Acute coronary occlusion seen in paced *and* non-paced ECGs

This was written by Brooks Walsh @BrooksWalsh, an emergency physician in Connecticut.

A paced ECG

The family of a very elderly person called EMS when they became short of breath. The patient had a number of comorbidities, including a pacemaker.

EMS obtained a number of ECGs, including this one:

Could a cath lab activation be justified with this ECG?

Well, yes, it should be!

The classic- and modified-Sgarbossa criteria for determining acute MI in the context of a paced rhythm are likely already well appreciated by readers of this blog. This ECG is a great illustration of those rules, particularly the criterion that ST elevation that exceeds 20-25% of the depth of the S wave (“excessive discordance”) suggests acute coronary occlusion.

We see this in lead V3, where the ST segment  in the first QRS complex is about 3.6 mm high, and the S wave 13.7 mm deep - this gives a ratio of 0.26. There is some unfortunate baseline wander, but the proportion holds for the 3rd complex as well. (The second complex is uninterpretable, as the S wave runs off the paper).

Lead III shows similar excessive discordance, with the third beat giving a ratio of 3.5/11.7, or 0.29. The fourth beat (3.5/10.4 = 0.33) is distorted but diagnostic.

Additionally, the ST segment in V2 suggests > 1 mm of concordant STE (in beats #2 and #3), but the baseline wander here makes this less certain.

 So, did these rules correctly predict a coronary occlusion?

Although angiography was not performed in this case, there is enough evidence to reasonably “prove” acute coronary occlusion. First of all, the paramedics had obtained another ECG about 10 minutes earlier:

This non-paced ECG shows ST elevations in the inferior and anterolateral leads, as well as ST depression in aVL, suggesting a “wrap-around” LAD lesion.
 

The non-paced ECG subsequently obtained in the ED was similar:

This was markedly different from an ECG obtained 1 year prior:

 

After evaluation by the emergency physician and the interventionist, and a discussion with the patient and family, neither angiography nor chemical fibrinolysis were pursued (the patient was quite old and debilitated).

Although angiography was not performed, acute occlusion of the LAD was supported by other tests. The initial troponin was 2.3 ng/ml (< 0.01), rising to 4 ng/ml about 10 hours later. The patient became hypotensive and showed signs of CHF. An echocardiogram showed severe systolic dysfunction, with akinesis of the apex, mid anterior, mid anterolateral, mid inferoseptal, mid anteroseptal, and mid inferolateral segments (Prior echo had been normal for age).

Apical 4 chamber in systole

Lastly, an ECG obtained the next day showed evolving lateral T waves, further supporting an acute occlusion.

The PERFECT Study [From the Paced ECG Requiring Fast Emergent Coronary Therapy (PERFECT) Study Group]

The PERFECT trial will show that acute coronary occlusion can be reliably predicted from paced ECGs, despite the prevailing belief that paced ECGs are “uninterpretable.” That trial used angiographic data, so this case (despite good circumstantial evidence) would not have met inclusion criteria. Hopefully the rigorous methodology can change the out-dated perspectives of emergency physicians and cardiologists!

The study is now under revision for Annals of Emergency Medicine.

Below is the Results and Conclusion portion of the abstract, which was published in AEM and presented at SAEM in 2018.  Annals is requesting that we also look at patients with AMI but without occlusion (Non-OMI).  We don't think that is terribly relevant, but do believe it will only reinforce the results.  We are almost done with that analysis and then will re-submit.

We presented the study at SAEM 2018.  Here are the results in modified form.  I am not publishing the entire abstract, as it will hopefully be published in the future.

Electrocardiographic Diagnosis of Acute Coronary Occlusion in Ventricular Paced Rhythm Using the Smith Modified Sgarbossa Criteria.     

 

Results: There were 59 OMI subjects and 102 controls (mean age 73 years; male 103 [64%]). The sensitivity and specificity of the MSC versus OSC for OMI were 81% (95% CI 69-90) versus 56% (95% CI 42-69; P<.001) and 96% (95% CI 90-99) versus 97% (95% CI 92-99). Adding concordant ST-depression in V4-V6 to the MSC yielded 86% (95% CI 75-94) sensitivity. For the excessive discordance component, the ratio identified 17 OMI patients vs. 2 for absolute ST Elevation of 5mm. 

