QS-wave in V2: 2 cases, different paradigms lead to different treatment times (STEMI - NSTEMI vs. OMI - NOMI)

Submitted by anonymous, written by Pendell Meyers.  Additional case by Smith.

Case 1

A middle aged woman presented with acute chest pain and shortness of breath, unclear time since onset, and likely with episodic symptoms off and on throughout the day. Her vitals were within normal limits.

ED1 @1512

What do you think?

Meyers: Very clear and specific for acute LAD OMI, with hyperacute T waves in the LAD distribution including leads V2-V6, II, III and aVF. Only very slight STE which does not meet STEMI criteria at this time. I am immediately worried that this OMI will not be understood, for many reasons including lack of sufficient STE for STEMI criteria, as well as the common misunderstanding of "no reciprocal findings" which is very common with this particular pattern. This ECG is pathognomonic, regardless of any information, prior ECG, etc available: it means the LAD territory is undergoing immediate and hyperacute full thickness infarction, with the most likely etiology being type 1 ACS. 

Prior ECG available on file from 2 months before:

We do not know the clinical events happening during this ECG, but there is borderline tachycardia, PVCs, and likely some evidence of subendocardial ischemia with small STDs maximal in V5-6/II, slight reciprocal STE in aVR. Probably not the patient's "baseline" ECG, but it was the prior on file. Notice the normal precordial T waves.

That first ECG (the one at the top) was interpreted as "no evidence of ischemia."

A single high sensitivity troponin I was measured from triage (around 1500), which now returned elevated at 2,271 ng/L (upper limit of normal 12 for women, 20 for men).

(Amazingly, no further troponins were ever measured for this case)

ED2 @1559

Continued evolution of LAD OMI, with increasing STE and now likely meeting STEMI criteria to those who actually measure it.

With the elevated troponin and repeat ECG showing new STE, the patient was discussed with local PCI center, and the cath lab was activated. The patient was transferred.

Angiogram @ 1830 (3.3 hours after that first diagnostic ECG):

Mid-LAD culprit lesion, 99% stenosis, no pre-intervention TIMI flow available, but described as "severe subtotal lesion", which was stented with reported TIMI 3 flow resulting. Another lesion in the proximal LAD with 80% stenosis was stented as well. Other vessels had scattered 30-40% stenoses.

Post-cath ECG @1921

Significant evolution of MI including worsening precordial Q waves, notable absence of deflation of the T waves.  This is very concerning after reportedly "successful PCI" (successful in restoring flow in the epicardial coronary artery, but not necessarily to the downstream cells). Concerning for ongoing injury, concerning for the "No Reflow" phenomenon.

No peak troponin was measured. We do not know if the patient's symptoms resolved.

Next morning:

Slight evidence of reperfusion (or just completion) with terminal T wave inversion in many leads. QS waves from V2-V5 consistent with LV aneurysm morphology.

Echocardiogram:

EF 50%, akinesis of mid-apical anteroseptal, inferior, and inferoseptal myocardium. Normal RV, no valve stenosis or regurgitation.

The patient survived and was able to be discharged. 

2 weeks later:

Some slight R wave recovery in V4-V5, but overall still LV aneurysm morphology, and lingering T wave inversions which could be consistent with reperfusion or completed OMI.

Case 2.

Contrast the last case with this case, from a different institution, which operates by the OMI/NOMI paradigm:

70-something male presents through triage with 9 hours of chest pain.

Here is the triage ECG:

Sinus rhythm with Left Anterior Fascicular Block.

There is subtle STE in V2 - V4, I and aVL, diagnostic of proximal LAD OMI.  There is one hyperacute T-wave (in V3).  

There is a QS-waves in V2: is this "Old MI with persistent STE (otherwise known as LV aneurysm morphology)"?   The T-wave in V2 and V3 are too large for this: a T/QRS ratio ＞0.36 in one of leads V1-V4 is acute until proven otherwise.  

T/QRS ratio in V2 is 2.5/6.5 = 0.38.  In V3, it is even higher.

