ECG Blog #428, 429 (4-16.1-2024)- PUBLISH JUST FOR PRACTICE!

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Acknowledgment: My appreciation to Chun-Hung Chen = 陳俊宏 (from Taichung City, Taiwan) for the case and this tracing.

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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 #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 80 laddergram cases — many with step-by-step sequential illustration).
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• ECG Blog #128 and ECG Blog #129 — Review Fusion Beats.
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• ECG Blog #366 — MAT explained.
• ECG Blog #199 — More on MAT.
• ECG Blog #65 — for an example of MAT in a patient with chronic pulmonary disease (plus more on the differential diagnosis of MAT).
• ECG Blog #200 — for an example of Wandering Atrial Pacemaker.

I link to 2 additional illustrative Cases taken from Dr. Smith’s ECG Blog. For each of these posts — Please scroll down to the bottom of the page to see My Comment. These cases provide insight to assessment for MAT:

• The January 5, 2020 post in Dr. Smith’s ECG Blog — for an example of MAT.
• The September 30, 2019 post in Dr. Smith’s ECG Blog — for an example of “MAT”, but without the tachycardia ...

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ADDENDUM (XXX/XX/2024):

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ECG recognition of MAT (3:20 minutes Video).

 

Figure-3: Summary of KEY points related to MAT.

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Chun-Hung Chen, M.D.  — EMAIL (3/20/2024)
Emergency Department,
China Medical University Hospital 
2 Yuh-Der Road,Taichung City Taiwan 40447
Tel:  0975681472
drumbeater1978@gmail.com

 

This patient is 92 years old with a history of arrhythmia and hypertension. The electrocardiogram (ECG) was conducted as a routine examination, and the patient did not report any discomfort at the time. The ECG is as follows:

 

The first 4 QRS complexes are junctional rhythm. Afterwards, there are numerous Premature Atrial Contractions (PACs) and Premature Ventricular Contractions (PVCs). Is this interpretation correct?

MY REPLY:

GREAT CASE — and at some point I'll make an ECG Blog of this! I'll acknowledge you and let you know when I do — but it may be a while, as I have a bunch of others to go before.

 

Beats #1,2,3,4; and 11; and 15,16 are ALL of the same etiology !!! These beats have a QRS that is no more than borderline prolonged — with marked left axis (as seen for beats 1,2,3,4 in leads I,II,III) — and incomplete RBBB morphology (beat #11 in V1 — with wide terminal S wave in V6 for beats #15,16) — so I think these are FASCICULAR beats from the LPH (left posterior hemifascicle) because of their incomplete RBBB/LAHB morphology.

 

GREEN arrows show retrograde P waves from these ventricular beats (#1,2,3,4) — but when these fascicular beats occur later — they are PRECEDED by P waves, and therefore do NOT conduct retrograde.

 

RED arrows show that there IS an "underlying" sinus rhythm — but along the way, in addition to the accelerated fasciular focus (which is ~100/minute — whereas it should only be ~20-50/minute) — there are PACs from multiple ( = BLUE lines showing lots of different P wave morphologies).

 

There is NO single specific classification for this particular rhythm! As I emphasize in Blog #366 — MAT is part of a spectrum. At the other end of the spectrum is sinus rhythm with PACs — and in your case, in this asymptomatic 92yo man — there is also an accelerated fascicular rhythm!

 

Since the patient is 92 and asymptomatic — we do not want to "do too much to him" (because it is "hard to make an asymptomatic patient feel better" !!!!). But it's good to appreciate that this rhythm "behaves" as MAT — which means we should look for simple potentially "fixable" exacerbating factors such as electrolyte imbalance (Check K+ and Mg++ ) — hypoxemia (Check O2 sats) — heart failure, sleep apnea, dehydration, etc. If nothing turns up abnormal — it may be that this 92 yo man has been in this rhythm for YEARS .... and we may then want to leave him alone ..

Please see ECG Blog #366 (https://tinyurl.com/KG-Blog-366 ) that reviews MAT.

Magnus- DRAFT- QOH Quiz- OMI or Not? (4-24.1-2024)-ME_to_REVIEW

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The Queen of Hearts AI model for ECG interpretation is still in its early days. Do you think you can outperform the toddler version of the AI model? Version 2.0 will soon be available with four times the training data.

The QoH groups ECGs into OMI and NOT OMI. Each category is subdivided into three levels of confidence. Thus you can get a reading of NOT OMI (low, mid or high). Or you can get sa reading of OMI (low, mid or high). In other words there are six outputs with NOT OMI high confidence on one end and OMI high confidence on the other end.

