How a pause can cause cardiac arrest

Written by Magnus Nossen —  with edits by Grauer 

The tracings in today’s case is from a patient in his 80s being admitted due to dyspnea. Below is the presentation ECG. What do you think?

The above ECG shows sinus rhythm. There is one premature atrial contraction which is blocked and this causes a short pause. The following sinus P wave conducts with a slightly shorter PR interval. There is slight ST depression in leads V4-V5 that could be ischemic in nature. There are no clear signs of OMI. The patient was admitted and put telemetry. 

While on telemetry monitoring he suffered cardiac arrest and was resuscitated. What ECG finding may have contributed to (or precipitated) the cardiac arrest?

The R-R interval for the first 3 normally conducted beats looks regular. There is a prolonged QTc.  

• I measure the QT at 520ms (13 small boxes each 40ms). Since the heart rate is 60bpm — the QTc will equal the QT. 
• Note: Due to the limited number of normally conducted beats — it is hard to be sure whether the underlying rhythm is sinus with baseline artefact or atrial fibrillation. 
• There a two PVCs. The second PVC sets off a run of polymorphic VT that continues to the end of the tracing — and since the QTc is prolonged, this is TdP ( = Torsades de Pointes).

Below the rhythm strip has been annotated

The QRS complexes have been numbered for clarity. Beat #4 is a PVC that is followed by a compensatory pause. The pause is concluded by a narrow complex QRS (beat #5). The QT interval (blue line) of beat #5 is significantly prolonged. Of note — the QT interval of beat #5 (blue line) is markedly prolonged compared to the QT interval in the beginning of the tracing (red line). This is pause-dependent QTc prolongation (which is described as the most common cause of TdP in patients with LQTS).

After resuscitation and defibrillation, there were no more episodes of TdP. Had there been recurrent episodes of pause-dependent TdP, temporary ventricular pacing at a higher heart rate would have been indicated to suppress the pauses and in that way decreasing the risk of further episodes of TdP.

Post ROSC the patient was alert and cooperative. A coronary angiogram was done that did not show significant coronary artery disease. Echocardiography showed apical ballooning with hypokinesis. NT-proBNP was significantly elevated at 4900ng/L (ref < 500ng/L). High sensitivity troponin T was mildly elevated peaking at 107ng/L (ref < 14ng/L).

Below is the patient’s 12 lead ECG following defibrillation. What does this ECG tell you?

The ECG shows sinus rhythm. Buried in the ST segment of beat #1 is a non-conducted P wave (red arrows). 

• This non-conducted P wave could be a PAC. It could also possibly be part of a Wenckebach cycle (dropped beat). The PR intervals for beats #4-6 seem slightly longer (280ms) than for beat #2 (240ms). There are only six beats in this ECG as the precordial and standard leads are recorded simultaneously — so  a longer rhythm strip would be to better evaluate what is going on. 
• Note: The patient while on telemetry had alternating atrial fibrillation, sinus rhythm with 1st degree AV block and also periods of Wenckebach conduction. That said — rhythm interpretation here is more of an academic interest  — as the most striking findings are the widespread T-wave inversions and QT prolongation.

The patient was diagnosed with stress cardiomyopathy. Widespread T wave inversions and prolongation of the QT interval is not uncommon in Takotsubo cardiomyopathy. On admission serum magnesium was 0,56 mmol/l (ref 0,71-0,94 mmol/l). Potassium was 4,8 mmol/l. (ref 3,5-4,6 mmol/l). The patient was not on any medications known to prolong the QT interval. After magnesium replacement the QTc did not significantly shorten. 

In conclusion — this patient suffered cardiac arrest secondary to pause-dependent QTc prolongation in the setting of an already prolonged QTc from Takotsubo cardiomyopathy. Moderate hypomagnesemia may have contributed, however the QTc remained very prolonged even after magnesium replacement. The QTc then gradually shortened over the course of several days as is usual for stress cardiomyopathy. 

Learning points:  

• Takotsubo can lead to cardiac arrest from ventricular arrhythmia. As a result — telemetry monitoring is indicated in the acute phase
  
  
• Pause-dependent TdP is the most common cause of cardiac arrest in patients with LQTS. It is likely to be the same for patients with acquired long QT interval. 
   

=================================== 

MY Comment, by KEN GRAUER, MD (9/16/2024):

===================================

Today's post by Dr. Nossen highlights an important concept — namely pause-dependent precipitation of a malignant ventricular arrhythmia (in this case Torsades de Pointes).

• The clinical significance of this concept extends beyond the episode of Torsades presented in today's post — in that the key principle implicated in pause-dependent Torsades is the same key principle operative in the commonly cited (but all-too-frequently misunderstood) Ashman phenomenon. 