In this case, the MI is subacute, with symptoms of 9 hours duration.  QS-waves are typical of anterior OMI of this duration, as are the relatively flat T-waves (not hyperacute).  (When symptoms are present for more than 6 hours, the T/QRS ratio may be small due to subacute MI -- absence of hyperacute Ts).

It is difficult to say whether this ECG meets "STEMI criteria:" there is 2 mm of STE in V3.  But V2 does not have 2 mm and V4 is very close to 1 mm.  The computer did read "STEMI".

The cath lab was immediately activated.

Later, the initial hs troponin I returned very high.

Angiogram:

Primary PCI for Acute Antero-lateral STEMI.

Culprit is 100% stenosis in the Proximal LAD.

Culprit lesion was reduced to 0% and stented.

90% ostial LAD-D1 reduced to 35% with PTCA and stented.

Next day ECG:

There is now RBBB in addition to LAFB.

Some persistent STE in V2-V5 (with RBBB, there should be STD depression discordant to the positive R'-wave, so this is particularly worrisome)

Reperfusion T-waves in I, aVL, V2-V5,6

Echo

Normal left ventricular size and wall thickness with severely reduced systolic function.

The estimated left ventricular ejection fraction is 31%.

Akinesis in LAD territory:

- Basal to apical septum

- Mid to apical anterior wall

- Entire apex

The delay in patient presentation resulted in large irreversible infarction.

Learning Points:

Note that expert ECG interpretation diagnosed OMI at the time of arrival, STEMI criteria possibly at 45 minutes later, and the patient underwent cath at 3 hours after arrival, for a delay of approximately 3 hours since first medical contact. Better ECG interpretation would likely have led to more rapid reperfusion.

Understanding the entire OMI progression including hyperacute T waves is critical for diagnosing OMI.

The ECG is usually a better indicator of reperfusion than the angiogram.

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My Comment by KEN GRAUER, MD (1/28/2023):

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After reading about the course of case presented by Dr. Meyers — I have mixed emotions. I find it gratifying that so many of our readers have become highly competent interpreters, who are able to immediately recognize that the initial ECG in today's case is (as per Dr. Meyers) — "very clear and specific for acute LAD OMI".

• In this middle-aged woman who presented to the ED with new chest pain producing symptoms "on and off" throughout the day — the need for prompt cath lab activation with PCI is indisputable.
• 
  
• That said, on seeing the initial ECG for the 1st time — I shared Dr. Meyers' concern that this acute OMI might not be "understood" for the same reasons he expressed (ie, lack of millimeter criteria to be called a "STEMI" — and a "lack" of reciprocal changes).
• On reading what happened — I have to admit my frustration at learning that despite the incriminating history and diagnostic initial ECG in today's case — PCI was delayed for over 3 hours. 

I focus my comment on the case presented by Dr. Meyers — specifically regarding interpretation of the first 2 tracings in his case, which I consider at 2 LEVELS: i) The BASICS (ie, Why even less experienced interpreters should not misinterpret the diagnostic initial ECG); and, ii) PEARLS for the more advanced readers of Dr. Smith's ECG Blog (in which I'll point out some interesting subtleties in these first 2 tracings).

• For clarity in Figure-1 — I've reproduced and labeled these first 2 tracings in today's case.

Figure-1: I've reproduced and labeled the first 2 tracings in today's case.

My Initial Thoughts on Reading Today's CASE:

The aphorism, "Listen to the patient — he/she is telling you the diagnosis" — has been attributed to Dr. William Osler, the "Father" of Medicine. Ignoring this truism was the 1st oversight in today's case.

• Awareness that not only did the patient in today's case present to the ED with new chest pain — but that she indicated having this symptom "on and off" throughout the day. Knowing this history explains many of the ECG findings that were overlooked in the initial tracing.

The initial ECG shows sinus rhythm with a PAC ( = the early beat in leads V1,2,3). All intervals (PR, QRS, QTc) are normal. There is no chamber enlargement (On the contrary — overall QRS amplitude is decreased).