Take the Quiz below. It is not easy. Good luck! 

Quiz

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SSmith-DRAFT-Regular WCT (3-22.23-2024)-ME_TO_DO

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MY Comment, by KEN GRAUER, MD (3/22/2024):

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Figure 1: The initial ECG in today's case.

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For additional examples of this phenomenon whereby automatic truncation of an EMS ECG may mistakenly result in LVH serving to mimic ischemia — Check out My Comment at the bottom of the page of the following posts in Dr. Smith's ECG Blog — the November 29, 2023 post — June 20, 2020 — March 31, 2019 — March 29, 2019 — and the December 27, 2018 post.

69 y.o. male with pertinent past medical history including Afib, aflutter, cardiomyopathy, PE, HTN who presents to the stabilization room via ambulance for respiratory distress and tachycardia. Per EMS report, patient has been in afib for 5 days, since coming down with flu-like illness with rhinorrhea, productive cough, SOB. Patient is on xarelto, coreg, and dofetilide, says he maybe missed a dose or two during recent illness. On EMS arrival, patient satting high 80s, improved on 4L O2 via NC. Noted to have irregular heart rhythm with rates 120-170s. BG 248. 

First ED ECG

1. · Patient hemodynamically stable, discussed options with patient, would prefer medications before attempting cardioversion
2. · Patient given metoprolol 5 mg IV with improvement in HR to 110-120s, repeated ~q5 mins x3. Patient also given metoprolol PO 50 mg. 
3. · Mag 2g administered 
4. · Appeared mildly hypovolemic on US, LV function grossly preserved, reports decreased PO intake, given gentle 500 cc bolus
5. · CXR with likely infiltrates vs edema, blood cultures collected, started ceftriaxone and azithromycin
6. · Given patient reports not having taken home meds today, given home dofetilide, coreg and xarelto
7. · Labs notable for mild Acute Kidney Injury (Cr 1.5). pH 7.4. 
8. · CT noncon prelim consistent with pneumonia, final read pending
9. · Patient's HR 110s, respiratory effort improved, reported symptomatic improvement

1. · Patient was transferred to the ED team center while in stable condition.  Their care was signed out face-to-face with the ED team center provider.  Please see their note for the remainder of patient's care while in the emergency department.

Previous ECG

t = 14 minutes, after metoprolol

t = 16 minutes

Later in afternoon

WFrick-DRAFT- OMI -LAH Escape Rhythm (3-18.21-2024)-AWAIT WILLY

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MY Comment, by KEN GRAUER, MD (3/20/2024):

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Superb and enlightening discussion of today's case by Dr. Willy Frick! His unique cath film demonstration removes all doubt about the anatomy — with the clearest illustration of acute septal perforator occlusion that I have seen!

• I always find it especially rewarding when the anatomy revealed in prompt cath findings matches our prediction from the initial ECG (ie, Dr. Smith's uncanny immediate impression that, "This ECG could very well represent a septal MI — given the Precordial Swirl Sign).

I focus my comment on 2 aspects of today's case: i) Offering another perspective on some of the findings in the initial ECG; — and, ii) Laddergram and a "deep dive" explanation of the initial rhythm.

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To amplify Dr. Frick's description of Precordial Swirl (taking from My Comment at the bottom of the page in the October 15, 2022 post of Dr. Smith's ECG Blog):

• In the setting of a very proximal site of LAD occlusion (usually proximal to the 1st septal perforator) — with resultant septal ischemia (as well as anterior wall and apical involvement) — the ECG will show ST elevation in leads V1 and aVR — and reciprocal ST depression in leads V5 and V6. This is precisely what we see in Figure-1, in which I've reproduced and labeled the initial tracing.
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• PEARL: Although assessment of ST-T wave changes in lead V1 for beats #5 and 6 is rendered more difficult (because of the RBBB morphology of beats #5,6 in lead V1) — the long lead rhythm strip in Figure-1 is recorded from Lead V1 — and, RED arrow P waves with a normal PR interval before the narrow and normal-appearing QRS complex of beats #1,7,8 reveal what the ST-T wave in sinus-conducted beats looks like! 
• Although the upright T wave with ST elevation is clearly abnormal for the RBBB morphology of beats #5 and 6 that we see in lead V1 — there can be no doubt that the straightened, hyperacute takeoff of the ST segment for sinus-conducted beats #1,7,8 in the long lead V1 represents (together with the ST elevation in lead aVR) — an even more convincing localized picture of acute septal OMI!
• The other PEARL for recognizing Precordial Swirl — is appreciation of a mirror-image opposite picture for the ST-T waves in leads V1 and V6 (that is not the result of LVH). Isn't it EASY to appreciate this mirror-image reciprocal ST-T wave picture between lead V1 and lead V6 by focusing on sinus-conducted beats #7 and 8 in lead V6 compared to the last 2 beats (just below lead V6) in the long lead V1 rhythm strip!

