ECG Blog #508 — Tall, Pointed T Waves ...

The ECG in Figure-1 was obtained from a middle-aged man who presented to the ED (Emergency Department) with severe, new-onset CP (Chest Pain).

• BP = 130/90 mm Hg.
• Initial hs-Troponin was normal.

QUESTIONS:

• How would you interpret this ECG?
• Should you activate the cath lab?

Figure-1: The initial ECG in today's case — obtained from a patient with new-onset, severe chest pain.

MY Thoughts on the Clinical Scenario:

The history of severe, new-onset CP in this middle-aged man that was worrisome enough to him to prompt his presentation to the ED, immediately places him in a higher-risk group for having an acute cardiac event.

• PEARL #1: To emphasize that although one may be momentarily comforted by the initial normal hs-Troponin value — this in no way rules out an acute cardiac event. Wereski et al (JAMA Cardiology, 2020) — found that 14% of patients with an acute STEMI had a normal initial hs-Troponin (and ~25% had hs-Troponin levels below the infarction “rule-in” level).
• On occasion — even the 2nd hs-Troponin level may still be normal in a patient who goes on to develop an acute STEMI. The reasons for this are simple: i) Troponin values (including hs-Troponin values) provide a “rear-view” mirror as to what has already happened — but not to what will happen in the future; — and, ii) Whether hs-Troponin increases or not depends not only on the size of the infarct — but especially on the duration of time that the “culprit” vessel is occluded — which means that if the amount of time that the “culprit” vessel is closed was brief (because of rapid spontaneous reperfusion) — then hs-Troponin may be no more than minimally (if at all) elevated.

MY Thoughts on the Initial ECG in Figure-1:

The rhythm is sinus arrhythmia — at a rate just under 60/minute. The PR interval is prolonged ( = 1st-degree AV block) — but QRS duration and the QTc interval are normal. The frontal plane axis is normal at +50 degrees. There is no chamber enlargement.

• There is appreciable artifact in lead V1. That said — the baseline artifact in the limb leads is minimal, and does not impair interpretation.
• My “eye” was immediately drawn to the chest leads — beginning with lead V2. Each of these 5 chest leads that follow manifest distinct J-point ST elevation with hyperacute-looking, tall, and pointed T waves (RED arrows in leads V2-thru-V6 — as shown in Figure-2). 
• 
  
• PEARL #2: As opposed to the peaked T waves that may be seen with repolarization variants — the T waves seen in Figure-2 are more pointed, taller and more symmetric (ie, Repolarization variants tend to be less symmetric, with a slower upslope compared to their more rapid downslope).
• Note: Distinct J-point notching is seen in lead V6. Despite this finding (that is commonly seen with repolarization variants) — the above described hyperacute appearance of the T waves in this patient with new-onset, severe CP is clearly of concern.
• P.S.: Although good to verify that serum K+ is normal (which it was) — the peaked T waves of hyperkalemia tend to have an even narrower base than that seen in Figure-2.

Figure-2: I’ve labeled today’s initial ECG.

Regarding the limb leads in Figure-2:

• ST segments are elevated and T waves are peaked in leads I,II,III and aVF (although not quite as much as they are in the chest leads).
• I was unsure if the tiny, artifact-laden QRS complex in lead aVL had some ST depression (therefore my BLUE question mark in this lead).
• 
  
• BOTTOM Line: In this middle-aged man who presents with severe, new-onset CP — ST elevation is seen in 9 (if not 10) of the 12 leads, with hyperacute T waves until proven otherwise in 5 consecutive chest leads.

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The Case Continues:

Based on the above clinical presentation and findings in the initial ECG — the cath lab was activated. Results from the cardiac cath:

• LMain: Normal.
• LAD: Mild-to-moderate atherosclerosis in the mid-LAD region with severe Coronary Spasm resulting in total occlusion (TIMI-0 flow). Normal (TIMI-3 flow) was achieved following intracoronary NTG.
• LCx: No more than minimal atherosclerosis.
• RCA: No more than minimal atherosclerosis.
• 
  
• Impression: Insignificant coronary atherosclerosis. Acute coronary spasm that initially resulted in total LAD occlusion — but with normal flow restored by intracoronary NTG. Normal LV function following IC-NTG. Medical management advised.

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NOTE: Although the initial hs-Troponin-I value was normal — the 2nd and 3rd Troponin values were greatly increased! ==> Today's patient had an MI precipitated by coronary spasm.