Conclusions: For the diagnosis of OMI in the presence VPR, the MSC were more sensitive than the OSC; specificity was equivalent. 

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MY Comment by KEN GRAUER, MD (10/19/2020):

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Important case by Dr. Walsh that adds to our growing collection of cases in which OMI is evident despite the presence of a pacemaker (Most recently — See our October 5, 2020 post in Dr. Smith’s ECG Blog).

• I limit my comments in today’s case to the two 12-lead tracings obtained by the EMS team. I wanted to begin (as did Dr. Walsh) — by focusing on the 1st ECG shown above (which I have reproduced in Figure-1). Dr. Walsh asked the KEY question about this ECG = “Could cath lab activation be justified from ECG #1?"

Figure-1: The 1st ECG shown above in today’s case. For clarity — I’ve numbered the beats (See text).

MY THOUGHTS ON ECG #1:

As per Dr. Walsh, given the presence of new symptoms (ie, acute dyspnea) in this elderly patient — ECG findings in ECG #1 at the least justify strong consideration of cath lab activation. I’d add the following thoughts to the points highlighted in Dr. Walsh’s excellent discussion:

• POINT #1: As emphasized in “Pearl #1” in My Comment to the October 11, 2020 post in Dr. Smith’s ECG Blog — as many as 30% of all patients with acute MI do NOT have chest pain. Among these patients with “Silent MI” — the most common non-chest pain symptom associated with acute MI (especially among elderly patients) — is shortness of breath (which is the reason the elderly patient in today’s case came to the ED).

POINT #2: Although it is often more difficult to identify OMI in the presence of cardiac pacing — it is not always impossible to do so “just because the patient has a pacemaker”. And sometimes, acute OMI may be obvious despite the presence of a pacemaker. (SEE the links below — among other examples on Dr. Smith’s ECG Blog).

• KEY: In many more cases than is commonly appreciated — modified Smith-Sgarbossa criteria provide an objective means for identifying acute MI despite the presence of cardiac pacing. As per Dr. Walsh — these modified Smith-Sgarbossa criteria are strongly suggestive of OMI in ECG #1.

Among many Other Examples of Acute OMI despite Cardiac Pacing:

• Our October 5, 2020 post.
• Our August 20, 2019 post.
• Our April 25, 2019 post.
• Our October 3, 2018 post.

POINT #3: In addition to modified Smith-Sgarbossa criteria — ECG #1 also shows suggestive Qualitative Criteria for acute OMI. By “qualitative” criteria, I mean that one focuses on ST-T wave shape — and the presence of ST-T wave deviations that simply should not be there in association with a given conduction defect (like LBBB) or with a given paced QRS morphology.

• Becoming comfortable with assessment of qualitative ST-T wave changes in shape provides another way to strongly suspect acute OMI — even when millimeter-determined criteria are not necessarily satisfied.

CAVEAT: The most challenging aspect of assessing ST-T wave morphology in ECG #1 — is the presence of baseline wander with artifact. Specifically — ST-T wave morphology varies significantly from one beat to-the-next in many leads. This makes it difficult to know which one(s) of the 2, 3 or 4 QRST complexes that we see in each of the 12 leads is the one(s) that we should be assessing for potential acute ischemia.

• POINT #4: There is no perfect “rule” for addressing the above caveat. As a result, I favor a “Gestalt” ( = overall) approach — in which one “steps back” and mentally averages ST-T wave appearance for all complexes in each of the leads in a given lead area — all done in context to the overall findings on the 12-lead, with special attention to those leads expected to show reciprocal changes.
• MY DISCLAIMER: Concrete measurable criteria for this “Gestalt Approach” do not exist. Instead, this is that indescribable “sense” that the experienced clinician gets within moments of seeing a patient as to what the diagnosis is likely to be.