• The frontal plane axis in ECG #1 (Top tracing in Figure-1) — is markedly leftward, with a predominantly negative QRS in lead II. This suggests an axis of at least -45 degrees, and is consistent with LAHB (Left Anterior HemiBlock).
• 
  
• PEARL #1: It's often difficult to appreciate inferior infarction in association with LAHB (and vice versa). This is because the initial component of ventricular depolarization is oppositely directly with LAHB vs inferior infaction. The fact that there is a small-but-real initial q wave in lead II in this patient with LAHB (BLUE arrow in lead II) — consistent with a qrS complex in lead II, suggests inferior infarction has occurred at some point in time, in addition to the LAHB.
• In support of this premise that inferior MI has occurred at some point in time are: i) The QS in lead III (without any initial positive deflection at all); and, ii) The fragmentation we see in the tiny QS complex in lead aVF (this variable fragmention in lead III most probably produced by the beat-to-beat opposing orientation between the initial vectors from the LAHB and inferior MI).

Continuing my interpretation of ECG #1 — by assessing Q-R-S-T Changes:

• There are QS complexes in leads V1,V2,V3.
• We again see small initial q waves in leads V4,V5,V6.
• As a result of these QS complexes and the overall reduced voltage — there is poor R wave progression (with delayed transition, in that the R wave does not ever become taller than the S wave).
• 
  
• PEARL #2: Although small and narrow septal q waves may normally be seen in lateral chest leads — this is not what we see in ECG #1. Instead — the fact that following QS complexes in the first 3 chest leads — the initial negative deflection ( = q wave) that occurs before the tiny r in lead V4 is indicative of the extensive anterior infarction that has occurred at some point in time. 
• In support of this premise of extensive anterior MI — is continuation of the tiny R wave amplitude through to lead V6, with persistence of tiny q waves in V5,V6 (BLUE arrows in leads V4,5,6 in ECG #1).
• 
  
• PEARL #3: As we've pointed out on a number of occasions (ie, See My Comment at the bottom of the page in the November 12, 2020 post in Dr. Smith's ECG Blog) — the finding of low voltage in a patient with ongoing acute MI may be indication of cardiac "stunning" from extensive infarction.

The MOST Abnormal Lead in ECG #1:

The reason for my frustration in reading what happened in today's case — is a result of providers not realizing the abnormality in lead V4.

• PEARL #4: Changes of acute OMI may often be subtle in many leads. As a result — I find it most helpful to look for those 1 or 2 leads that you know are definitely abnormal. Once these definitely abnormal leads are identified — it becomes far easier to assess neighboring and reciprocal leads for changes that may not be as obvious. In ECG #1 — regardless of the experience of the interpreting clinician — there should be no doubt that in a patient who presents to the ED with new chest pain — that the ST-T wave lead V4 is disproportionately tall. Indication that this T wave in V4 is hyperacute is forthcoming from ST segment straightening of its upslope and its hypervoluminous T wave (clearly taller-than-it-should-be with a much wider base than should be present given tiny amplitude of the QRS).
• 
  
• I've added parallel RED lines in a number of other leads in ECG #1 — to highlight ST segment straight (and coving in lead V2) — that all provide support of the ongoing acute LAD occlusion.

WHY So Many Q Waves IF the MI is Acute?

The answer to this important question is forthcoming IF we remember Sir William Osler's famous quote: "Listen to the patient — he/she is telling you the diagnosis".

• Today's patient was having chest pain "on and off" throughout the day. As a result — there was more than ample time for infarction Q waves to develop — with resultant loss of QRS amplitude — and possibly some return-to-baseline of previously elevated ST-T waves.

Comparison with the Prior ECG:

As per Dr. Meyers — there is a significant difference between the 2 tracings in Figure-1. To emphasize — We do not know the circumstances under which the prior tracing was obtained — and this prior ECG #2 does show sinus tachycardia, PVCs and nonspecific ST segment flattening with slight depression in many leads.

• The above said — My frustration in this case is that IF any provider (at any level of clinical experience) made a lead-by-lead comparison between the initial tracing in today's case — and the prior tracing — it should be impossible not to notice the change in ST-T wave morphology.
• 
  
• PEARL #5: The EASY way to get good at comparing serial tracings — is to go lead-by-lead. Doing so (as I illustrate in Figure-1) — should reveal more left axis deviation in ECG #1 (new development of LAHB) — lack of inferior and lateral chest lead Q waves and small-but present initial R waves in leads V2,V3 (GREEN arrows in ECG #2). Most notable should be the change in ST-T wave morphology between the 2 tracings (shape of the RED lines I've drawn in ECGs #1 and #2 in Figure-1).