• At 6 hours after symptom onset — hs-Troponin I was 6.24 ng/mL (abnormal ≥0.0875; reference ≤0.0175).
• At 12 hours after symptom onset — hs-Troponin I = 66.16 ng/mL.

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MY Thoughts on this CASE:

Unfortunately, no ECG was obtained following relief by intracoronary NTG of the complete LAD occlusion. Thus, we do not have a baseline ECG when this patient was pain-free.

• Review of this patient's chart did not reveal any prior ECG.
• A repeat ECG was done after cardiac catheterization, at which time the patient was still pain-free — but this was nearly 2 hours later (shown in Figure-3).

QUESTION:

• Has there been any change in ECG #2 compared to ECG #1?
• HINT: If your answer is that there is no difference between the 2 tracings shown in Figure-3 — GO BACK and LOOK again ...

Figure-3: Comparison between today's initial ECG — and the repeat ECG done after cardiac catheterization.

ANSWER:

ST elevation with T wave peaking persists in multiple leads in ECG #2. That said — there is subtle-but-real improvement in chest lead T wave appearance.

• Chest lead T waves look less hyperacute in the repeat ECG — in that these T waves are now less symmetric than they were in ECG #1 (ie, the T wave upslope in leads V2-thru-V6 is now slower than the T wave downslope).
• Subtle J-point notching is seen in leads V5,V6 — as well as in several limb leads.
• My Thoughts: We still do not know what this patient's baseline ECG looks like. Although ECG #2 now manifests characteristics of a repolarization variant — I would have expected more normalization of this patient's ECG by this point 2 hours after intracoronary NTG completely relieved this patient's chest pain. I'd want to repeat the ECG after the patient remains pain-free for at least a day.

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CASE Conclusion:

Today's case provides an insightful example of a patient with limited, non-obstructive coronary disease — who presented with acute coronary spasm severe enough to completely occlude the mid-LAD until the administration of intracoronary NTG.

• The result was spasm-induced infarction, with marked Troponin increase.

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About VSA (VasoSpastic Angina) = Coronary Spasm:

The entity of "VSA" — has been known for more than 50 years. As opposed to Prinzmetal (or Variant) Angina that occurs at rest — it has become increasingly apparent that variations on the theme of coronary "spasm" also occur with surprising frequency in association with exercise-induced angina, unstable angina, acute infarction, and with malignant ventricular arrhythmias that may cause sudden death.

I found manuscripts by Teragawa et al ( World J Cardiol 10(11):201-209, 2018) — by Tandon et al (Cureus 11(2):e4134, 2019) — by Slavich and Patel (IJC Heart & Vasc 10:47-53, 2016) — and by Ziccardi and Hatcher (StatPearls, 2023) helpful in my review of this subject.

• Coronary Spasm is defined — as transient narrowing of one or more epicardial coronary arteries, with this resulting in myocardial ischemia.
• Multiple potential mechanisms have been attributed to causing coronary spasm, including — endothelial dysfunction; hyper-reactive vascular smooth muscle — magnesium deficiency; autonomic nervous system malfunction — and/or from some combination of the above factors.
• The diagnosis of VSA in today's patient was made by cardiac catheterization. In this patient who was found to have a limited amount of non-obstructive atherosclerosis — total occlusion of the mid-LAD region was initially seen on cath. Administration of IC (IntraCoronary) NTG restored normal flow — thus confirming the diagnosis of coronary spasm.
• In other cases, SPT (Spasm Provocation Testing) is needed to make the diagnosis of VSA (ie, Ergonovine or Acetylcholine are administered during cardiac cath in an attempt to provoke coronary spasm — after which the diagnosis of spasm is confirmed by restoration of coronary flow with IC-NTG).
• Additional modalities that may be helpful for diagnosing VSA include ETT (Exercise Treadmill Testing) in patients with exercise-induced spasm — and/or Holter monitoring (for patients with night-time or early morning VSA).
• Although many (most) patients with VSA have at least some degree of underlying atherosclerosis — a certain percentage of patients with VSA do not (sometimes showing "normal" coronary arteries on cath). Thus, the mechanism by which coronary spasm may produce symptoms and/or events may vary from microvascular dysfunction in seemingly normal vessels — to coronary spasm that acts on vessels with established plaque in a way that may ultimately precipitate plaque rupture (ie, See ECG Blog #415 on MINOCA — for the group of patients who develop acute MI despite "Non-Obstructive" Coronary Arteries).
• PEARL #3: Be aware of potential triggers of coronary spasm. These may include smoking, cocaine, marijuana, alcohol, amphetamines, certain migraine medications, alpha agonists (ie, clonidine; pseudoephedrine), cold exposure, psychologic stress and left heart catheterization (guidewire, balloon dilatation).