I have periodically called attention to examples of the Ashman phenomenon as they occur in Dr. Smith's ECG Blog (See My Comments in the January 5, 2020 post — the June 17, 2020 post — and the March 30, 2023 post, among others).

• PEARL #1: The simplest way to describe the Ashman phenomenon — is that it represents pause-dependent aberrant conduction. And, the easiest way to recognize this phenomenon is to remember that "the funniest-looking beat — is most likely to follow the longest pause". Clearly, exceptions exist — but I always consider Ashman-related aberrant conduction when wide, different-looking beats are most often seen following slight pause in the rhythm.

Rationale for the Ashman Phenomenon:

The KEY principle of the Ashman phenomenon is pause-dependency — namely, that the RP (Refractory Period) is dependent on duration of the preceding R-R interval. This concept is best explained by Figure-1:

• Panel A in Figure-1 schematically illustrates that a premature impulse (PAC or PJC) occurring during the ARP (Absolute Refractory Period — corresponding to point X) will be blocked.
• In contrast — a PAC (or PJC) occurring after repolarization is complete (corresponding to Z in Panel A) — will be conducted normally.
• Aberrant conduction will only occur IF a premature impulse occurs during the RRP (Relative Refractory Period — corresponding to point Y in Panel A).

Events in Panel B — suggest a different clinical situation.

• Once again — points X, Y and Z represent theoretical timing for 3 PACs. 
• Premature impulse X will again be blocked (since it occurs within the ARP).
• This time, however — both Y and Z fall beyond the RRP — so both of these premature impulses will be conducted normally to the ventricles (because the ventricular conduction system has fully recovered and conducts normally by this time).

KEY Point: Whether a premature impulse will fall within the RRP (and conduct with aberration) — will depend on: i) The coupling interval of the premature beat (ie, How soon after the preceding QRS complex the PAC or PJC occurs); and, ii) The length of the R-R interval immediately preceding the anomalous (widened) beat. This is because duration of the RP is directly proportional to the length of the preceding R-R interval. When heart rate slows (as it does in Panel C of Figure-1) — the subsequent ARP and RRP will both be prolonged!

• Panel C — shows the effect of rate slowing on conduction of the 3 PACs from Panel B. Premature impulse X will again be blocked (because it occurs within the ARP when no impulse, no matter how strong can be conducted).
• Premature impulse Z will again be conducted normally (since it occurs after the RP is over).
• However, premature impulse Y (which in Panel B had occurred after repolarization was complete) — will now be conducted with aberrancy (since the preceding R-R interval is now longer in Panel C — thereby prolonging the RRP, which now extends to encompass the timing of Y).

Figure-1: Illustration of the effect that the preceding R-R interval exerts on duration of the subsequent refractory period (See text)

===========================

The Rhythm in Figure-2: A picture is worth 1,000 words ...

• The rhythm in Figure-2 is from another patient. It begins with 3 sinus-conducted beats.
• Beat #4 is a PAC (the premature P wave highlighted by the YELLOW arrow).
• Following another sinus beat ( = beat #5) — a run of rapid and irregular beats is seen, with loss of atrial activity after beat #6.
• To Emphasize: Although beat #6 is wide — this beat is also a PAC (the BLUE arrow highlighting the premature P wave preceding beat #6 that notches the T wave of beat #5). But there are 3 other wide beats in the tachycardia that begins with beat #6 ( = beats #7; 13,14).

Application of the Ashman phenomenon in Figure-2:

• Although in Figure-2 — the coupling intervals of the 2 premature P waves highlighted by the YELLOW and BLUE arrows  is virtually identical — the reason beat #6 is conducted with RBBB aberration (whereas beat #4 is conducted normally) — is that beat #6 is preceded by a longer R-R interval (ie, the R-R interval between beats #4-5 is longer than the R-R interval between beats #2-3).
• In simple terms — the "funny-looking" beat follows the longer pause (therefore early beat #6 is aberrantly conducted — whereas the equally early beat #4 is conducted normally).
• PEARL #2: Clinically, once we know that beat #6 is an aberrantly conducted PAC — interpretation of the rest of this rhythm strip becomes easy. Similar-looking wide beats #7,13,14 must also be aberrantly conducted supraventricular impulses — and since P waves are lost after beat #6 and subsequent R-R intervals are irregular — beats #7-thru-16 constitute a run of rapid AFib.

Figure-2: Application of the Ashman phenomenon to this arrhythmia (See text).
= = = = = = = 
Note: Lead MCL-1 is a right-sided monitoring lead that provides a similar perspective as is seen in lead V1 on a 12-lead tracing — such that QRS morphology of wide beats #6,7; 13,14 is consistent with RBBB aberration.

