and Often! — The 2nd ECG in this case was not obtained until 5:07 am — or 84 minutes after the 1st ECG — by which time there was dramatic and diffuse ST elevation (attaining nearly 10 mm in 2 of the anterior leads!). The chances are great that waiting no more than 10-15 minutes before repeating the ECG would have been enough to satisfy STEMI criteria (Not to repeat the initial ECG before 84 minutes in this case is indication of not understanding the pathophysiology of an acutely evolving coronary occlusion).

Why the Initial ECG should NOT have been Discounted:
The consulting cardiology team decided against prompt cardiac cath — because the initial ECG "failed to meet STEMI criteria". However (as emphasized by Dr. Meyers) — this initial ECG was already clearly diagnostic of acute LAD OMI. Among the Lessons-to-be-Learned in today's case — is WHY the initial ECG should not have been discounted in this way.  
  • For clarity in Figure-1 — I've reproduced and labeled the first 2 tracings in today's case. The initial ECG shows sinus rhythm and a narrow QRS. When assessing an initial ECG in a patient with new chest pain — I look first for one or two leads that show definite diagnostic changes. In ECG #1 — there is simply no way that the ST-T wave in lead V2 can be normal. As seen within the dotted RED rectangle — the ST-T wave in this lead is "fat"-at-its-peak, extremely wide-at-its-base — and towers over the tiny QRS complex in this lead. In a patient with new chest pain — it is hard to conceive of a more hyperacute T wave than what we see in lead V2.

  • Because of the much taller R waves in neighboring leads V3 and V4 — determination of "hyperacuity" is more challenging. That said — given the definite hyperacute T wave in lead V2 — the taller-than-expected T wave in lead V3 manifests a disproportionately wide base that in my mind, qualifies it as also being "hyperacute".
  • By the concept of "neighboring leads" — I suspected that the T wave in lead V4 was probably also hyperacute, albeit admittedly less prominent than the T wave in lead V3. 
  • In the context of hyperacute T waves in leads V2-thru-V4 — the subtle-but-real J-point ST depression in leads V5,V6 is clearly abnormal (thin BLUE arrows in V5,V6).
  • In the other direction — lead V1 (neighboring the hyperacute T wave in lead V2) manifests subtle-but-real ST coving, if not slight ST elevation (BLUE arrow in V1).

ST-T wave changes in the limb leads of ECG #1 are more subtle — but equally important in supporting our impression of acute ongoing LAD occlusion.
  • We have often emphasized that acute LAD occlusion does not always produce reciprocal ST depression in the inferior leads — especially when the location of LAD occlusion is more distal. That said — the clearly hyperacute T wave in lead V2 of ECG #1 (together with suspicious change in lead V1) — suggest a more proximal location for the occlusion.
  • Consistent with mid- (if not proximal) LAD occlusion in ECG #1 — is the ST coving with slight elevation in lead aVL (BLUE arrow) — and ST segment flattening with slight depression in each of the 3 inferior leads (angulated BLUE lines in these leads).

To EMPHASIZE: Many of the ST-T wave changes that I describe above are subtle! That said — in context with a 50-ish year old man with: 
  • i) New "crushing" chest pain of 10/10 severity
  • ii) An initial troponin that is already slightly elevated; 
  • iii) Bedside Echo showing wall motion abnormalities in multiple cardiac segments; and
  • iv) An initial ECG with definite hyperacute T wave in lead V2 and probable hyperacute T waves in several other leads — the additional finding of these admittedly subtle ST-T wave abnormalities in virtually all other leads should more than satisfy the need for prompt cath.

Figure-1: The first 2 ECGs recorded in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

Comparison with ECG #2:
There are 2 reasons I chose to reproduce ECG #2 in today's case:
  • Reason #1: To emphasize that the BEST way to get good at recognizing the early ECG changes of acute OMI (ie, before frank ST elevation is seen) — is to retrospectively go back and reanalyze serial tracings to better understand the subtle clues that were initially present (ie, Looking at ECG #2 — it is easier to appreciate how those prominent T waves in leads V3,V4 and V5 of ECG #1 were truly hyperacute).

  • Reason #2: Leads V3 and V4 in ECG #2 provide a superb example of Terminal QRS Distortion (T-QRS-D). This concept 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 Drs. Smith and Meyers. 
  • To Emphasize — T-QRS-D is not needed in today's case for diagnosis — since the dramatic ST elevation seen in ECG #2 can be recognized from across the room. But there are times when there may be doubt as to whether more subtle ST elevation represents acute OMI or a repolarization variant. In such cases — recognition of T-QRS-D may be diagnostic of acute OMI.

By way of review — I i
llustrate 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.
  • T-QRS-D — is defined as the absence of both a J-wave and an S-wave in either lead V2 or lead V3 (and probably also in lead V4). 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 thlead 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).

  • Returning to Figure-1 — the RED arrows in leads V3 and V4 highlight T-QRS-D, as there is no S wave and no defined J-point in these leads. (NOTE: Validity for T-QRS-D as an indicator of acute OMI is lacking when this phenomenon is seen in leads other than V2, V3 and presumably V4).

Figure-2: Comparison between ST elevation in lead V3 due to a repolarization variant (TOP — from 4/27/2019) — vs acute OMI (BOTTOM — from 9/20/2015), which manifests T-QRS-D (See text).

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