BOTTOM Line: The acute OMI in today's case should not have been missed, given the history and the appearance of the first 2 ECGs.

• There are simple things even less experienced providers can do to improve their ECG interpretation ability — so that oversights as described in today's case do not occur. 

What is this Rhythm?

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My Comment by KEN GRAUER, MD (1/26/2023):

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While reading ECGs — Dr. Smith came across the intriguing tracing shown in Figure-1. No history was available. However, the rhythm is indeed challenging — and illustrates a number of important principles in rhythm interpretation of interest to all emergency care providers.

• How would YOU interpret the ECG in Figure-1? 
• Can you come up with a definitive rhythm diagnosis?

Figure-1: 12-lead ECG and simultaneously-recorded 3-lead rhythm for today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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REVIEW: MY Approach to Rhythm Interpretation

• As always — I favor beginning my interpretation of 12-lead ECGs with a look at the cardiac rhythm. My systematic approach to rhythm interpretation entails assessment of the 5 KEY Parameters, which are easily recalled by use of the memory aid, "Watch your Ps, Qs and 3Rs". The questions to ask when assessing these 5 Parameters are:
• Are there P waves (or other sign of atrial activity)?
• Is the QRS wide?
• What is the Rate? (looking both at the atrial and ventricular rates IF these are different).
• Is the rhythm Regular? (and if not — Is the rhythm “irregularly irregular”, as in AFib — or is there a pattern of “regular" irregularity in the form of group beating?).
• If P waves are present — Are P waves Related to neighboring QRS complexes?
• 
  
• NOTE: It does not matter in what sequence you assess the above 5 Parameters — as long as you always assess all 5 of them. I generally look at whichever of the Parameters are easiest to recognize.
• CAUTION: In my experience over decades — Failure to systematically assess each of the above 5 Parameters will result in even the most “experienced” of clinicians missing the diagnosis of a number of non-sinus rhythms.
• To EMPHASIZE: Using the Ps, Qs, 3R system does not slow you down. On the contrary — it organizes my thinking, and allows me within seconds (!) to diagnose almost any arrhythmia.

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MY Approach to the Rhythm in Figure-1:

Using the Ps, Qs & 3R Approach:

• The QRS is narrow in all 12 leads of Figure-1 (So the rhythm is supraventricular!).
• The rhythm is not completely Regular. That said — Parts of the rhythm are regular (ie, Except for the 2 pauses between beats #4-5 and 10-11 — the R-R intervals between all other beats is essentially the same!).
• P waves are present!

PEARL #1: Overall — the best lead to look for P waves in, is lead II. In fact — sinus rhythm is defined by the presence of an upright P wave with fixed PR interval in lead II. 

• Remember that the 2nd-best lead to look for P waves in — is lead V1. 
• KEY Point: There are times when P waves will not be well seen in lead II — and may only be seen in lead V1. Such is the case in today’s tracing. We barely see P waves in the long lead II rhythm strip (and then, only before the 1st QRS complex that occurs at the end of each pause). However — regularly-occurring P waves at a Rate of ~80/minute are clearly seen throughout the entire long lead V1 rhythm strip (ie, RED arrows in Figure-2).

PEARL #2: The KEY for interpretation of complex AV block tracings — will often reside with the 5th Parameter = Whether or not P waves are Related to neighboring QRS complexes. 

• I look to see IF there are any PR intervals that repeat. The best place to look for this — is in front of the QRS complex that terminates a pause in the rhythm. In Figure-2 — Isn’t the PR interval before beats #5 and 11 equal? The fact that the same PR interval repeats before 2 or more beats is unlikely to be due to chance — and suggests that there probably is at least some conduction!

Figure-2: Regularly-occurring P waves are clearly seen in the long lead V1 rhythm strip (RED arrows).