Returning to MY Thoughts on ECG #1:

Knowing that today’s case came from an elderly patient with new dyspnea but no chest pain — the following were my thoughts on seeing the paced tracing shown in Figure-1.

• The rhythm in ECG #1 appears to be 100% paced. Regular pacing spikes are seen in many (not all) leads — with 100% capture showing a wide QRS at a regular rate of ~100/minute.
• Looking first at the 6 limb leads in ECG #1 — Assessment of ST-T wave appearance in lead I is not helpful. There is just too much beat-to-beat variation in ST-T wave morphology.
• There is also much beat-to-beat variation in ST-T wave morphology for each of the 4 QRST complexes in eachof the inferior leads. That said — Don’t YOU get a “sense” of disproportionate (ie, more-than-there-should-be) J-point ST elevation in each of these 3 inferior leads (given the modest depth of S waves in these inferior leads)?
• Admittedly — the ST-T wave shapes of beat #1 in lead III — and of beats #5 and 7 in lead aVF do not look abnormal for paced beats. However, even though ST-T wave appearance of other complexes in these inferior leads all differ from one another — I thought they looked suspicious.
• IF the J-point ST depression in beat #6 of lead aVL was real — this would indicate “tell-tale” reciprocal ST depression. The other 3 beats in lead aVL also suggest inappropriate J-point depression — although modest R wave amplitude makes this more difficult to assess.
• I found assessment of chest leads even more challenging. We get at least a glimpse of 5 elevated ST segments in lead V3 (of beats #9-13) — and each of the 5 looks suspicious.
• Each of the 3 ST segments in lead V4 look abnormal — with the amount of J-point ST elevation in beats #14 and 16 seemingly disproportionate to the modest S wave depth in this lead.
• Regarding the other chest leads — lead V1 is of no help — the ST segments of beats #10 and 11 in lead V2 look suspiciously coved, though not overly elevated — and ST segment shape in leads V5 and V6 is clearly abnormal for beat #15, but unimpressive for beats #14 and 16.
• BOTTOM Line: I would not be certain from ECG #1 that this elderly patient with new dyspnea (but no chest pain) was having an acute OMI — but I definitely would be suspicious. I’d want to repeat the ECG (hopefully with less beat-to-beat variation).

As per Dr. Walsh — it turned out the EMS team obtained multiple tracings on this patient. The one they obtained ~10 minutes before ECG #1 was absolutely diagnostic (Figure-2).

Figure-2: Comparison of ECG #1 in today’s case — with a non-paced tracing obtained in the field ~10 minutes earlier (See text).

POINT #5: Serial tracings are often diagnostic. This was especially true in today’s case — in which severe dyspnea resulted in beat-to-beat artifactual variation in ST-T wave morphology.

• Ten minutes earlier — the patient had a spontaneous (non-paced) rhythm. Although hard to appreciate P waves due to the baseline artifact in ECG #2 — subsequent ED tracings showed an underlying sinus mechanism.
• Although there is diffuse low voltage in ECG #2 — each of the inferior leads show subtle-but-real ST elevation. Lead aVL suggests even more subtle reciprocal ST depression.
• Obvious hyperacute ST elevation is seen in leads V4 and V5 of ECG #2. Looking closely — ST elevation appears to begin in leads V2 and V3 — and extend through to lead V6.
• ECG #2 is diagnostic of acute infero-antero-lateral OMI from acute LAD occlusion with “wraparound”.

FINAL Point: Take ANOTHER LOOK at both tracings in Figure-2.

• It’s insightful to compare lead-to-lead paced ST-T wave appearance (in ECG #1) — with what ST-T waves look like in these same leads when there is no ventricular pacing (in ECG #2). My hope is that doing so will help to better appreciate what qualitative ST-T wave findings to look for the next time you encounter a paced tracing in a patient with new symptoms.

Our THANKS to Dr. Brooks Walsh for presenting this highly insightful case!

A 70-Something Woman with a Very Wide Tachycardia

 

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MY Comment by KEN GRAUER, MD (10/17/2020):

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Today’s patient is a 70-something year old woman who presented to the ED for possible acute Covid-19 symptoms. She was conscious, but appeared acutely ill at the time the initial ECG was obtained in the ED (Figure-1). The computer interpretation read, “Extreme wide complex tachycardia”.  