=========================== 

Returning to Today's CASE:

As per Dr. Nossen — the KEY "Take-Home" message from today's case is that it is the pause after the 4th beat in today's initial tracing that precipitates Torsades de Pointes, with resultant cardiac arrest.

• Most Torsades is the result of a pause-dependent effect that predisposes to development of the malignant arrhythmia (Dohadwala et al — Heart Rhythm Case Rep 3(2):115-119, 2017). 
• Intermittent long-short pauses increase the risk of Torsades even more than a persistent bradycardia or stable AV block with a slow ventricular response — because in addition to prolonging the RP, there is a disproportionate increase in dispersion of repolarization times with long-short pauses through a non-homogeneous effect on myocardial tissue.

In Conclusion: The principle is the same. A longer R-R interval associated with transient slowing of a given cardiac rhythm results in pause-dependent prolongation of the subseqent RP. 

• With certain supraventricular rhythms — this may result in aberrant conduction (Ashman phenomenon) of the next early beat (ie, as for beat #6 in Figure-2).
• In the setting of a predisposed patient (today's older patient with hypomagnesemia and baseline QTc prolongation from Takotsubo Cardiomyopathy) — the pause-dependent effect on an already prolonged QTc precipitated a series of episodes of Torsades de Pointes.

===========================

• NOTE: For those wondering about the "correct" spelling for TdP (Torsades de Pointes) — I review potential alternative spellings of this French term in the P.S. of My Comment at the very bottom of the page in the September 2, 2024 post of Dr. Smith's ECG Blog.

Acute chest pain, right bundle branch block, no STEMI criteria, and negative initial troponin.

Written by Pendell Meyers

A man in his 40s called EMS for acute chest pain that awoke him from sleep, along with nausea and shortness of breath. His history included known heart failure with prior EF 18%, insulin dependent diabetes, and polysubstance abuse. Vitals were within normal limits except for tachypnea. 

Here are his EMS ECGs along with the Queen of Hearts interpretations below each one:

 EMS1 0650

EMS2 0707

Click here to sign up for Queen of Hearts Access

The ECGs show RBBB and LAFB, with small but important concordant STE in V2. In EMS2 ECG, the T waves in V5 is possibly hyperacute. Because the most severe LAD OMIs can cause ischemic failure of the RBB and LAF, any patient with ACS symptoms and new RBBB and LAFB with any concordant STE has LAD OMI until proven otherwise.

The paramedic called the EM physician ahead of arrival and discussed the case and ECGs, and both agreed upon activating "Code STEMI" (even though of course it is not STEMI by definition), so that the acute LAD occlusion could be treated as fast as possible. So the cath lab was activated.

Here is his ECG on arrival to the ED, still with active pain:

ED1 at 0727

A baseline ECG was available from 1 month ago:

First troponin was drawn before cath, which would soon return at 14 ng/L (within normal limits).

He was taken rapidly to the cath lab and here are some representative images before and after intervention:

Acute proximal LAD culprit with TIMI 0 flow, 100% stenosis, thrombotic occlusion, requiring thrombectomy and PCI.

Post cath 

EF was estimated at 15% with severe global hypokinesis, and akinesis of the apex.

Long term outcome is unavailable.

Learning Points:

Currently by definition, there is unfortunately no such thing as a formal diagnosis of STEMI or STEMI criteria in the setting of RBBB and LAFB. There is no recognition of STEMI equivalency in this setting in the USA guidelines currently. We recommend using the modified Sgarbossa criteria for all significantly wide QRS complexes.

This is an acute deadly proximal total LAD OMI in the setting of "NSTEMI". You must far exceed the guidelines and current world paradigm to deliver good care to these patients. As you can see above, AI can help.

Initial negative troponin is not uncommon even in the most dangerous OMI cases, when the time from occlusion to troponin is within the first few hours.

Smith: LAD OMI with RBBB/LAFB is not only subtle on the ECG, but most of these patients are extremely ill: most I have seen are post-ROSC, in cardiogenic shock, or arrested shortly after.  DO NOT MISS THESE!

===================================

MY Comment, by KEN GRAUER, MD (9/13/2024):

===================================

The KEY consideration in today's case is — How effectively can we diagnose acute OMI in a patient with RBBB? While fully acknowledging the challenge of recognizing OMI in such a patient, to the extent of being able to convince the On-Call interventionist of the need for prompt cath — today's case shows this can be accomplished in very time-efficient fashion.