Putting together what we’ve derived thus far:

• The rhythm in Figure-2 is supraventricular (narrow QRS). 
• Regular P waves at a rate of ~80/minute occur throughout the long lead V1 rhythm strip (RED arrows).
• Although the rhythm in Figure-2 is not completely regular — there are groups of beats with a constant R-R interval — that are separated by pauses of almost equal length (ie, The R-R interval between beats #4-5 and between #10-11 is virtually the same!).
• The PR intervals before the 2 beats that terminate the short pauses are equal (ie, the PR intervals before beats #5 and 11 in Figure-3). This tells us that at least 2 beats in this tracing are being conducted to the ventricles, albeit with a markedly prolonged PR interval ( = 0.54 second).

Figure-3: PR interval measurements for the beats just before the pause — and just after the pause.

PEARL #3: Our above description thus far of the 5 Parameters — should immediately suggest that of some form of AV Wenckebach (ie, 2nd-degree AV block of the Mobitz I type) is present in Figure-3. This is because:

• The QRS is narrow (The QRS is usually narrow with Mobitz I. The QRS is almost always wide with Mobitz II).
• There are regular P waves, as highlighted by the RED arrows in Figure-3 (The finding of a regular or at least almost regular atrial rhythm makes other causes of group beating such as PACs and sinus pauses far less likely).
• There is group beating — in which the R-R intervals of the 2 short pauses are approximately equal in duration (I always immediately suspect Wenckebach if the QRS is narrow and P waves are regular and there is group beating!).
• 
  
• The PR intervals before beats #5 and 11 are equal — which tells us that these beats are conducting to the ventricles. In contrast — the P waves that occur just after the QRS of beats #4 and 10 are not conducted — which in the setting of a regular atrial rhythm defines this tracing as some form of 2nd-Degree AV Block.
• 
  
• PEARL #4: Statistically — Mobitz I 2nd-degree AV block is much more common than Mobitz II (ie, In my experience — at least 90-95% of all 2nd-degree AV blocks I have seen over the years are Mobitz I. Mobitz II is distinctly uncommon).
• 
  
• PEARL #5: The finding of 1st-degree AV block (especially given the markedly prolonged PR interval in today's case) — further increases statistical likelihood of Mobitz I (There commonly occurs a progression from 1st-degree AV block — to Mobitz I 2nd-degree block).

PEARL #6: We are used to recognizing Mobitz I, 2nd-degree AV block by obvious progressive lengthening of the PR interval until a beat is dropped. The reason Mobitz I is difficult to recognize in today's tracing — is that we are presented with a long Wenckebach cycle, in which there is only minimal increase in the PR interval increment from one beat-to-the-next.

• In such cases — the EASY way to immediately recognize that the PR interval is in fact increasing — is to measure the PR interval just before the pause (ie, the PR intervals before beats #4 and 10 in Figure-3) — and to compare this to the PR interval before the first beat that ends each pause (ie, the PR intervals before beats #5 and 11 in Figure-3). Doing so confirms that the PR interval is ever-so-slowly increasing until a P wave is non-conducted.

Laddergram Illustration:

The laddergram in Figure-4 — illustrates the mechanism of today's rhythm. I've carefully measured each PR interval in milliseconds.

• NOTE: Many patients "don't read the textbook". There simply is not always a measurable beat-to-beat increase in the PR interval with all cases of Mobitz I, especially when there is a long Wenckebach cycle (as is seen from beat #5-to-#10 in Figure-4).
• That said — there should be no doubt that the PR interval before the first beat in this grouping ( = 540 msec. for the PR interval before beat #5) — is less than the last PR interval in this group ( = 640 msec. before beat #10).
• The next on-time P wave (ie, the YELLOW arrow that occurs just after beat #10) — is non-conducted. There follows a short pause (between beats #10-to-11) — after which the PR interval again shortens (to 540 msec. before beat #11) — as the next long Wenckebach cycle begins. This sequence of events confirms the diagnosis of a long Wenckebach cycle.

PEARL #7: We often think of 1st-degree AV block as a benign rhythm. This is because most patients with an isolated 1st-degree AV block remain asymptomatic without need for intervention. This is especially true when the severity of 1st-degree AV block is not great (ie, a PR interval less than 0.30 second).