Treatment of VSA:

Full discussion of VSA extends beyond the scope of this ECG Blog. That said — several points regarding treatment are worthy of mention.

• Smoking cessation is an absolute MUST! This is one example of a clinical condition in which smoking a single cigarette — is smoking 1 cigarette too many. 
• Avoid other potential triggers of spasm (ie, = PEARL #3 above! ).
• SL (Sublingual) NTG — is 1st-line treatment for an acute VSA episode.
• CCB (Calcium Channel Blockers) — are recommended for longterm treatment. If/as needed — CCBs may be combined with long-acting nitrates.
• ß-Blockers — are best avoided (as ß-blockade may result in unopposed alpha-adrenergic activity, potentially exacerbating spasm). If ß-blockers are needed for other cardiac indications — then gradual dose titration is essential to avoid exacerbating coronary spasm.
• Consider magnesium supplementation.
• 
  
• Unresolved Issues: While great progress has been made in the recognition of VSA under a variety of conditions — some problems remain: i) How to treat refractory VSA? — and, ii) Determining which patients with VSA are in need of an ICD (Implantable Cardioverter-Defibrillator).

Another LOOK at Today's ECG:

While fully acknowledging that I was not expecting the principal pathology in today's patient to be the result of coronary spasm — in retrospect, the initial ECG is perfectly consistent with this diagnosis!

• As discussed earlier — today's initial ECG (that I've reproduced below in Figure-2) shows ST elevation with tall, pointed T waves in 5/6 chest leads (RED arrows in these leads). Although distorted by artifact — there appears to be ST elevation in lead V1.
• ST elevation with T wave peaking is also seen in 4 of the limb leads. This makes for 10/12 leads showing ST elevation with peaked T waves.
• Clear sign of reciprocal ST depression is missing.
• As opposed to an acute OMI, in which ST-T wave findings tend to be localized to that area of the heart that is ischemic — diffuse ST elevation with hyperacute T waves in the absence of reciprocal ST-T wave changes is perfectly consistent with coronary spasm!
• 
  
• PEARL #4: Although today's ECG showing diffuse ST elevation without reciprocal STdepression is typical for pure coronary spasm — VSA is not always associated with ST elevation SPT (Spasm Provocation Testing) may be needed for diagnosis on cath in certain cases.

Figure-2 — that I’ve reproduced from above. 

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

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ECG Blog #507 — A Teenager with Palpitations ...

The ECG in Figure-1 — was obtained from an otherwise healthy male teenager with palpitations.

• How would you interpret this tracing?

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

MY Thoughts on the ECG in Figure-1:

This is a complex tracing. I thought it best to break it down into parts.

• Beginning right after beat #6 — is a continuous run of a regular tachycardia which is wide until beat #21, when the QRS complex suddenly narrows!

NOTE: Although there is no single long lead rhythm strip — limb leads and chest leads are continuous, such that there are 30 consecutive beats on this tracing. In all — there is just under 10 seconds of monitoring.

• By the Every-other-Beat Method — the rate of the tachycardia is ~200/minute (See the ADDENDUM below for a brief ECG Video that reviews application of this concept).
• In Figure-2 — I have chosen the R wave of beat #8 in lead I as my "starting point" — because this begins precisely on a heavy grid line.
• We can see that the time it takes to record 2 beats (PINK numbers 1 and 2) — is 3 large boxes on ECG grid paper (BLUE numbers 1,2,3). This tells us that HALF of the rate = 300 ÷ 3 large boxes = 100/minute.
• Therefore, the actual rate = 100 X 2 = 200/minute.

Figure-2: Illustration of the Every-other-Beat Method for rapid estimation of fast rates. The rate of the regular tachycardia that begins after beat #6 is ~200/minute.