• The "good news" in today's case — is that both the EMS team and the EM physician rapidly recognized strong suggestion of acute LAD occlusion on prehospital ECGs, thereby enabling activation of the cath lab even before the patient arrived in the ED.
• I focus my comment on the KEY ECG findings that led to this decision. For clarity in Figure-1 — I've labeled the 2 EMS ECGs and the baseline ECG recorded ~1 month earlier.

The Clinical Setting in Today's CASE:

Today's patient is a man in his 40s with underlying co-morbidities, including known heart failure with markedly reduced cardiac function (EF ~18%) — who was awakened from sleep with severe chest pain.

• Even before looking at the initial ECG — this patient is in a high prevalence group for having an acute event. Therefore — even subtle ECG abnormalities merit especially close scrutiny.

The Initial EMS ECG:

I've labeled key findings in ECG #1:

• The rhythm is sinus at ~90/minute. The PR interval is normal — but the QRS is wide with morphology consistent with RBBB (Right Bundle Branch Block) — in that the wide QRS is predominantly upright in lead V1 (with a QR pattern) — and there are terminal S waves in lateral leads I and V6. 
• There is fragmentation (especially of the S wave in inferior leads — and in the R wave irregularities in leads V3,V4,V5) — which is consistent with this patient's severe underlying heart disease.
• The predominantly negative QRS complex in each of the inferior leads indicates marked LAD (Left Axis Deviation) that is consistent with LAHB (Left Anterior HemiBlock) — with combined RBBB/LAHB indicating bifascicular block.
• Regarding chamber enlargement — biatrial abnormality is suggested by the tall, peaked P waves in the inferior leads (consistent with RAA) — and the deep negative component to the P wave in lead V1 (consistent with LAA).
• Assessment for LVH and RVH is difficult because: i) RBBB complicates such assessment; — and, ii) As is common with EMS tracings — QRS amplitude is truncated when R wave or S wave amplitude exceeds 10 mm (dotted PURPLE lines in Figure-1 that "cut off" the R in leads V3 and V4 — as well as the S in lead V6).
• More than just RBBB — there are deep and wide Q waves in leads V1 and V2 (BLUE arrows in these leads). When seen in association with RBBB — such Q waves suggest septal infarction has occurred at some point. 
• In addition — there are subtle-but-real ST-T wave abnormalities in leads V1-thru-V4 suggesting a recent acute event. The RED arrow highlights the most obvious of these — as the relative amount of ST-T wave depression with RBBB should decrease instead of increasing as one moves across the precordial leads. BLUE lines over these first 4 chest leads mark the subtle abnormal coving of the ST segment in leads V1-thru-V4, with a hint of ST elevation in leads V1,V2 (whereas with uncomplicated RBBB — the ST-T wave should be slightly depressed).
• 
  
• IMPRESSION: Given the history ( = this patient with known heart disease was awakened from sleep with severe CP) — this initial EMS ECG suggests acute LAD OMI until proven otherwise. Some findings are subtle — which may be the result of some "pseudonormalization" on the way to developing reperfusion T wave inversion (We do not know IF this patient's CP has lessened at this point in time) — and we do not yet have a previous ECG for comparison — but, as was recognized by today's EMS team — this may be acute!

Figure-1: To facilitate serial ECG comparison — I have placed ECGs #1 and #2 together, with the baseline tracing from ~1 month earlier.

The Repeat EMS ECG

17 minutes later — the diagnosis of acute LAD OMI is confirmed by a series of subtle-but-definitely-present ST-T wave changes in the chest leads (within the RED rectangle in ECG #2).

• Subtle ST-T wave changes on serial ECGs are BEST appreciated by lead-by-lead comparison when both tracings are placed side-by-side (as in Figure-1).
• RED dotted lines in ECG #2 that mark the ST segment baseline in lead V2, and leads V4,V5,V6 — document new ST elevation that was not present in ECG #1. That this finding is real — is supported by the increased ST coving in lead V4 and straightening of the ST segment takeoff in leads V5,V6 (Compare the light BLUE with the RED lines over the 1st QRST complex in leads V4,V5,V6 of ECGs #1 and 2).
• NOTE: While I fully acknowledge how subtle these changes in ST-T wave shape are — when they occur in multiple leads as they do here (in this patient with new severe CP) — these are real changes!

PEARL: Did YOU notice the Fusion Beat in ECG #2?

Although there is no long lead rhythm strip — there is a fusion beat (F) in ECG #2. Red arrows show on-time sinus P waves in lead aVF of this tracing — with the too-short-to-conduct PR interval before the 3rd complex indicating fusion of sinus conduction with a late-cycle ventricular beat.

• Realizing that the ST-T wave of this fusion beat is attenuated by the oppositely-directed ST-T wave contribution from partial sinus conduction — the shape of the ST-T wave in leads aVL and aVF of this fusion beat still looks "off", and supports chest lead ST-T wave findings that suggest an acute event.

