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Wednesday, June 25, 2025

SSmith-DRAFT (KG- Done) - Excellent OMI Care (6-12.21-2025)- I_am_DONE

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MY Comment, by KEN GRAUER, MD (6/14/2025):

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Today's case is gratifying, because as per Dr. Smith — the diagosis of acute OMI with need for prompt cath was quickly made. CREDIT to Drs. Sala and Villa!

Regardless of whether or not STEMI criteria were met — the important point is to recognize that today's initial ECG is clearly diagnostic of acute proximal LAD OMI.

Today's Initial ECG:

To facilitate rapid recognition of the need for prompt cath — I've labeled KEY findings in Figure-1.

As per Dr. Smith — nearly all the benefit of reperfusion is lost by 6 hours. It is for this reason that cases such as the one presented today by Drs. Sala and Villa should be recognized within seconds of seeing an initial ECG like the tracing shown in Figure-1.
Rapid recognition begins with the history. Knowing the patient is a 60-something man with known diabetes and COPD (therefore presumably a longterm smoker) — who presented with 1 hour of "oppressive" CP (Chest Pain) — instantly places this patient in a higher-risk group for having an acute cardiac event (ie, Our "threshold" for activating the cath lab should be lowered — so as to include not only diagnostic ECG findings, but also those ECG findings that are somewhat less certain, but still suspicious for OMI).

ECG #1 — shows sinus rhythm — normal intervals — a leftward axis (but not negative enough to qualify as LAHB — because the QRS is predominantly positive in lead II, therefore an axis of less than -30 degrees).

Overall QRS amplitude is reduced, especially in the chest leads where none of the 6 leads manifests an amplitude greater than 7 mm. Whether this overall reduction in QRS amplitude is the result of body habitus, the patient's COPD — and/or reduced QRS amplitude as a result of cardiac stunning in association with acute infarction, is uncertain from this single tracing.
Transition occurs surprisingly early (ie, The QRS becomes all positive as soon as in lead V2). The reason (and potential significance) of this unusual finding is uncertain — but important to appreciate in our assessment of ST-T wave appearance in anterior leads.
The above said — my "eye" was immediately drawn to the ST-T waves in leads V2 and V3 (within the RED rectangle). That the T waves in both of these leads are hyperacute — should be recognized by the disproportionately enlarged T wave dimensions compared to the tiny QRS amplitudes in V2,V3.
As noted by Dr. Smith — both leads V2 and V3 manifest T-QRS-D (Terminal QRS Distortion), because neither lead has a J-point or an S wave that descends below the baseline (See My Comment in the November 14, 2019 post in Dr. Smith's ECG Blog for more on T-QRS-D).

To Emphasize: In this higher-risk patient with severe, new CP — the abnormal ECG findings within the RED rectangle in Figure-1 would be enough to justify prompt cath lab activation. But there is lots more that is abnormal on this initial ECG.

In the context of the above described definitely abnormal ST-T waves in leads V2,V3 — Neighboring leads V1 and V4 are also clearly abnormal. The slight ST elevation with ST segment straightening, disproportionately prominent postive T wave with subtle terminal T wave negativity in lead V1 — is not normal for the ST-T wave appearance in this lead.
By itself — I might not interpret the T wave in lead V4 as hyperacute. But in the context of definite hyperacuity with T-QRS-D in leads V2,V3 — the T wave in V4 is surprisingly tall, and both "fatter"-at-its-peak and wider-at-its-base than expected given modest R wave amplitude in this lead.
Reciprocal changes are seen in each of the inferior leads. Light BLUE arrows highlight ST segment flattening in leads II,III,aVF — with slight ST depression in III and aVF — and (as emphasized by Dr. Smith), with telltale terminal T wave positivity (darker BLUE arrows) that supports an ongoing acute cardiac event.
Finally — Lead aVL provides an excellent example of subtlety that by itself would not be significant — but which in the context of acute anterior chest lead findings + reciprocal ST-T wave changes in all inferior leads — confirms an acute event. That is, the shape of the ST-T wave in lead aVL is coved and ever-so-slightly elevated.
PEARL: A proximal LAD location is suggested for this OMI because: i) An acute ST-T wave appearance begins with lead V1; ii) There are reciprocal ST-T wave changes in the inferior leads; and, iii) Lead aVL shows slight-but-real ST segment coving with ever-so-slight ST elevation.