Figure-1: Details and my proposed laddergram for today's initial ECG (See text).

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I found the rhythm in today's initial tracing serves as a "treasure chest" of advanced arrhythmia concepts for readers who love deciphering intricate rhythms.

• NOTE: For readers who prefer "Just the basics" — Knowing there is sinus bradycardia with clearly abnormal ST-T wave morphology in both wide and narrow beats, that is consistent with the acute OMI proven on cath — is all that is needed for appropriate clinical management.
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• BUT — For Arrhythmia Lovers: Are YOU up for the challenge identifying the fascinating features included in this initial tracing?

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In Figure-1 — I've labeled the long lead V1 rhythm strip with arrows, interval measurements — and my proposed Laddergram.

• RED arrows highlight a fairly (but not completely) regular sinus rhythm, consistent with sinus bradycardia and arrhythmia (given this P-P interval irregularity — and an overall atrial rate below 60/minute).
• As noted by Dr. Frick — there are 2 principal QRS morphologies, which is why this rhythm is so intriguing. That said — We know that beats #1,7,8 are each sinus-conducted — because each of these beats is preceded by the same normal PR interval (of 0.18 second) — and each of these beats manifest a narrow and normal appearing rS morphology, as expected in a lead V1.
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• However — None of the other RED-arrow P waves on this tracing manifest normal sinus conduction (Not even the P waves preceding beats #2 and #6 — because the PR interval preceding these 2 beats is clearly less than the 0.18 second that sinus-conducted beats #1,7,8 tell us is needed for normal AV conduction).
• Instead — Beats #3,4,5 all appear to be arising from some type of lower level pacemaker — because the QRS complex of beats #3,4,5 is clearly wider than the QRS of pure sinus-conducted beats #1,7,8 — and — the R-R interval preceding beats #3,4,5 is identical ( = 1160 msec.).
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• KEY Point: The above 2 bullets tell us there is transient AV dissociation — because despite on-time sinus P waves (ie, the consistent RED arrows in Figure-1) — the P waves near beats #3,4,5 are clearly not conducting. 
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• Subtle-but-Important Point: Although the PR interval preceding beats #2 and 6 is shorter than the 0.18 second PR interval needed for normal sinus conduction — this PR interval is long enough to allow some penetration of these sinus P waves into the ventricles. And, the R wave of beats #2 and #6 is not quite as tall as the R wave of beats #3,4,5. I therefore believe that beat #2 (and probably also beat #6) are Fusion beats! (I've labeled beat #2 with an "F").
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• PEARL: The clinical importance of identifying fusion beats — is that this proves that a component of the QRS complex that we see for beats #2 and 6 is arising not from the AV node (which is a supraventricular structure) — but from the ventricles (ie, Fusion of QRS complexes does not occur from simultaneous depolarization of sinus and AV nodal beats). CLICK HERE — for more on fusion beats.
• That beats #2 and 6 are in part ventricular in origin, and arising from the same lower level escape pacemaker as are beats #3,4,5 — is supported by the similar QRS morphology and identical preceding R-R interval of these 5 beats (ie, Each of these 5 beats is preceded by an R-R interval of 1160 msecs.).
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• Dr. Frick has alluded to where the site of ventricular escape beats #2,3,4,5 and 6 is likely to arise. These QRS complexes are wider than normal, but not overly wide — and they manifest RBBB morphology (as seen by beats #5 and 6 in lead V1) and LPHB morphology (as seen by the rS complex with very deep S wave in lead I — and the predominant R waves in leads II,III) — which defines these ventricular escape beats as arising from a site in the fascicles.
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• PEARL: My easy way of deriving which of the 3 fascicles (the slender right bundle branch = RBB — and the left anterior and left posterior hemifascicle = LAH and LPH) is the site of the escape focus — is that the site is whichever of the 3 fascicles is not suggested on ECG.
• In simple words — Since escape beats in Figure-1 manifest RBBB/LPHB morphology — the site of ventricular escape must be in the LAH ( = Left Anterior Hemifascicle).
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• To Emphasize: Fascicular beats are ventricular beats — that are usually not as wide as other forms of ventricular escape rhythms that do not arise from a part of the conduction system. Given the R-R interval = 1160 msecs. between each of the fascicular escape beats in Figure-1 — the rate of this escape rhythm (ie, which is a bit faster than 50/minute) — is probably slightly accelerated, compared to a typical ventricular escape rate (which generally is between 20-40/minute) — suggesting that the Fascicular Rhythm that we see in today's tracing may be consistent with a form of AIVR (Accelerated IdioVentricular Rhythm) — which often appears a "reperfusion" arrhythmia following an acute OMI (For more on AIVR — See My Comment at the bottom of the page in the April 8, 2022 post of Dr. Smith's ECG Blog).