And — the Baseline ECG!

The EMS team in today's case knew to activate the cath lab within the 17 minutes it took to record the first 2 ECGs. The EMS team did not need the baseline ECG to make this decision. That said — as soon as this baseline ECG was found, all doubt was removed.

• The prior tracing from ~1 month earlier shows sinus rhythm, LAHB, RAA and marked LVH (R ≥12 in aVL — and especially the very deep S waves in V2,V3 + ST-T wave changes of LV "strain" in multiple leads) — but no acute changes!
• Comparison of this baseline tracing with ECGs #1 and #2 confirms that the RBBB, septal Q waves and above described ST-T wave changes are all new — and consistent with the acute LAD occlusion found on cath.

Texted from a former EM resident: 70 yo with syncope and hypotension, but no chest pain. Make their eyes roll!

A former resident texted me this case: 

"Hey Dr. Smith. Hope you’re doing well! How excited would you have been about this case?" 

Here is the case:

Report from EMS was witnessed syncope, his son did CPR, but the patient had pulses when EMS arrived. When the patient arrived in the ED, he was still hypotensive in 70s, slowly improving with EMS fluids. No Chest Pain, but somnolent. 

Here is the ED ECG (a photo of the paper printout)

What do you think?

Smith: There is 1mm of STE in V1 and almost 1.5mm in V2.  There are QS-waves in V1-V3 suggesting old anterior MI with persistent ST Elevation (LV aneurysm morphology), but I have written a couple papers showing that in LV aneurysm, the T-wave is not > 0.36 x the QRS amplitude in any of V1-V4.  The highest ratio here is in V4 at 1/1.5 = 0.67.   Next is V2 at 5/14.5 = 0.34.   The fact that this is syncope makes give it a far lower pretest probability than chest pain, but it was really more than syncope, as the patient actually underwent CPR and had hypotension on arrival of EMS.

1. Smith SW.  T/QRS Amplitude Best Distinguishes Acute Anterior MI from Anterior Left Ventricular Aneurysm.  American Journal of Emergency Medicine 2005; 23(3):279-287.

https://www.sciencedirect.com/science/article/abs/pii/S0735675705000811

 

2. Klein LR.  Shroff G.  Beeman W.  Smith SW.  Electrocardiographic Criteria to Differentiate Acute Anterior ST Elevation Myocardial Infarction from Left Ventricular Aneurysm.   The American Journal of Emergency Medicine 2015; 33(6):786-790.  https://www.sciencedirect.com/science/article/abs/pii/S0735675715001904

So I responded with these words:

Smith: "There are QS waves, which suggest old MI.  But the T-waves in LV aneurysm are not this big.  This is LAD Occlusion until proven otherwise."

Smith: "What did you do?"

Former resident: "I activated, ran it through the queen and she agreed but cardiology wasn’t excited."

The Queen say OMI with High Confidence.  

Explainability shows: she sees the T-waves AND the QRS in lead V2, but also in leads V3-4.

Smith: "Did they take him right away to cath?"

Former Resident: "They took him but they rolled their eyes at me (Smith editorial comment: how often have they rolled their eyes at YOU?). They said it looked similar to his old one (in my opinion, similar, but not similar enough to be able to say no OMI)."

Smith: "What was the outcome?"

Former resident: "Just saw cath report, LAD stent was 100% acutely occluded."  

They of course opened and stented it.

Former resident: "The biggest piece for me was the size of the T waves in relation to everything else. You taught us well!"

Click here to sign up for Queen of Hearts Access

===================================

MY Comment, by KEN GRAUER, MD (9/11/2024):

===================================

Among the important concepts brought out by today's case are the following: 

• #1) — Is acute OMI a common cause of syncope?
• #2) — How to distinguish between LV aneurysm vs new infarction?

To emphasize (as noted by Dr. Smith) — today's patient did not present only with syncope. Instead — the "syncopal episode" prompted the patient's son to start CPR, and was associated with persistent hypotension. That said — syncope remains a common reason patients seek emergency care — so it is worth addressing how often acute MI is the cause.