Figure-1: I've labeled today's initial ECG.

Figure-1: The long lead II in today's tracing.

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This is Excellent OMI Care

SSmith DRAFT (6/12/2025)

This case came from Drs. Luca Sala and Paolo Villa from a public hospital (Ospedale Luigi Sacco) in Milan Italy.

CASE

A 60-something male presented with one hour of "oppressive" chest pain radiating to the back and to the left arm. He has a history of diabetes and COPD.

This ECG was recorded:

What do you think?

There is at most 0.5 mm ST Elevation in V2 and V3, but there are hyperacute T-waves in V2-V4. There is terminal QRS distortion, meaning that there are no S-wave or J-waves in either V2 or V3 (in this case, none in BOTH V2 and V3, which is even more worrisome). Whenever you are in doubt about hyperacute T-wave in V2, look at inferior leads for any ST depression or "down-up" T-waves. Lead II has ST depression. Lead III has STD with down-up T-wave, as does aVF. There is also minimal STE in aVL.

So this ECG is diagnostic of proximal LAD Occlusion.

The physicians state they used the Queen of Hearts but that they obtained "No OMI".

This is strange because I ran it through BOTH PMCardio for Individuals AND PMCardio for Organizations and this was the result:

She says "OMI" for the same reasons that I do.

New PMcardio for Individuals App 3.0 now includes the latest Queen of Hearts model and AI explainability (blue heatmaps)! Download now for iOS or Android. (Dr. Smith is a shareholder in Powerful Medical.)

Nevertheless, the physicians were almost certain of OMI, so they called cardiology. The on-call cardiologist performed a bedside echo immediately and found wall motion abnormalities of the apex and septum, with EF 40%.

They immediately activated the cath lab, with very little delay and without waiting for troponin.

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Note: Waiting for troponin results in excess loss of myocardium!! Many trials of emergent vs. delayed intervention for NSTEMI show no difference because they wait for troponin to decide if the patient has an acute MI (and therefore Non-ST-Elevation MI -- NSTEMI) and so do not intervene until usually 6 hours after pain onset. Nearly all of the benefit of reperfusion is lost by 6 hours. This is why you need expert ECG interpretation to diagnose acute MI without ST Elevation -- or use the Queen of Hearts.

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At angiogram, they found a 99% culprit lesion with TIMI-3 (perfect) flow and it was stented.

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Note: Does TIMI-3 flow mean that there was no occlusion? No!! Fully 20% of cases in which everyone agrees that "STEMI" is present (meeting ST Elevation millimeter criteria) have TIMI-3 flow by the time of angiogram. This is due to spontaneous reperfusion (recanalization) between the time of the ECG and the time of the angiogram.

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The peak troponin T was 1055 ng/L, which due to very fast intervention is quite a limited infarct given the very large amount of myocardium at risk.

Here is the ECG after the PCI (digitized by PMCardio):

And the next day:

These T-wave inversions in V2-V6 are "terminal T-wave inversion" or biphasic, and are analogous to Wellens "Pattern A" waves. This is diagnostic of reperfusion (the Queen says "reperfusion of the LAD") in the most up-to-date algorithm

Monday, June 16, 2025

JesseM-DRAFT (KG- Done)- 65yo-CP during Dialysis (6-16.41-2025)-DRAFT- I_am_DONE

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SSmith-DRAFT (KG- Not Done)- BLANK (6-16.1-2025)-DRAFT- ME_to_DO

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MY Comment, by KEN GRAUER, MD (6/16/2025):

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Insightful case by Dr. McLaren — with lots of PEARLS in assessment and management. I focus my comment on a few additional interesting aspects regarding the repeat ECG, obtained after spontaneous conversion of the regular WCT (Wide-Complex Tachycardia) seen in today's 1st ECG.

For clarity in Figure-1 — I've reproduced and labeled this repeat ECG.