Finally — I always like to try to determine WHY an escape rhythm arises. Looking at the intervals that I carefully measured in Figure-1:

• The sinus rate is slower at the beginning of the long lead V1 rhythm strip (ie, P-P intervals of 1230, 1240 and 1220 msecs. for the first 3 beats in this tracing). This clearly provides a "space" for the slightly accelerated fascicular rhythm to emerge (ie, R-R intervals of 1160 msecs. preceding each of the fascicular beats — indicating a faster rate for the escape rhythm compared to the sinus bradycardia).
• This changes toward the end of the long lead rhythm strip, as the P-P interval drops below the 1160 msecs. R-R interval of the escape rhythm after beat #4 — allowing sinus "capture" for the last 2 beats on the tracing.
• NOTE: The above said — the rate of sinus bradycardia once again slows after beat #7 (P-P interval = 1210 msecs.) — so I would expect return of fascicular escape rhythm IF monitoring would have been continued beyond beat #8.
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• As a last observation — the fluctuating intervals with nearly comparable P-P and R-R duration for sinus beats and fascicular escape in parts of today's tracing bears resemblance to the entity known as isorhythmic AV dissociation — in which the manner that these P-P and R-R intervals vary does not always follow the textbook — which may explain some of the difficulty predicting when the fascicular rhythm arises in today's tracing (For more on isorhythmic AV dissociation — Please see My Comment at the bottom of the page in the May 24, 2020 post in Dr. Smith's ECG Blog).

 

  

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MY Comment by KEN GRAUER, MD (10/15/2022): — 20 cases by SSmith!

http://hqmeded-ecg.blogspot.com/2022/10/precordial-swirl-20-cases-of-swirl-or.html

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Today's blog post introduces a colorful new term = "Precordial Swirl" — which facilitates recognition of a unique ECG pattern that strongly suggests a very proximal site of LAD occlusion (usually proximal to the 1st septal perforator) — with resultant septal ischemia in addition to anterior wall and apical involvement.

How to Recognize Precordial Swirl?

As per Drs. Smith and Meyers — in the setting of acute LAD OMI — there is 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.

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For more on Fusion Beats — CLICK HERE = Blog #128

https://ecg-interpretation.blogspot.com/2016/06/ecg-blog-128-vt-fusion-wct-sinus.html

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MY Comment, by KEN GRAUER, MD (10/8/2018):

Sometimes ST elev only seen in a PVC

https://hqmeded-ecg.blogspot.com/2018/10/hyperacute-t-waves-and-concordant-st.html

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BOTTOM LINE: The great majority of acute OMI tracings identified by ECG will be diagnosed on the basis of ST-T wave morphology changes in sinus-conducted beats. But over the last decade-plus, since I started paying attention to ST-T wave morphologic changes in ventricular beats — I have seen a surprising number of cases in which acute OMI was evident from morphologic change in the PVCs. And on occasion (as is the case here) — acute OMI may only be evident from assessment of ST-T wave morphology of PVCs.

• PEARL: If you can identify one or two leads in which there is NO doubt that ST-T wave morphology of the PVCs is abnormal (as is the case here in leads V2 and V3) — it then becomes much easier to appreciate abnormal ST-T wave morphology for PVCs in other leads.