• How would YOU interpret the cardiac rhythm in ECG #1?
• Should you treat with Adenosine? Amiodarone? Immediate cardioversion? — or — Would you first do something else?

Figure-1: The initial ECG in today’s case (See text).

MY Thoughts on ECG #1: At 1st glance — ECG #1 indeed appears to be an “extremely wide tachycardia” in this acutely ill, elderly patient. That said — there are 2 things that “don’t fit”. These are:

• My 1st Concern: The rate of the ventricular response is extremely rapid = about 260/minute. While clearly not impossible for VT to be this fast — it is not common for a patient to remain conscious at this fast of a ventricular rate.
• My 2nd Concern: There appear to be some narrow QRS complexes occurring at a fairly regular rate in at least some of the leads in ECG #1 (See BLUE arrows in Figure-2).

Figure-2: I’ve added BLUE arrows to ECG #1 in places where it looks as if there are narrow QRS complexes. (See text).

PEARL #1: I’ve emphasized on a number of occasions in Dr. Smith’s ECG Blog how helpful accurate estimation of heart rate can sometimes be. While there are always exceptions — certain cardiac rhythms commonly manifest an atrial or ventricular rate within a general rate range (ie, the atrial rate of untreated atrial flutter in an adult is most commonly between a range of 250-350/minute).

• When the atrial or ventricular rate is rapid and regular — it is far more accurate to estimate the rate by looking at every 2nd or every 3rd complex (or in today’s case — looking at every 5th ventricular complex) — instead of trying to estimate rate by only looking at the R-R interval for a single beat.
• To do this — I first select a part of the QRS complex that occurs precisely on a heavy ECG grid line (See the 1st vertical RED line in the long lead II rhythm strip in Figure-2).
• The RED numbers show that the amount of time it takes to record 5 ventricular beats is just under 6 large boxes (BLUE numbers in Figure-2).
• This means that 1/5th of the rate will be a little bit faster than 300 ÷ 6 — or ~52/minute X 5 ~260/minute. Precise estimation of the ventricular rate is helpful here — since a slightly slower ventricular rate (ie, 220-230/minute) would not be nearly as unusual in a patient with VT who was still conscious.

PEARL #2: The BEST way to establish (and confirm) a diagnosis of Artifact — is to be able to identify an underlying rhythm that “marches through” the artifact.

• In today’s case — even more important than the very rapid rate of the wide complexes — is the strong suggestion (by the BLUE arrows in Figure-2) that an underlying narrow-QRS complex rhythm is present!

Returning to the QUESTIONS that I initially Asked: In answer to the question of whether to give adenosine, amiodarone, or initiate synchronized shock — Recognition of a potential underlying narrow-QRS rhythm (BLUE arrows in Figure-2) should prompt you to immediately GO to the BEDSIDE and LOOK at the PATIENT!

• IF the cause of the wide deflections is artifact — a quick LOOK at the patient will often immediately suggest the cause! In today’s case — this acutely ill patient was having febrile rigors that caused uncontrollable body shaking.

AFTER Body Tremors Resolved: I found this patient’s follow-up ECG, obtained after her tremors resolved to be especially insightful (Figure-3).

• ECG #2 — shows almost complete resolution of the artifact seen in ECG #1. There is now sinus tachycardia with a narrow QRS complex and nonspecific ST-T wave changes, that considering the history — most probably were related to the patient’s underlying non-cardiac medical illness.

Some FINAL Points about ECG #1: 100% confirmation that the wide complexes initially seen in ECG #1 were the result of artifact is forthcoming from several observations:

• RED vertical lines in ECG #1 of Figure-3 show precisely regular occurrence of narrow QRS complexes (seen within the RED ovals in each of the chest leads).
• Using calipers, and looking leftward (ie, earlier) on ECG #1 — Even though we do not see any underlying narrow QRS complex simultaneous with the PURPLE vertical line — we do see a small amplitude, completely on-time narrow QRS complex within the BLUE ovals in leads aVR, aVL and aVF.
• Compare the narrow QRS complexes within the 9 OVALS in ECG #1 — with corresponding QRS morphology in these same 9 leads in ECG #2 after resolution of the artifact. QRS morphology of each of these beats is virtually the SAME! The underlying, narrow QRS complexes (within the 9 colored OVALS in ECG #1) — were simply “hidden” by the huge amplitude artifactual deflections resulting from this patient’s vigorous body rigors at the time ECG #1 was recorded.