Rhythm Detection Using Simultaneous Leads:

As per Dr. McLaren — preservation of the same QRS morphology as was seen during the WCT in today's 1st ECG confirmed that this WCT was supraventricular, with an unusual IVCD (IntraVentricular Conduction Defect) morphology. I chose to reproduce this tracing — because it provides an excellent example of time-efficient use of simultaneously-recorded leads to deduce the etiology of each beat in Figure-1:

Caveat: As per Dr. McClaren — the KEY clue for suggesting that the WCT in today's 1st ECG was supraventricular, was the fast septal depolarization (ie, narrow initial R wave in leads V1-to-V3). That said — I'll add the caveat that as helpful as this clue is, it is not infallible — as I've seen documented VT on occasion manifest surprisingly narrow initial QRS deflections in these anterior leads. The reason I was not confident in today's case about a supraventricular etiology for the WCT until I saw ECG #2 — was that the initial QRS deflection in the WCT rhythm was wide in many of the other leads.
But the presence of sinus P waves with a constant (albeit prolonged) PR interval in the long lead V1 rhythm strip (RED arrows) — confirmed the supraventricular etiology in Figure-1.
While fully acknowledging that additional details regarding the rhythm in Figure-1 do not alter management — facile use of the long lead V1 rhythm strip in association with the simultaneously-recorded leads from the 12-lead tracing above it, allow clarification that the PINK arrow P waves in Figure-1 are PACs — because: i) Beats #2,6 and 12 all occur earlier-than-expected; ii) The PR interval of these 3 beats is consistently shorter than the PR interval of the RED arrow P waves; and, iii) P wave morphology of the 4 PINK arrow P waves in Figure-1 is subtly different than the P wave morphology of the RED arrow sinus P waves (these PINK arrow P waves all lack the terminal negative P wave deflection of the sinus P waves).
In contrast — beat #10 is a PVC, even though the QRS complex of this beat is small in the long lead V1 rhythm strip. We know this — because simultaneously-recorded beat #10 in leads V1,V2,V3 is clearly very wide and very different in morphology compared to beats #8,9 and 11 in these leads.
However — beat #13 in the long lead V1 rhythm strip is not a PVC. We know this despite how wide and different-looking this beat is in lead V1 — because the QRS morphology of beat #13 in simultaneously-recorded beat #13 in leads V4,V5,V6 is identical to the QRS morphology of beats #12 and 14 in these leads. It should be apparent that the reason for the bizarre QRS morphology of beat #13 in the long lead V1 is the result of artifact.
"Take-Home" — In my experience, the concept of assessing P wave and QRS morphology using simultaneously-recorded leads is underused. While not clinically important in ECG #2 — there are times when this technique will be the sole determining factor for distinguishing between an SVT vs VT.

Figure-1: The repeat ECG in today's case, obtained after spontaneous conversion of the regular WCT.

An Aslanger Pattern?

While fully acknowleding the confounding role of the unusual IVCD morphology that we see in Figure-1 — I instantly arrived at a similar decision as Dr. McLaren that ECG #2 was indicative of acute inferior infarction — because of the resemblance of this tracing to Aslanger's Pattern.

As discussed by Dr. Meyers and in My Comment from the December 31, 2024 post of Dr.Smith's ECG Blog — the combination of ST elevation in lead III (but not in other inferior leads) — in association with an ECG picture that is otherwise consistent with DSI (Diffuse Subendocardial Ischemia) — suggests there is inferior OMI plus underlying multivessel disease.
The diagnosis of DSI in today's case is suggested by ST depression in multiple leads (as per the 7 BLUE arrows in Figure-1) — in association with marked ST elevation in lead aVR.
Although we are only provided with information from the cardiac catheterization report regarding the "culprit" LCx artery — the bizarre IVCD morphology, in association with fragmented QRS complexes in several leads is almost certain indication of additional underlying "scar" from coronary disease.

Figure-1: Initial ECG in the ED. (To improve visualization — I've digitized the original ECG using PMcardio).

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Written by Jesse McLaren

A 65 year old with history of CABG and end stage renal disease developed sudden chest pain and diaphoresis during routine dialysis, and was given three nitro sprays and then sent to the emergency department. On arrival, heart rate was 145 and BP 75/50. What do you think?

There’s a wide complex tachycardia which is regular (so not AF) and without preceding P waves (so not sinus tach). There’s a LBBB appearance in the precordial leads, but the limb leads have rS complexes in I/aVL rather than monophasic R waves – making it non-specific intraventricular conduction delay (IVCD). There are no obvious features of hyperkalemia (eg very wide QRS, peaked T waves). Instead, There’s fast septal depolarization in V1-3 (narrow rS) suggesting supraventricular origin. With the abnormal depolarization there's expected discordant repolarization abnormalities, which are exaggerated by the tachy-arrhythmia - producing diffuse ST depression with reciprocal STE in aVR. But there's unexpected concordant STE in III, which could be secondary to the tachy-arrhythmia or from primary ischemia. Bottom line: unstable non-sinus tachy-arrhythmia: cardiovert and reassess.