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Sometimes ST elev only seen in a PVC

See My Comment in Sept. 13, 2022 post

https://hqmeded-ecg.blogspot.com/2022/09/chest-pain-peak-troponin-100000-ngl-and.html

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MY Comment, by KEN GRAUER, MD (9/13/2022):

Sometimes ST elev only seen in a PVC

See My Comment in Sept. 13, 2022 post

https://hqmeded-ecg.blogspot.com/2022/09/chest-pain-peak-troponin-100000-ngl-and.html

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Rhythm Abnormalities in ECG #3:

• Beat #9 is a PVC. In addition to being wide and looking very different than the sinus-conducted beats before and after it (ie, beats #8 and 10) — there is transient AV dissociation. That is — the 2nd P wave (2nd RED arrow) in leads V1,V2,V3 occurs right on time — but the PR interval preceding beat #9 is too short to conduct all the way to the ventricles. This can only happen if the QRS complex that occurs after this 2nd P wave arises "from below" (ie, from the ventricles).
• Actually — I strongly suspect that beat #9 is a Fusion Beat — because all P waves (RED arrows) are on time — and the 2nd P wave does occur before the QRS of beat #9, and does have at least some time to penetrate a portion through the ventricles. This is relevant — because a fusion beat manifests an intermediate QRS and ST-T wave morphology (between a sinus-conducted beat and a PVC) — which means that a "pure" PVC in leads V1 and V2 would manifest more ST elevation than what we see in beat #9 (For more on Fusion Beats — CLICK HERE). 
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• As we have shown in other posts on Dr. Smith's ECG Blog — on occasion, acute ST-T wave changes of acute MI may only be seen in PVCs, and not in the rest of the tracing (See My Comment in the October 8, 2018 post in Dr. Smith's ECG Blog). If there was any more ST elevation than what we see for fusion beat #9 in leads V1,V2,V3 (especially for a PVC in lead V1!) — then we most probably could diagnose a "STEMI" based on this PVC ST elevation.
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• Did YOU Recognize that beats #11-thru-15 in Figure-2 represent a 5-beat run of VT? This run is possibly much longer — since the 12-lead tracing stops after beat #15, which means we have NO idea as to what happened after beat #15. And since no ECG was apparently done after ECG #3 — I suspect the health care team did not recognize this run of VT.
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• PEARL: The reason we know that beats #11-thru-15 represent a run of VT — is that there once again is transient AV dissociation — because there is an on-time P wave that occurs with a very short PR interval right before the QRS complex of beat #11 (double RED arrow in lead V6 of Figure-2) — which proves that beat #11 (and the 4 similar-looking QRS complexes that follow) have to be coming "from below" = from the ventricles.
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• NOTE: The rate of this 5-beat run of VT is not fast. It is ~115/minute — which is at the limit between AIVR (Accelerated IdioVentricular Rhythm) which is often benign and associated with reperfusion — and a "faster" VT rhythm. But since I see no ECG evidence of coronary reperfusion on ECG #3 — one has to be concerned about potential deterioration of this rhythm to VFib (ie, yet another reason for prompt cath).
• For more on AIVR — See My Comment at the bottom of the page in the April 8, 2022 post of Dr. Smith's ECG Blog.

SSmith-DRAFT-BLANK- XXX (4-28.1-2023)-BLANK DRAFT

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

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WFrick DRAFT as of 12-22.11-2023: 

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Written by Willy Frick

A man in his 50s with history of hypertension, hyperlipidemia, and a 30 pack-year smoking history presented to the ER with 1 hour of acute onset, severe chest pain and diaphoresis. His ECG is shown:

What do you think?

The history thus far is highly suggestive of OMI, so we must study the ECG very closely to see if we can confirm this. Looking at the rhythm strip, we see there is more going on than simple sinus rhythm, and in fact there are two different morphologies of QRS complexes. Take a closer look at the rhythm by itself and see if you can figure out what's going on before scrolling further.

If we set our calipers on the R waves and number them, we see that even though the PR interval shortens and the P wave disappears beneath the R wave, the R wave continues to occur at very regular intervals. That is, until the 7th R wave which comes a little bit sooner than expected.

I will leave more detailed rhythm discussion to the illustrious Dr. Ken Grauer below, but this use of calipers shows that the rhythm interpretation is: Sinus bradycardia with a competing (most likely junctional) rhythm. The fact that R waves 2 through 6 are junctional does make ischemia more difficult to interpret -- but not impossible. The Queen of Hearts does not care about rhythm analysis, she simply looks at the ECG and decides whether it represents OMI or not. 

Here is the Queen's verdict and her explanation:

She sees OMI but with low confidence. I sent this to Dr. Smith with no context and he said "Could very swell be a septal OMI." He pointed out the precordial swirl sign. As a reminder, precordial swirl occurs when the LAD is occluded at or proximal to the major septal perforators causing significant septal ischemia. This pulls the ST elevation vector rightward resulting in ST elevation most pronounced in the right precordial leads with reciprocal depression in the lateral precordial leads.