Figure-3: Comparison of the initial ECG (during body tremors) with the follow-up tracing after body rigors resolved (See text).

PEARL #3: In WHICH extremity were body rigors the most intense at the time ECG #1 was obtained?

• In My Comment, at the bottom of the page in the September 27, 2019 post in Dr. Smith’s ECG Blog — I posted the 3-page article by Rowlands & Moore, which is the BEST description I’ve seen for how to quickly determine WHICH extremity is the source of artifact. Full discussion for my rationale employed in the next few bullets below appears in this article by Rowlands & Moore.
• For clarity — I’ve outlined in GREEN the artifactual deflections in 11 of the leads in ECG #1 of Figure-3. Note that the amplitude of the artifactual deflections is equally large in leads II and III. In contrast — artifact is largely absent in lead I (with the exception of some low-amplitude baseline undulations). This localizes the source of artifact to the Left Foot ( = the one limb that is not involved in the derivation of lead I appearance).
• That the Left Foot is the “culprit” extremity — is confirmed by recognizing that artifactual deflections in the 3 augmented leads are greatest in augmented lead aVF (Note the amplitude of artifact in lead aVF is approximately equal to the amplitude of artifact in limb leads II and III).
• The amplitude of the artifact in the other 2 augmented leads ( = leads aVR and aVL) — is approximately half the amplitude of the artifact in lead aVF (which is as expected according to the formulas provided in the Rowlands & Moore article).
• And finally — the amplitude of the artifact in the 6 chest leads is approximately 1/3 of the amplitude of the artifact in lead aVF (which is also as expected by the Rowlands & Moore formulas, since electrical potential in each of the 6 unipolar chest leads is derived by subtracting the potential of the “indifferent” connection [which is determined after dividing the sum of the limb lead potentials by 3]).

HOW TO Do This QUICKLY: I fully acknowledge the challenge of trying to remember the formulas put forth by Rowlands & Moore. You do not have to!

• The EASY way to recognize the “culprit extremity” in less than 5 seconds — is to see IF there is an approximately equal amplitude for artifact in 2 of the 3 limb leads (with no more than minimal artifact in the remaining limb lead) — and then to look at which of the augmented leads has the greatest amount of artifact. Since lead aVF in today’s case clearly has the largest amplitude of artifact among the 3 augmented leads — the Left Foot is the “culprit” extremity (which makes sense — because the left foot is not involved in the recording of lead I, which is the one limb lead that doesn't show significant artifactual deflection).
• NOTE: There will not always be a single “culprit extremity” cause for artifact — but when there is, and you note the geometrical relationships described above — you have confirmed artifact as the cause, because nothing else shows these mathematical relationships.

REFERENCE: For those interested in More on Recognition of ECG Artifact:

• The September 27, 2019 post — for the Rowlands & Moore article with the above-noted formulas for recognizing the “culprit” extremity.
• The January 30, 2018 post — for arterial pulsation artifact.
• Brief review by Tom Bouthillet on some common causes of artifact.
• VT Artifact — by Knight et al: NEJM 341:1270-1274, 1999.
• Artifact simulating VFib — CLICK HERE.
• More VT-VFib artifact — CLICK HERE.
• Artifact simulating AFlutter — CLICK HERE.
• Parkinsonian Tremor vs AFlutter — CLICK HERE.

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APPRECIATION: My sincere THANKS to Prateek Sehgal (Toronto, Canada) for sharing the tracings and this case with us!

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Dynamic ST Elevation

A 70-something male with 3 CAD risk factors developed intermittent left sided chest discomfort 29 hours prior.  It began again 2 hours prior to first ECG.  Pain was 7/10 radiating to left arm with SOB and diaphoresis.