The patient spontaneously cardioverted and systolic BP increased to the 90s, but had ongoing chest pain. Repeat ECG:

Sinus rhythm with PVC, first degree AV block, and same QRS morphology as during tachy-arrhythmia - confirming it was supraventricular. The final blinded read was non-specific IVCD, suggesting that all ST/T changes are secondary to abnormal depolarization. But there is still ongoing inappropriate concordant ST elevation III and reciprocal ST depression I/aVL, as well as mild concordant ST depression in V2 - indicating superimposed primary ischemic changes from inferior +/- posterior OMI.

Old MI can result in Q waves with residual STE (LV aneurysm morphology), which in the inferior leads can be difficulty to distinguish from acute OMI. But this was new compared to an old ECG:

The old ECG also had a narrower QRS, so cath lab was activated both for “new LBBB” as well as concordant inferior ST elevation. But it’s not a true LBBB, and “new LBBB” is no longer an indication for cath lab activation. However, despite not being a true LBBB, the principle of inappropriate concordance is still helpful in identifying OMI.

Even without a prior to compare, this ECG in a patient with a high pre-test likelihood of ACS is diagnostic of OMI. Here's the Queen's interpretation, highlighting concordant STE and reciprocal STD:

What about the initial troponin? Troponin is often chronically elevated in a dialysis patients, and can rise from the demand ischemia of tachy-arrhythmias or other shock states. The initial troponin is an unreliable marker of acute OMI (it can be normal acutely, and even if elevated it lags far behind the myocardial damage), and doesn’t provide real-time information to distinguish Occlusion MI from Non-Occlusion MI. So in this patient the initial troponin would not help differentiate chronic myocardial injury, type 2 MI from tachy-arrhythmia demand ischemia, and type 1 MI from OMI or NOMI – and if OMI, waiting for troponin would cost myocardium. So this is a clinical diagnosis, aided by ECG.

Fortunately the patient was immediately taken to cath lab without waiting for the troponin, with a door to cath time of only 45 minutes. There was a 95% left circumflex occlusion which was stented. First troponin I was 80 ng/L (only slightly higher than the patient’s baseline of 50ng/L), which rose to 500, then 2,000 and then a peak of 8,000 ng/L. Follow up ECG showed resolution of the primary ischemic ST changes, and subtle infero-posterior reperfusion T wave inversion compared with baseline:

Take home

1. If a patient is unstable from a WCT and the differential is narrowed to VT vs SVT with aberrancy (eg not AF, sinus tach, or hyperkalemia/sodium channel toxicity), then the treatment is immediate cardioversion regardless

2. Tachy-arrhythmias can cause secondary ST/T changes that can be reassessed after cardioversion

3. ‘New LBBB’ is not an indication for cath lab activation

4. Inappropriate concordant STE can identify OMI in both LBBB and IVCD

5. First troponin is an unreliable marker of OMI in acute chest pain and can’t differentiate chronic myocardial injury and demand ischemia from OMI or NOMI: OMI is a clinical diagnosis, aided by ECG (and AI)

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MY Comment, by KEN GRAUER, MD (6/16/2025):

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For clarity in Figure-1 — I've reproduced and labeled this repeat ECG.

Rhythm Detection Using Simultaneous Leads:

Caveat: As per Dr. McClaren — the KEY clue for suggesting that the WCT in today's 1st ECG was supraventricular, was the fast septal depolarization (ie, narrow initial R wave in leads V1-to-V3). That said — I'll add the caveat that as helpful as this clue is, it is not infallible — as I've seen documented VT on occasion manifest surprisingly narrow initial QRS deflections in these anterior leads. The reason I was not confident in today's case about a supraventricular etiology for the WCT until I saw ECG #2 — was that the initial QRS deflection in the WCT rhythm was wide in many of the other leads.
But the presence of sinus P waves with a constant (albeit prolonged) PR interval in the long lead V1 rhythm strip (RED arrows) — confirmed the supraventricular etiology in Figure-1.
While fully acknowledging that additional details regarding the rhythm in Figure-1 do not alter management — facile use of the long lead V1 rhythm strip in association with the simultaneously-recorded leads from the 12-lead tracing above it, allow clarification that the PINK arrow P waves in Figure-1 are PACs — because: i) Beats #2,6 and 12 all occur earlier-than-expected; ii) The PR interval of these 3 beats is consistently shorter than the PR interval of the RED arrow P waves; and, iii) P wave morphology of the 4 PINK arrow P waves in Figure-1 is subtly different than the P wave morphology of the RED arrow sinus P waves (these PINK arrow P waves all lack the terminal negative P wave deflection of the sinus P waves).
In contrast — beat #10 is a PVC, even though the QRS complex of this beat is small in the long lead V1 rhythm strip. We know this — because simultaneously-recorded beat #10 in leads V1,V2,V3 is clearly very wide and very different in morphology compared to beats #8,9 and 11 in these leads.
However — beat #13 in the long lead V1 rhythm strip is not a PVC. We know this despite how wide and different-looking this beat is in lead V1 — because the QRS morphology of beat #13 in simultaneously-recorded beat #13 in leads V4,V5,V6 is identical to the QRS morphology of beats #12 and 14 in these leads. It should be apparent that the reason for the bizarre QRS morphology of beat #13 in the long lead V1 is the result of artifact.
"Take-Home" — In my experience, the concept of assessing P wave and QRS morphology using simultaneously-recorded leads is underused. While not clinically important in ECG #2 — there are times when this technique will be the sole determining factor for distinguishing between an SVT vs VT.

Figure-1: The repeat ECG in today's case, obtained after spontaneous conversion of the regular WCT.

An Aslanger Pattern?

As discussed by Dr. Meyers and in My Comment from the December 31, 2024 post of Dr.Smith's ECG Blog — the combination of ST elevation in lead III (but not in other inferior leads) — in association with an ECG picture that is otherwise consistent with DSI (Diffuse Subendocardial Ischemia) — suggests there is inferior OMI plus underlying multivessel disease.
The diagnosis of DSI in today's case is suggested by ST depression in multiple leads (as per the 7 BLUE arrows in Figure-1) — in association with marked ST elevation in lead aVR.
Although we are only provided with information from the cardiac catheterization report regarding the "culprit" LCx artery — the bizarre IVCD morphology, in association with fragmented QRS complexes in several leads is almost certain indication of additional underlying "scar" from coronary disease.

Saturday, June 14, 2025

WillyF-DRAFT (KG- Done) - Subtle ECG & Angiogram (6-12.1-2025)- I_am_DONE

Video: AP Cranial Angiogram

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Video: AP Cranial Angiogram

Here is a narrated video explaining the angiogram:

Video: AP Cranial Angiogram shown above, now with slow motion freeze frame.

I have personally never seen isolated septal perforator OMI before. But it makes perfect sense given the finding of precordial swirl on ECG 1. Swirl indicates a rightward vector of injury (since the septum is rightward relative to the bulk of LV mass). This was not felt to be a suitable target for PCI. I have never personally seen intervention to a septal perforator, but I was able to find a few case reports. This is extremely rarely done for a variety of reasons (technical difficulty, smaller caliber vessel, mechanical stress on stent from intramyocardial course, etc.) He was managed with dual antiplatelet therapy.

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MY Comment, by KEN GRAUER, MD (6/14/2025):

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Today's illustrative case by Dr. Frick features a subtle initial ECG — and an equally subtle angiogram. Along the way are additional Lessons to be Learned, as contained within Dr. Frick's insightful discussion. I focus on the initial ECG — and add a simple reminder regarding what could have (and should have) expedited performance of the cardiac cath in today's case.

For clarity in Figure-1 — I've reproduced the 2 ECGs in today's case.

Today's Initial EMS ECG:

The patient in today's case is a previously healthy man in his early 40s who presented to the ED with 10/10 "crushing" CP (Chest Pain) that radiated to his left arm.

As we frequently emphasize — this clinical scenario immediately places this patient into a higher-risk likelihood for having an acute cardiac event (as it should be simultaneously lowering our "threshold" for activating the cath lab).