An aside on understanding the morphology of the escape complexes:

The QRS duration is very close to 120 ms which suggests it may be lower in the junction, perhaps even near to the his-purkinje system (although the rate is a bit fast for ventricular escape). Inspecting the morphology can give us more information about the source of the escape rhythm. I have shown representative R waves from several leads below.

Step 1 is to inspect for right vs left bundle morpholoy, which depends on leads I and V1. Remember, we have to restrict our inspection to the QRS complexes that have the escape morphology (that is, R2 through R6). That leaves us with only R2 in lead I, which is negative in its terminal portion consistent with rightward depolarization (since I is oriented right to left). Lead V1 is positive in its terminal portion, also consistent with rightward depolarization (since V1 is oriented toward the right fourth intercostal space). This is consistent with RBBB morphology, which suggests that the impulse originates closer to the left bundle. (This may sound confusing, but if the impulse originates near the left bundle, then the right bundle must activate later. This is the exact same activation sequence as you would see in the case of right bundle change block.)

Step 2 is to inspect for fascicular morphology, which depends on the limb leads. We see marked right axis with rS complexes in I and aVL, and qR complexes in II, II, and aVF. (Strictly speaking, there is no visible Q wave in aVF but this is because of the buried P wave. Since II and III have Q waves, aVF must also have one.) This is left posterior fascicular block morphology, suggestive of left anterior fascicular origin. (This is the same logic as above, where right bundle branch morphology predicted left bundle branch origin.)

Back to the assessment of ischemia:

Returning to the ECG, the leads that catch my eye first are -- I, II, V4, V5, V6. The first beat in leads I and II, and both beats in V4-6 are sinus beats, and they all have ischemic appearing down-up T waves. We also see that aVL (with escape complexes only) has subtle ST depression which is inappropriately concordant to its predominantly negative QRS complex. Here the ECG is again:

Now that we see multiple areas with what appears to be reciprocal change, the final task is to find the primary vector of injury. Looking at V1, which has right bundle branch block morphology, there is concordant STE, which fits perfectly. Due to the precordial swirl Dr. Smith mentioned, the STD in the lateral leads is reciprocal to the STE in V1. And because swirl is a sign of LAD OMI, it is not surprising that there is reciprocal depression inferiorly in II.

Fortunately, the emergency physician evaluating the patient activated the cath lab immediately. (This is documented as a STEMI in the clinical notes and in the cath report, but certainly does not meet STEMI criteria and is therefore an NSTEMI by definition. For national registry purposes, this will be incorrectly classified as a STEMI.)

The first angiographic shot below is AP cranial, good for viewing the LAD and diagonal vessels.

(Right click the video and click "Loop" to see the video repeat endlessly.)

Below I have shown a still with arrows indicating the LAD, septal perforators, and a few diagonal vessels. At the tip of the red arrow, you can see a round filling defect which represents a thrombus and appears to involve the origin of the septal perforators (hence swirl sign).

This next angiographic shot is RAO caudal, best for viewing the LCx and its branches, the obtuse marginals. In this case, it also more clearly shows the subtotal occlusion of the septal perforator.

Below I have shown a still with arrows indicating the LAD, septal perforators, one diagonal vessel, LCx, and OM. The LAD thrombus is not as well visualized in this view, but the orange arrow points to the origin of the septal perforators which almost appears not to connect to LAD due to subtotal occlusion.

And finally, after placement of a stent in the LAD:

Before and after:

(Unfortunately, this resulted in the "jailing" of the septal branches behind the stent and probably some degree of plaque shift which is why they do not opacify well in the "after" shot. This was the cost of preventing infarction of the anterior wall.)

Despite very rapid presentation (presenting cTnI undetectable) and reperfusion, the patient still had peak cTnI 48.4 ng/mL (ref. < 0.049). Still, his anterior wall was saved and he had normal ejection fraction without heart failure.

Learning points:

• Precordial swirl can be seen in proximal LAD occlusion involving septal perforators, and you can miss it if you are depending on obvious anterior ST elevation.

• Ischemia can be disguised by a wide escape rhythm, which decreases the sensitivity of ECG.

• Right bundle branch escape morphology indicates left bundle branch origin, and left bundle branch morphology indicates right bundle branch origin.