• Among patients who present purely for “syncope” — our  greatest concern is focused on those with a cardiac-related etiology for their syncope — since longterm prognosis is poorest for these patients unless a “fixable” etiology is discovered.
• Acute MI per se usually does not depress cardiac function and blood pressure enough to cause syncope (Mostafa et al — J Com Hosp Intern Med Perspect 13(4):9-12, 2023-). But especially with infero-postero OMI, it may do so indirectly — by activating the BJR (Bezold-Jarisch Reflex) — which in response to sympathetic activation (and/or in association with coronary reperfusion) — may activate mechanoreceptors that are primarily located in the infero-postero wall of the LV, producing a potent parasympathetic effect that may lead to reflex bradycardia, peripheral vasodilation and hypotension (Cadogan — Life-In-The-Fast-Lane, 2022 — and — Holland, Stouffer — JSCAI 1(2),2022).
• Other cardiac-related causes for syncope associated with acute MI may include malignant ventricular arrhythmias and bradyarrhythmias including AV block.
• The "good news" — is that a cardiac-related cause of syncope is unlikely if the initial ECG is normal, and cardiac monitoring in the ED fails to reveal significant arrhythmia.

LV Aneurysm vs New Infarction?

The initial ECG in today's case was recognized as definitely abnormal — but the question arose as to whether this ECG indicated old infarction vs a new acute event.

• QOH (Queen Of Hearts) and Dr. Smith's former resident immediately diagnosed acute OMI — but providers in the ED thought the ECG findings "looked old".
• As per Dr. Smith — T/QRS amplitude measurement clearly indicated that rather than LV aneurysm, the elevated ratio suggested acute infarction until proven otherwise. 

I thought qualitative assessment of the initial ECG (that I have labeled in Figure-1) — clearly favored new on-top-of old infarction until proven otherwise:

• At the least — ECG #1 is diagnostic of previous infarction(s) at some point in time because of diffuse abnormal Q waves. Not only are such Q waves seen in all 3 inferior leads — but they are also present in all 6 chest leads (QS complexes in leads V1-thru-V4). Most of these Q waves are unusually wide with respect to QRS amplitude in the lead being looked at — as well as fragmented in multiple leads, including lead V3 (BLUE arrow) and leads III, aVF, V2 and V4.
• But in addition to prior infarction — lead V2 is clearly "off", as the ST segment straightening in this lead "looks" acute — and the disproportionate amount of ST elevation in V2 is visually beyond that expected with simple LV aneurysm.
• In the context of this hyperacute appearing ST-T wave in lead V2 — the other 2 leads within the RED rectangle support the impression of acute injury until proven otherwise (especially the ST segment straightening in lead V1, with a disproportionate amount of ST elevation for this lead).
• I would not have been convinced by the subtle ST elevation in the inferior leads alone — but I thought the ST segment coving and T wave inversion in lead aVL added support that the above highlighted findings in leads V1,V2,V3 must be assumed acute until proven otherwise.

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

"The dye don't lie" ...except when it does. Angiogram Negative, or is it?

Written by Willy Frick

See the fascinating discussion on X started by this post. Link below.  

A 40 year old woman was at home cooking when she developed chest pain. She took an oxycodone and called EMS. Her presenting ECG is shown below:

ECG 1

What do you think?

I sent this to Drs. Meyers and Smith and the response was: "I’m quite confident that this is OMI."

Here is the Queen's verdict with explainability:

She sees OMI with low confidence. As an aside, the explainability above came from using QOH in the Telegram bot environment. I had previously run this ECG through QOH in the PMcardio app environment and she reported mid confidence, shown below.

Although the QOH is exactly the same in both environments, extremely subtle changes in digitization from one analysis to the next can slightly change her confidence. The QOH output is a number between 0 and 1. A value of 0 would be "not OMI" with high confidence, and a value of 1 would be "OMI" with high confidence. The cut points for what constitute OMI and not OMI as well as confidence levels are calibrated to maximize sensitivity and specificity according to the receiver operating characteristic.

Queen of Hearts version 2 is in active development, and she is trained on a much larger data set than version 1. The image below shows output for QOH version 1 and QOH version 2. You can see that version 2 has a higher number than version 1, hence she sees the ECG as more OMI-like than version 1.

Version 2 of the Queen of Hearts

She is more confident than Version 1

Click here to sign up for Queen of Hearts Access

Back to the case...

The ECG was interpreted as showing diffuse STD with some STE in aVR. The notes do not comment on V1 and V2. In fact, V1 and V2 both have STE, and V2 in particular has hyperacute T waves. Taken together with STD in the lateral precordial leads, this represents precordial swirl, and is therefore diagnostic of LAD OMI proximal to the first major septal perforator.

Even though QOH did not have access to the prior ECG, we do. This is shown below:

Prior ECG

As compared to the prior ECG, we can now feel completely confident that the V2 T waves are in fact hyperacute, and that the current ECG shows LAD OMI.

Initial hscTnI was 10 ng/L (ref. <14). The patient was thought to have low likelihood of ACS, and cardiology recommended repeat troponin, urine drug testing, and echocardiogram. There was no recommendation for repeat ECG. I strongly believe you should never trend troponin without also trending ECG. Troponin tells you what was happening hours ago, ECG tells you what is happening right now.