As per Dr. Frick — ECG #1 strongly suggests Precordial "Swirl" (See the October 15, 2022 post in Dr. Smith's ECG Blog for 20 examples of Swirl or Swirl "Look-Alikes" — and My Comment at the bottom of the page for clinical synthesis on making the ECG diagnosis of Swirl).

The rhythm in ECG #1 is sinus bradycardia at a rate just under 60/minute — with normal intervals — a vertical frontal plane axis — and no chamber enlargement.
My "eye" was immediately drawn to the 3 leads within the RED rectangles. Although subtle — there is straightening of the ST segment takeoff in lead V1, with a bit more than 1 mm of J-point ST elevation in this lead. Given very modest depth of the S wave in this V1 lead in this patient with crushing 10/10 new CP — this "picture" of the ST-T wave in lead V1 is definitely abnormal (and should be embedded in the brain of all emergency providers).
Lead V2 "looks" funny (ergo the ? I added in Figure-1). That is — the J-point is elevated — then the ST segment itself is flat, followed by a disproportionately tall T wave considering modest depth of the S wave in this lead. Although a bit bizarre in appearance — the QRST complex in lead V2 supports our impression of an acute anterior event until proven otherwise.
As emphasized in the numerous examples and my summary in the October 15, 2022 post — the entity of Precordial "Swirl" ( = acute proximal LAD occlusion) is recognized in a patient with new CP by abnormal ST elevation in leads V1,V2 — in a patient without LVH who manifests a flat (or scooped) and depressed ST segment in leads V5 and/or V6 (highlighted by the RED and BLUE arrows in these leads in Figure-1).

BOTTOM Line: While the amount of anterior lead ST elevation is modest in Figure-1 — given its association with the definite flat ST depression that we see in the lateral chest leads of this patient with new 10/10 CP — today's initial EMS ECG is diagnostic of acute proximal LAD OMI until proven otherwise. The cath lab should be immediately activated on seeing ECG #1.

There is no need to delay decision-making for Troponin levels (remembering that the initial 1-to-2 Troponins may be normal despite acute OMI).
Given the history in today's case and the above-described findings in ECG #1 — there is essentially nothing that might happen (ECG, Troponin or Echo-wise) to alter the need for prompt cath in this patient. So WHY wait?
Other findings in ECG #1: With the exception of lead aVL — the limb leads in today's initial tracing contribute little to our interpretation. Frankly — I did not know how to interpret the large Q wave and T wave inversion in lead aVL given lack of a similar appearance in the other high-lateral lead ( = lead I). Perhaps this T inversion in aVL reflects some component of reperfusion, possibly linked to the unusual appearance of the ST-T wave in lead V2?

Figure-1: Side-by-side comparison of the initial EMS ECG — with the repeat ECG done ~1 hour later, when the patient's CP returned.

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Looking Closely at the Sequence of Events ...

As per Dr. Frick — chart documentation suggests that this patient's symptoms "got better" over the next 15 minutes after ECG #1 was recorded, while the EMS unit was en route to the hospital.

KEY Point: Especially until definitive decision regarding whether to activate the cath lab is made — the ECG should be repeated whenever there is any change in the patient's clinical condition. If impractical to repeat the ECG during transit (ie, with EMS rushing the patient to the hospital) — then as soon as the patient arrives in the ED — the ECG should be repeated. This apparently was not done.
It was not until ~1 hour after the initial EMS ECG that return of this patient's CP prompted the recording of a 2nd ECG ( = the repeat tracing shown in the bottom half of Figure-1).
I thought lead-by-lead comparison of ECG #1 and ECG #2 showed essentially no change.

Review of the Sequence of Events:

The initial EMS ECG ( = ECG #1, recorded by EMS in the field when the patient was having 10/10 CP) — suggests Precordial "Swirl", albeit ECG changes are somewhat subtle.
Over the next 15 minutes — the patient's CP decreased (albeit we do not know by how much his CP decreased — or if it resolved entirely). But no repeat ECG was done at this time.
It was not until ~45 minutes later, when the patient's CP "returned" — that a 2nd ECG was obtained. Comparison of this 2nd ECG with the initial EMS ECG did not show significant change.

NOTE: Comparison between ECG #1 and ECG #2 failed to show significant ST-T wave change. But the patient was having CP at the time both of these ECG were recorded.