Here was the prehospital ECG

Sinus rhythm. Slight ST depression in I, aVL, and V4-V6, consistent with ischemia.

These medics were smart and well trained, and so they recorded another several minutes later due to persistent symptoms:

New ST Elevation in V4-V6, with obliteration of the S-waves.

There is also new subtle STE in inferior leads

They arrived in the ED and another ECG was recorded:

Chest pain still 7/10

Now there remains the STE in inferior leads and STD in I and aVL.  This alone would be enough to call inferior OMI even without the previous diagnostic prehospital ECG.

STD in V2

Hyperacute T-waves remain in V4-V6 but the STE is resolved.

This is diagnostic of an infero-postero-lateral OMI (that is also a STEMI, or STEMI (+) OMI).  It is reperfusing and re-occluding.  Thus, it can be called a "Transient STEMI"

The cath lab was activated.

The BP was 194/83. A nitro drip started at 50 mcg/min.  BP then 140/67 and pain improved from 7 to 3/10.

The interventionalist was happy to take the patient to the cath lab, but he mysteriously commented that "there is going to be nothing there."

The initial high sensitivity troponin I returned at 83 ng/L (99th %-ile URL = 34 ng/L for men; LoD = 4 ng/L).  Depending on the population, this level by itself (without any clinical or ECG data), has a PPV for Acute MI of anywhere from 30-80%.  With this patient's presentation (pretest probability), the PPV of the troponin alone is at least 80%.

Angiogram:

The LAD has 70% disease in the mid segment of the vessel, involving the LADD2 origin

RCA: RCA has Normal take off.

The Mid segment of the RCA has 90% disease.

Culprit is 90% occlusion of the LCX-OM1 (1st Obtuse Marginal).

They put a stent in the OM1, and left the other disease to be treated later.

Here is the post PCI ECG:

Echo:

Technically difficult study

The estimated left ventricular ejection fraction is 60%.

Normal estimated left ventricular ejection fraction .

No wall motion abnormality probable.

Peak troponin = 6240 ng/L.  This is not a terribly high troponin and the peak troponin of STEMI using contemporary troponin is usually above 10 ng/mL (roughly equivalent to 10,000 ng/L in the high sensitivity assay).

Because it was a transient STEMI, the infarct size was small, leaving no discernable wall motion abnormality.

Later, the patient went back to have the other arteries stented.  (There is new data showing that for some patients, stenting all the arteries at the initial angiography results in outcomes at least as good as delayed stenting.  In this case, stenting was only delayed by a couple days.)

Learning Points

1. Should a transient STEMI go to the cath lab emergently?  I would argue yes. See this post: Timing of revascularization in patients with transient STEMI: a randomized clinical trial

2. Rapid reperfusion may leave no wall motion abnormality. (Although in this case it was a technically limited study)

3. STEMI frequently has open artery at angiography.  At least 16% of patients with STEMI at presentation have TIMI-3 flow just minutes later at emergent angiography (many more have an open artery with less than TIMI-3 flow). 

Stone GW et al. Normal flow (TIMI-3) before mechanical reperfusion therapy is an independent determinant of survival in acute myocardial infarction. Circulation 2001;104(6):636–41. https://www.ahajournals.org/doi/abs/10.1161/hc3101.093701

4. Most (70%) STEMI have peak Abbott contemporary troponin I > 10 ng/mL, but we don't have data on high sensitivity troponin (ng/L)

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MY Comment by KEN GRAUER, MD (10/14/2020):

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Insightful case showing 4 serial tracings during evolution of a STEMI in which the “culprit” artery was reperfusing and re-occluding. Although I limit my comments below to the initial EMS ECG that was done in the field ( = ECG #1) — I wanted to first reemphasize some important points brought out by Dr. Smith’s discussion above.