Repeat hsTnI two hours after the first increased from 10 to 8,512 ng/L. At that point, cardiology elected to treat for ACS. Bedside echocardiogram showed hypokinesis of the mid to distal anterior wall and apex. Angiography is shown below.

Shown below is a left anterior oblique view of the RCA with a little bit of cranial angulation ("LAO crani").

Here is a representative still showing RCA and the distal bifurcation into the PDA and a right posteralateral (RPL) branch. The diaphragm tells you this is a cranial shot (i.e., you are looking down from above).

Next is RAO cranial shot.

Below is a representative still showing the LAD and septal perforators. The diagonal branches are overlapping one another and not well visualized in this view. Although this view is not meant for it, there is fair visualization of the LCx. The diaphragm again tells you this is a cranial view.

So far, we haven't seen anything to explain LAD OMI, but let's keep looking. The next shot is anteroposterior ("AP") cranial, which typically visualizes the LAD and diagonal bifurcation.

Here is a representative still showing the LAD and septal perforators. The first and second diagonal branches are both sizable vessels, but unfortunately they're overlapping here, so they are not very well visualized. The LCx is not well visualized (nor is it meant to be in this view).

Again, not much going on so far. Certainly there is TIMI 3 flow everywhere. The next view is LAO caudal (sometimes called the "spider view"). This view is best for left main and the proximal LAD, LCx, and branch vessels.

In this representative still, we see the LAD, diagonal branches, and LCx. All proximal vessels appear widely patent, and the septal perforators are not well visualized (due to overlap with LAD). There is no diaphragm since this is a caudal view.

The last shot is RAO caudal, which is good for proximal LAD and LCx.

And here is a representative still showing LAD, diagonal branches, the ostium of the septal perforators, and LCx.

To most, this probably looks like completely normal angiography. And it could easily be mistaken as such. Eagle eyed readers might notice a slightly scooped out appearance of the proximal LAD in the above view, right at the head of the top left green arrow. The cardiologist called this 20% stenosis.

In a large proportion of cath labs, the operator would probably have ended the case at this point. You can easily imagine this patient getting one of several diagnoses -- vasospasm, MINOCA, pericarditis, or maybe even no diagnosis at all beyond "non-obstructive coronary artery disease."

Smith comment: a very high proportion of MINOCA are ruptured plaque with lysed thrombus. That plaque is at risk of thrombosing again.  It is worthwhile remembering that the majority of plaques which rupture are non-obstructive before they ulcerate and thrombose.  If the thrombus completely lyses, then there may be no visible evidence on angiogram.  An angiogram is a "lumenogram" and does not "see" the extraluminal plaque.  Most plaque is outside the lumen!!  And so other modalities may be necessary.

Fortunately, this operator used intravascular ultrasound (IVUS). (Another option would be to use Optical Coherence Tomography for Coronary Imaging).  This showed a "completely normal vessel throughout the LAD, except in the proximal/ostial LAD there was a ruptured plaque." With this in mind, ECG 1 showing precordial swirl makes perfect sense. In fact, there was transient occlusion of the LAD proximal to the septal perforators.

At the time of IVUS, there was no thrombus. The report describes extension of the plaque into the distal left main. The operator documented thoughtful consideration of risks and benefits of stent placement. Technically, there was a very narrow landing zone for the stent, and missing this could result in "jailing" the LCx, which is ideally avoided. Furthermore, the operator worried about the patient's adherence to dual antiplatelet therapy, in which case she would be at risk for catastrophic stent thrombosis. For this reason, and given that she had very robust spontaneous recanalization, they decided to attempt medical management with a plan for immediate repeat cath if she had any return of symptoms.

Repeat hsTnI just after cath was 36,029 ng/L. ECG below shows obvious LAD reperfusion.

Unfortunately, a few hours later the patient complained of recurrent chest pain. Repeat ECG showed progressive reperfusion without any evidence of reocclusion.

However, given the context, she returned for immediate angiography and received a stent to her proximal LAD. A few selected echo images show extensive, severe hypokinesis in the distribution of LAD.

Learning points:

• OMI is not ruled out by non-obstructive, almost normal coronary arteries.

• Troponin tells you what happened hours ago, ECG tells you what is happening now.

• Recognize precordial swirl, a very important sign for diagnosing subtle proximal LAD OMI.