QUESTION:

What would a repeat ECG obtained ~15 minutes after ECG #1 have shown, considering that CP had decreased at that time?

ANSWER:

We have no idea what a repeat ECG might have shown IF it had been done ~15 minutes after ECG #1 when CP had decreased.

If spontaneous reopening of the "culprit" artery was the reason this patient's CP had decreased — we might have seen significant improvement in the ST-T wave abnormalities that were evident in ECG #1.
And — IF spontaneous reclosure of the "culprit" artery was the reason for return of this patient's CP ~45 minutes later — this might account for the ECG picture of ECG #2 that was obtained when CP returned.

MY Opinion: I completely agree with Dr. Frick that "improved" CP is not the same as "relieved" CP from an ischemic point of view (because as long as some CP is present in a patient with new ECG changes — there is ongoing ischemia that merits prompt cath with PCI to restore coronary flow).

That said — since medical providers did not arrange for prompt cath after diagnostic ECG #1 was recorded — being able to demonstrate "dynamic" ST-T wave changes that correlate to a change in the relative severity of symptoms might have been possible IF a repeat ECG had been recorded ~15 minutes after ECG #1 when this patient's CP had "decreased".
It is for this reason that I favor routine notation on the actual ECG of the presence and relative severity of CP as an extra insightful source for clinically determining the likely state of the "culprit" artery (ie, open or closed) — as well as for optimizing the chance of recording "dynamic" ST-T wave changes that may serve to convince a reluctant interventionist of the need for prompt cath with PCI.

My COMMENT: — I completely agree with Dr. Frick that "improved" CP is not the same as relieved CP from an ischemic point of view — because as long as some CP is present in a pt with new ecg changes — there is some ongoing ischemia in need of prompt cath and PCI to restore coronary blood.

On the other hand — I find it helpful on occasion from a diagnostic viewpoint to correlate reduction (without resolution) of CP — since IF this correlates to improvement of ECG changes — this supports this being a "dynamic" ST-T change — which in today's case could have supported the OMI diagnosis.

MAKE FIGURE OF ECG #1 & ECG #2

ECG #1 — initial EMS ECG in today's case (Pt with CP)

ECG #2 — repeat ECG (done ~1 hour after ECG #1, when CP returned ... )

Me to compare ECGs #1 and #2 (done an hour later) — NOT much change — but that is undoubtedly because no repeat ECG was done for an hour — and since CP decreaed, a sooner repeat ECG most probably would have shown improvement — and then we would have seen worsening (instead of little change between the 2 ECGs).

Note — this WAS a "swirl" pattern — but minimal change in multiple leads — probably becaue of the unusual location/appearance of the culprit prforator artery!

NOTE — This is the type of ECG for which I believe (my opinion) that clinical assessment by a human is essential — V1 is definitely abnormal - as V6 — so this fits "Swirl" — but it lacks the usual abnormalities in other leads.

V2 is definitely abnormal — but with an unusual shape.

But in a pt with CP — the ECG should be repeated.

Note — The 2nd ECG was only done an hour later. As per Dr. Frick — it did not show any real change compared to ECG #1

PROBLEM — CP got better (No ECG was done

Initial EMS ECG (done for this pt with new CP
CP got better within 15 min. after ECG #1 — but no ECG was done.
CP returned — and ECG #2 was obtained

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Willy — This is the slow mo of your angiogram — :)

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

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Written by Willy Frick

A man in his early 40s with no past medical history experienced acute onset crushing chest pain and dyspnea. The chest pain radiated into his left arm, and there was finger tip numbness. He rated it 10 out of 10. He took aspirin 325 mg and called EMS. The EMS report describes him as diaphoretic and clammy with extreme anxiety. His ECG is shown.

ECG 1

What do you think?

The Queen of Hearts calls this negative for OMI, but the raw output is 0.48. The model output ranges from 0 to 1 where 0 is no evidence for OMI and 1 is maximal confidence for OMI. The threshold for positivity is 0.5. So 0.48 is extremely close to being positive, and even a few subtle changes in digitization could conceivably swing this above 0.5. In a patient with a classic history for OMI (i.e. very high pre-test probability), this is not reassuring at all.

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This is a difficult ECG, but knowing the history my interpretation was precordial swirl. Specifically, there is STE with hyperacute T waves in V1 with flat, very subtly downsloping STD in V6. The inferior T waves are also generous in size, with what appears to be reciprocal STD in the high lateral leads and ischemic down-up T waves especially in lead I.