• The History is essential! The patient in this case was an older man with risk factors who described, “intermittent left-sided chest discomfort” over more than 1 day — with recurrence of this chest discomfort 2 hours prior to ECG #1. Awareness of this history greatly enhanced my insight at the time I interpreted this 1st ECG.
• Not uncommonly — the “culprit” artery may suddenly occlude — then spontaneously reopen (sometimes prior to the patient seeking medical attention) — and on occasion (such as in today’s case) — continue to open and close spontaneously a number of times. Interpreting the serial ECGs in today’s case, in association with this patient’s History — tells us this is what was happening.
• Even a “recent” STEMI may fail to show ST elevation at the time the ECG you are looking at was done IF — prior to this, there has been an ongoing process of intermittent occlusion, followed by spontaneous reopening.
• Depending on WHEN the cath was done during the course of a “transient” STEMI — the “culprit” artery may not always still be occluded at the time of cardiac catheterization.
• It may be difficult to determine the “culprit artery” from the initial ECG if the patient has multi-vessel disease (as did the patient in today’s case). In such instances when ECG findings may not be localized — the indication for cath may be cardiac chest pain with ischemic findings on ECG, even if no specific “culprit artery” is suggested on the ECG.

With this as introduction — Please TAKE another LOOK at the initial ECG that was done in today’s case ( = ECG #1 in Figure-1).

• Given the history in today's case — WHY is this initial ECG so concerning?
• HOW MANY leads in ECG #1 show abnormalities?

Figure-1: The initial ECG in this case (See text).

MY Thoughts on ECG #1: The rhythm is sinus bradycardia at ~55/minute. All intervals (PR, QRS, QTc) are normal. The axis is leftward at about -20 degrees. There is no chamber enlargement. Regarding Q-R-S-T Changes:

• There is a small, narrow Q wave of uncertain significance in lead aVL. There are QS complexes in leads V1 and V2.
• R Wave Progression — R waves develop appropriately after the QS complexes in leads V1,V2 — with transition (where R wave height surpasses S wave depth) occurring normally, seen here between leads V3-to-V4.
• NOTE: The finding of a QS complex in lead V1, or even in both leads V1 and V2 does not by itself necessarily mean that there have been anterior (or anteroseptal) infarction. A majority of patients with this finding will not have had anterior infarction. It is only when patients with a narrow QRS and no LVH have a QS complex in leads V1, V2 and V3 — that prior anterior (or anteroseptal) infarction becomes very likely.

Assessment of ST-T Wave Morphology in ECG #1: In the context of today’s patient (who presents with chest pain) — lots of leads show ST-T wave abnormalities in ECG #1. These ST-T wave abnormalities include:

• ST straightening in multiple leads (horizontal RED lines in Figure-2).
• ST segment coving, with slight elevation in lead V1.
• Abrupt angulation between the straight ST segments and the ascent of T waves in leads V3, V4, V5 and V6 (RED lines).
• T waves that look more voluminous than they should be, compared to R wave amplitude in the same lead. This is especially true for the T waves in leads II, V2 and V3 — and probably also for the T waves in leads V4, V5, V6.

My Impression of ECG #1: Many of the ST-T wave changes described above are subtle. That said — ST-T wave abnormalities highlighted by the RED lines in Figure-2 are seen in no less than 11 of 12 leads!

• In isolation — the ST-T wave changes in leads I, III, aVL, aVF and V1 in a patient without acute symptoms would probably not prompt concern.
• And, ST segment straightening with angulation at the onset of the T wave is often a nonspecific finding that does not necessarily reflect acute ischemia.
• But, in the context of an older patient with risk factors who develops new chest pain — I interpreted the above-described T waves as hyperacute until proven otherwise.

BOTTOM Line: Frank ST elevation that confirmed the diagnosis of acute STEMI was seen in the 2nd EMS ECG (shown above) in today’s case. But the point to emphasize is that even without this 2nd ECG — the acute ischemic (hyperacute) ECG findings I describe for ECG #1, in conjunction with the history of ongoing chest pain and ST-T wave abnormalities that are seen in no less than 11/12 leads — should prompt suspicion of recent OMI, and provide clear indication for prompt cath.

Figure-2: I’ve labeled abnormal ST-T wave findings in ECG #1 (See text).