• Once the PR interval extends much beyond 0.30 second — the delay in ventricular contraction that occurs may result in the atria contracting against closed AV valves, with reduction in cardiac output. This may lead to a series of symptoms similar to “pacemaker syndrome” (ie, dizziness, fatigue, light-headedness, presyncope/syncope, dyspnea and/or chest pain).
• On occasion — implantation of a permanent pacemaker may be needed in a patient with a marked 1st-degree AV block (ie, PR interval significantly greater than 0.30 second) — IF the patient is symptomatic as a direct result of PR interval prolongation (For an example of this — See My Comment at the bottom of the page in the May 24, 2020 post in Dr. Smith's ECG Blog). 
• 
  
• Mobitz I, 2nd-degree AV block is also often a relatively benign rhythm — in that many patients with Mobitz I will not need a pacemaker. That said — the fact that the shortest PR interval in today's case for sinus-conducted beats is 0.54 msec. — suggests there is significant conduction system disease with high risk of symptoms similar to "pacemaker syndrome" (as described above for patients with a markedly prolonged 1st-degree block).

Final POINT in Today's CASE: To emphasize — that although the PR interval increment from one beat-to-the-next in today's rhythm is small (and not-at-all obvious) — Attention to the ECG findings highlighted above in Pearls #3-thru-6 allowed me to know that the rhythm was Mobitz I in less than 10 seconds.

Figure-4: Laddergram illustration of today's rhythm. The YELLOW arrows are on-time non-conducted P waves in each of the long Wenckebach cycles (See text).

Chest pain, and Cardiology didn't take the hint from the ICD

Submitted and written by Megan Lieb, DO with edits by Bracey, Smith, Meyers, and Grauer

A 50-ish year old man with ICD presented to the emergency department with substernal chest pain for 3 hours prior to arrival. The screening physician ordered an EKG and noted his ashen appearance and moderate distress. 

Triage EKG:

What do you think?

Triage physician interpretation: 

-sinus bradycardia

-lateral ST depressions

While there are lateral ST depressions (V5, V6) the deepest ST depressions are in V4. Additionally, lead V3 has ST depressions, which are always abnormal (recall that lead V3 will have ST elevation under normal circumstances!)

Smith: also VERY important is the downsloping ST segment in V3.  This is a very specific marker of posterior OMI.  Additionally, V2 has a very flattened T-wave, which is typical of posterior OMI.

Close up of V3 with baseline in red

Close up of V4 with baseline in red

This ECG alone is highly suspicious for posterior OMI! This pattern is recognizable by the ST depressions maximal in lead V4. Recall that, in the setting of ACS symptoms, ST depression that are maximal in leads V1-V4 (as opposed to V5 and V6) not attributable to an abnormal QRS complex is specific for OMI. 

Meyers HP, Bracey A, Lee D, Lichtenheld A, Li WJ, Singer DD, Rollins Z, Kane JA, Dodd KW, Meyers KE, Shroff GR, Singer AJ, Smith SW. Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). J Am Heart Assoc. 2021 Dec 7;10(23):e022866. doi: 10.1161/JAHA.121.022866. Epub 2021 Nov 15. PMID: 34775811; PMCID: PMC9075358

A bedside ultrasound was performed, shown here:

Parasternal short axis view demonstrating inferior LV wall motion akinesis

Apical 2 chamber view again demonstrating inferior LV wall akinesis

The cath lab was not activated based on the ECG and bedside echo.

Back to the case:

After the patient was roomed, he revealed that he had undergone several episodes of syncope in the last 24 hours with each event resulting in a shock during which his wife reported that he would immediately awaken. The most recent event had occurred just before being triaged.

At this time he reported ongoing chest pain and was given aspirin and nitroglycerin. Labs were drawn and a repeat ECG was performed:

ST depression markedly worse in V3 and V4 

Comparison of leads V3 and V4

While the ICD was preparing to be interrogated, the interventional cardiologist was consulted for evaluation for emergency catheterization. After reviewing the available information, cardiology did not feel that the patient warranted emergent PCI and recommended heparin infusion and cardiac catheterization the following morning. 