Documentation indicates that the symptoms got "better" in the 15 minutes prior to arrival, but it does not say symptoms were RESOLVED. Ischemic chest pain is either resolved or unresolved. "Better" is almost meaningless. Initial high sensitivity troponin I (hsTnI) was 5 ng/L (ref. < 35 ng/L). The patient did not receive any nitro.

The next update an hour later says he had return of chest pain prompting repeat ECG, shown below.

ECG 2

Overall, pretty similar looking but probably a little improved. The ECG is irrelevant at this point, since the history is essentially diagnostic for OMI. And in a patient with stuttering symptoms, emergent angiography is the appropriate management. Cardiology recommended nitroglycerin, but none was apparently given. Repeat hsTnI rose from 5 ng/L to 64 ng/L.

Documentation indicates return of symptoms two hours later. It is not clear what happened during the prior symptomatic episode. Repeat ECG was very similar, and the patient received 0.4 mg sublingual nitroglycerin with "improvement" in pain. Third hsTnI resulted at 269 ng/L. At this point, he was diagnosed with "NSTEMI" and started on continuous heparin infusion.

A few hours later still, the patient had return of symptoms and received two additional doses of sublingual nitroglycerin with "slight improvement." HsTnI resulted at 1013 ng/L. This was in the middle of the night. The on-call interventional cardiologist recommended cardiac catheterization in the morning. This overt departure from guideline recommended management (immediate angiography for medically refractory chest pain) is reflective of usual care in the real world. About 1 out of every 15 patients with refractory angina is treated in accordance with guidelines.

The next day, the patient went for angiography. He was the second case the following day, after an elective outpatient procedure. (Why rush for an NSTEMI?) His door to angiography time was 13 hours and 54 minutes.

Shown below is a selected projection from his angiogram. The diagnostic finding is visualized here. See if you can find it. (I overlooked it until it was pointed out to me.)

Video: AP Cranial Angiogram

Here is a narrated video explaining the angiogram:

Video: AP Cranial Angiogram shown above, now with slow motion freeze frame.

WILLY — I added the video below. For YOU to decide if you want to use it! — :) Ken

HsTnI peaked at 22,286 ng/L and echocardiogram showed LVEF 49% with septal akinesis.

Discussion

First, what a fascinating case! I asked several experienced cardiologists, and no one I talked to had ever seen an isolated septal perforator infarct. The remaining coronary vessels were essentially angiographically normal other than subjectively slow flow which may be suggestive of microvascular dysfunction. Thus, the etiology of the infarct is not entirely clear. Classic plaque rupture is probably the most statistically likely explanation, but it is a bit unusual his remaining vessels did not show any plaque. (However, in patients with positive remodeling, CAD may fail to produce luminal narrowing rendering it essentially invisible on invasive angiography.) Embolism is also possible, although there was no apparent embolic source.

Second, what a shame that he received such delayed angiography. In this case, the delay MAY not have changed his outcome since no intervention was performed. But it is also possible something useful could have been done if the angiogram had been done 13 hours earlier. Perhaps at that time a large thrombus could have been aspirated. There is no telling how things changed as he completed his infarct in the hospital.

More to the point, the fact that no intervention was performed does not mean delaying the angiogram was reasonable BEFORE that information was known. This could equally well have been a proximal LAD lesion.

But it is easy to see why cases like this reinforce the biases of the physicians. Another NSTEMI where delaying cath did not appear to matter to the eventual outcome. That is how a STEMI disciple thinks of it. And in the world of STEMI, this is considered normal care. There is no way for this to be flagged as a systems failure for process improvement. Even though he had a large infarct (with classic symptoms), lost his septum, and experienced reduction in LVEF.

Key LINKS

Wednesday, June 25, 2025

SSmith-DRAFT (KG- Done) - Excellent OMI Care (6-12.21-2025)- I_am_DONE

Monday, June 16, 2025

JesseM-DRAFT (KG- Done)- 65yo-CP during Dialysis (6-16.41-2025)-DRAFT- I_am_DONE

Saturday, June 14, 2025

WillyF-DRAFT (KG- Done) - Subtle ECG & Angiogram (6-12.1-2025)- I_am_DONE