This case engendered interesting discussion on Twitter.

https://x.com/GreggWStone/status/1834315452459155656

==================================

My Comment, by KEN GRAUER, MD (9/9/2024):

==================================

Today's superb presentation by Dr. Frick provides a great example of how expert ECG interpretation can help the interventionist. Knowing (as Dr. Frick points out) that the initial ECG in today's case strongly suggests Precordial "Swirl" (therefore diagnostic of a proximal LAD OMI) — prompted the interventionist to keep looking at the area predicted to be the site of the "culprit" artery, with awareness of the need for IVUS (IntraVascular UltraSound) to make the final diagnosis once the subtle cath finding of a scooped out appearance to the proximal LAD was seen.

• For as good as QOH is in recognizing acute OMI (with even better performance anticipated once Version-2 is released) — QOH confidence for rating acute OMI was less-than-high for today's initial ECG.
• I'll suggest that joint assessment of this initial tracing by QOH, together with clinical ECG assessment by a skilled interpreter — could have (should have) increased confidence in the diagnosis of acute OMI even before a prior ECG on this patient was found.

For clarity in Figure-1 — I've labeled the initial ECG and the previous tracing.,

Figure-1: Comparison between the initial ECG and a prior ECG on today's patient.

============================

NOTE: For review of 20 cases of "Swirl" vs Swirl "Look-Alikes" — Check out the October 15, 2022 post in Dr. Smith's ECG Blog. At the bottom of the page in this Oct. 15 post — I summarize in My Comment, a series of tips to facilitate recognition of Precordial "Swirl".

============================

My "Take" on Today's CASE:

The history in today's case immediately places this patient in a higher-risk group for an acute event — in that this 40-year old woman suddenly developed new CP (Chest Pain) severe enough to contact EMS.

• Initial assessment of ECG #1 was without the benefit of a prior ECG. This initial ECG shows sinus rhythm — normal intervals and axis — and no chamber enlargement.
• Regarding Q-R-S-T Changes — the QS in lead V1 is not necessarily abnormal given development of a tiny r wave by V2 — with normal R wave progression (ie, showing transition to a predominant R wave already by lead V3).

ST-T wave abnormalities — are present in virtually every lead, with the challenge being that until we are able to find a prior tracing for comparison — it is difficult to know which leads to focus on.

• As per Dr. Frick — my attention was immediately captured in ECG #1 by the 2 leads within the RED rectangle. In both lead V1 and lead V2 — RED arrows highlight more J-point ST elevation than should be seen in these leads. In support that this ST elevation is likely to be acute in this woman with new CP — is the abnormal ST segment straightening in lead V1 — and the disproportionately-tall (hyperacute) T wave in lead V2 that is much larger than one would expect given modest depth of the S wave in this lead.
• That the above-described ST-T waves in leads V1,V2 are clearly abnormal — is supported by the surprise finding of ST segment straightening with slight ST depression in neighboring lead V3 (whereas normally there should be slight upward sloping ST elevation in lead V3).
• My "Go-To" Lead for confirming suspicious anterior lead ST-T wave changes — is lead aVL. Whereas I was not certain if the ST depression and T wave inversion in leads I,II,III,aVF was acute — given the likely hyperacute ST-T waves in leads V1,V2 — I interpreted the disproportionately "bulky" upright T wave in lead aVL (considering tiny size of the QRS in this lead) as also hyperacute.
• 
  
• As emphasized in My Comment at the bottom of the October 15, 2022 post — after establishing the abnormal ST elevation in leads V1,V2 — the final finding for identifying Precordial Swirl — is, in a patient who does not have LVH — the recognition of a relatively flattened appearance to a depressed ST segment in at least lead V6, if not also in lead V5 (BLUE arrows in these leads).

The Previous ECG:

As per Dr. Frick — comparison in Figure-1 of today's initial ECG with the previous tracing that was found confirms that the chest lead ECG findings diagnostic of LAD OMI with "Swirl" are new!

• That said — Which of the 4 complexes shown within the RED rectangle in ECG #2 is the correct one? The ST-T wave in "C" would seem to be the most worrisome — and "A" the least worrisome — but there is no way to know from ECG #2 which complex should be used. 
• While not critical to assessment in today's case (because it is obvious even without assessing ST-T waves in artifact-filled leads V2 and V4 that the changes in ECG #1 are new) — the point to emphasize is that when assessing patients for OMI, the ECG should be repeated IF critical leads are rendered uninterpretable because of artifact (as is the case for this previous tracing on today's patient).

"Take-Home" Message: The diagnosis in today's case of acute LAD OMI with "Swirl" became obvious as soon as the previous ECG was found.

• That said, given the history of severe new-onset CP — assessment of the initial ECG alone (as described above) — should have been sufficient to make this diagnosis with sufficient confidence to know prompt cath is indicated.
• As per Dr. Frick — any doubt about this need for prompt cath could have been quickly alleviated simply by repeating the ECG within ~15-20 minutes after the initial tracing was recorded.