Around this time the troponin I resulted at 0.05 ng/mL (ULN 0.04). 

A second ECG was performed this time:

Resolution of ST depression in the anterolateral leads

A posterior ECG  was also performed at this time:

Posterior orientation ECG (leads V4, V5, and V6 are actually V7, V8, and V9 respectively)
There is no ST elevation in the posterior leads (V7-V9) 
But one would not expect STE in V7-V9 because the STD in V3, V4 has resolved.

Cardiology reviewed the posterior ECG and once again concluded that as there was no ST elevation in the posterior leads, there was no need for emergent PCI. It is important to note, however, that there should have been no expectation for ST elevation in the posterior on this ECG as the ST depression in the anterior leads had resolved! The vessel was likely patent or nearly patent at the time of this ECG.

When the ICD was finally interrogated, the syncopal events and shocks correlated with two VF events that were defibrillated successfully. 

Smith: This is a failure of the cardiologists to comply with their own guidelines, which state that ACS with electrical instability needs the cath lab emergently

The cardiology service was alerted to the finding of episodes of VF and obvious dynamic ECG changes and did not feel immediate cath was indicated, and instead deferred cardiac cath until the next morning.

A repeat troponin I was elevated at 0.07 ng/mL and 7.59 ng/mL at hours 4 and 7 from arrival respectively. Serum troponin I level just before the cardiac catheterization procedure was 16.69 ng/mL.  

90% stenosis of the proximal ramus intermedius, pre procedure TIMI II flow

The ramus intermedius is a normal variant on coronary anatomy that arises between the LAD and LCX. Its course is variable, often supplying the lateral wall of the LV. In this case, the vessel supplied a portion of the posterior LV circulation.

Post procedure 0% stenosis, TIMI III flow

A post procedure ECG was performed 24 hours after PCI:

Standard orientation 12-lead ECG demonstrating reperfusion of infarcted territory

Note that leads V2-4 show posterior reperfusion T waves (now more upright in these leads, as they are reciprocal to negative, reperfusion T waves inversions on posterior leads). Lead aVL also demonstrates typical reperfusion pattern, indicating high lateral wall reperfusion.

The patient was started on dual antiplatelet therapy and discharged from the hospital on day 3 without further event.

Take home points:

ST depressions maximal in leads V1-V4 (not otherwise attributable to an abnormal QRS complex) are highly specific for posterior OMI in a patient with new ischemic symptoms.

Serial ECGs are often helpful in identifying more subtle ECG manifestations of OMI

Posterior leads will often have little to no ST elevation even in the setting of posterior OMI owing to lung tissue being in between the posterior LV wall and the posterior chest wall. However, when the ST depressions resolve, there will be no ST elevations in posterior leads either, as this case highlights. Recall that air is a poor conductor of electricity and will, therefore, generate smaller amplitudes on posterior leads (hence why STEMI criteria requires only >0.5 mm in any posterior lead to be considered positive). Thus, it is essential for you to be able to recognize posterior OMI in the standard orientation 12-lead ECG!

Ventricular fibrillation is a common outcome in OMI and should greatly heighten the suspicion for ischemic heart disease even in the absence of profound ST elevation.

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My Comment by KEN GRAUER, MD (1/23/2023):

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The importance of today's case by Drs. Lieb, Bracey, Meyers & Smith — relates to how often similar situations occur. The cath lab was not activated after review of the initial ECG. For clarity in Figure-1 — I've reproduced this initial tracing.

• Given the history of new-onset chest pain and this patient's initial appearance described as "ashen and in moderate distress" — the cath lab should have been activated immediately on seeing ECG #1.

Figure-1: The initial ECG in today's case. I've added a magnified view of the mirror-image of the 1st complex in lead V3 (within the RED-border insert).

WHY the Cath Lab Should Be Immediately Activated:

As per the above case discussion by Drs. Lieb and Bracey — ECG #1 is highly suspicious for acute posterior OMI (Occlusion-based MI) because of the chest lead ST depression that is maximal in lead V4 — and because of the ST depression in lead V3 that has replaced the slight upsloping ST elevation that is normally seen in this lead.

• The "similar situations" I was referring to in my opening sentence — relates to 3 Oversights made by all-too-many clinicians. These oversights are: i) Failure to appreciate the characteristic "shape" of ST-T wave depression in the anterior chest leads, that when seen in a patient with new chest pain is indicative of acute posterior OMI; ii) Failure to appreciate that the "culprit" artery in many acute occlusion MIs will spontaneously reopen (thereby reperfusing) even without treatment — sometimes opening, then reclosing, then reopening again a number of times until eventually the vessel's final state is reached; and, iii) Even without ST elevation — a patient with new-onset and persistent cardiac chest pain that occurs in association with ischemic ST depression is indication for prompt cath.

The Positive "Mirror" Test in Figure-1:

Much more than just the amount of ST depression in leads V3 and V4 of ECG #1 — it is the shape of the ST-T wave in lead V3 that instantly told me the 50-ish year old man in today's case was having an acute posterior OMI. 

• I don't know why the pattern of ST-T wave abnormality seen in lead V3 of ECG #1 continues to go unrecognized by all-too-many clinicians. I've found the easiest way to convey appreciation for this important ECG sign — is with the Mirror Test. As I've illustrated multiple times in Dr. Smith's ECG Blog, the Mirror Test is simply a visual aid that facilitates recognition of acute posterior OMI from the standard 12-lead ECG without need to apply posterior leads (See My Comment at the bottom of the page in the September 21, 2022 post).

• The rationale for the Mirror Test is based on the premise that anterior leads provide a mirror image of electrical activity in the posterior wall of the left ventricle. By simply inverting a standard 12-lead ECG, and then holding it up to the light — you can easily visualize the "mirror-image" of leads V1-thru-V4.
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• In Figure-1 — the principal lead showing a positive Mirror Test is lead V3 (Seen within the magnified, RED-border mirror-image insert of lead V3). QUESTION: Doesn't the shape of the slightly elevated ST segment, in association with deep, symmetric T wave inversion in this lead suggest acute infarction?

Failure to Appreciate Spontaneous Reperfusion

Although the shelf-like straightened ST segment in lead V3 of Figure-1 is typical of acute posterior OMI — the amount of ST depression in this lead is modest. Instead — the T wave in lead V3 is distinctly peaked and taller than the R wave in this same lead.

• As suggested in Figure-1 by the deep T wave inversion within the RED-border insert — the peaked T wave in lead V3 strongly suggests that there has been at least some reperfusion of the "culprit" artery. That this might happen should not be surprising — since the patient's chest pain was already ongoing for 3 hours prior to arrival in the ED.
• Additional evidence in support of spontaneous "culprit" artery reperfusion in ECG #1 — is suggested by the flat ST segment in neighboring lead V2. With acute posterior OMI — ST depression is typically most marked in leads V2,V3,V4 — such that the flat ST segment in lead V2 presumably reflects some return-to-the-baseline of the ST depression that most probably had been present earlier in lead V2.
• Final evidence in strong support of recurrent spontaneous opening and reclosure of the "culprit" artery — was forthcoming when the patient revealed having several syncopal episodes while at home during the previous 24 hours, with each episode culminating in a shock from his implanted ICD.

BOTTOM Line in Today's Case:

As we have shown numerous times on Dr. Smith's ECG Blog — a "culprit" artery that spontaneously opens — may at any time spontaneously reclose. This most probably happened multiple times in today's case. Optimal treatment for today's patient would have been prompt cath with PCI to the "culprit" artery with the goal of maintaining coronary perfusion.  

• The patient's "ashen appearance" with ongoing chest pain at the time he arrived in the ED — in association with the diffuse ST segment changes on the initial ECG — should have been enough to indicate prompt cath, even without recognizing that the ST-T wave appearance in lead V3 of ECG #1 was diagnostic of acute posterior OMI.
• If doubt remained about the need for cath after reviewing the initial ECG — the recent history of 2 syncopal epsiodes that were both terminated by ICD shock — and/or — the subsequent dynamic ST-T wave changes on serial ECGs would have more than satisfied criteria for prompt cath.