Today's Fast Rhythm is Supraventricular:

Although the QRS complex is wide from beat #7 through to beat #20 — the QRS then suddenly becomes narrow (ie, beginning with beat #21). This is best seen by focusing on the top row of beats in Figure-2 (ie, I suggest focusing on the 30 consecutive beats in leads I and V1 for my description below):

• PEARL #1: The fact that the last 10 beats in today's tracing clearly represents a regular SVT rhythm ( = narrow-complex tachycardia) — and that the transition from the wide tachycardia ( = beats #8-thru-20) — to the regular SVT that begins with beat #21 occurs without any pause or acceleration — suggests that this entire tachycardia is all supraventricular! (ie, If the wide beats represented VT — then it would be exceedingly unlikely for precise regularity of the rhythm to continue as the QRS narrows)!
• PEARL #2: QRS morphology during the wide tachycardia is consistent with RBBB aberrancy! (ie, The all positive QRS in lead V1 for beats #14-thru-20 — with slender initial R wave and wide terminal S wave in lead V6 for these beats — is completely consistent with RBBB conduction — as is the slender initial R wave with wide terminal S wave in lead I for beats #8-thru-13).
• PEARL #3: Putting together what we've established from PEARLS #1 and 2 — the tachycardia that begins after beat #6 is a regular SVT (albeit with a changing QRS morphology) at a rate of ~200/minute, but without sinus P waves. As I review in ECG Blog #240 — the rate of ~200/minute would be faster-than-expected for sinus tachycardia in a teenager — and unusual for AFlutter (since 2:1 AV conduction for untreated AFlutter typically results in a ventricular response close to 150/minute). Given that Atrial Tachycardia is an uncommon arrhythmia in an otherwise healthy teenager — this leaves a reentry SVT rhythm (either AVNRT or AVRT) as the most likely diagnosis for today's tachycardia, especially given the abrupt onset of this SVT rhythm.

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How Does Today's SVT Begin?

Now that we've established our "working diagnosis" as most probably being a reentry SVT rhythm — We can focus our attention on HOW this arrhythmia begins (See Figure-3):

• Beats #1,2,3 in Figure-3 — appear to be the last 3 beats in a previous SVT run at ~200/minute (that is probably of the same SVT mechanism with normal [narrow] QRS conduction as is seen in the chest leads for beats #21-thru-30).
• Beat #4 is sinus-conducted! (the 1st RED arrow in Figure-3 highlighting the sinus P wave).
• Beat #5 occurs early, and is preceded by a PAC (the 1st BLUE arrow that peaks the T wave of beat #4).
• Beat #6 is another sinus-conducted beat.
• Beat #7 is another PAC (2nd BLUE arrow in Figure-3). Note that this 2nd PAC produces a QRS complex that is wider than the normally-conducted QRS of beat #5.

Figure-3: Focusing on how the regular SVT begins.

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QUESTION:
Can you explain WHY in Figure-3 — the QRS complex of beat #7 is wider and looks different than the QRS of beats #1-thru-6?

• HINT: The interval measurements (in milliseconds) that I’ve added under beats #3-thru-7 in lead II of Figure-4 provide an important clue to the Answer!

ANSWER:

As I explain in the ADDENDUM below — the concept of "cycle-sequence" comparison (as it relates to aberrant conduction) — and — the Ashman Phenomenon — explain why beat #7 is wider and looks different than beats #1-thru-6 in Figure-4 (See ECG Blog #70 — for detailed illustration of the Ashman Phenomenon).

• PEARL #4: My user-friendly way to synthesize the Ashman Phenomenon is simply to recall, “The funniest-looking beat follows the longest pause”. 
• The physiologic reason for this phenomenon — is that the longer the R-R interval preceding a given beat is — the longer the RP (Refractory Period) after that beat will be (with the RP consisting of both an absolute and relative refractory period — as in ECG Blog #70).
• In Figure-4 — the R-R interval preceding beat #6 is 740 msec. — which is longer than the 720 msec. R-R interval that precedes beat #4. Therefore, by the Ashman Phenomenon — the PAC that follows beat #6 will be more likely to conduct with aberration.

PEARL #5: The other component of cycle-sequence comparison — relates to the coupling interval, which is the distance from the onset of a QRS complex until the onset of the PAC that follows it. 

• It makes sense that the shorter the coupling interval — the greater the chance that a PAC will fall within the RRP (Relative Refractory Period), and therefore be conducted with aberration.
• In Figure-4 — it is the coupling interval of the 2nd PAC that is shorter (ie, 180 msec. vs 220 msec.) — therefore explaining why beat #7 is aberrantly conducted, but beat #5 is not.
• KEY Point: There is an "art" to applying the dual concepts of "cycle-sequence" comparison — in that both a longer preceding R-R interval and a shorter coupling interval may not be present, as they are for beat #7 in Figure-4.
• PEARL #6: Given the need for preciseness when applying cycle-sequence comparison for determining the likelihood of aberrant conduction — it should be obvious that use of calipers is a must to apply this concept!

PEARL #7: The ECG Video and content in Figures-7,-8,-9 in the ADDENDUM below — review the basics of aberrant conduction. As emphasized in this review — aberrantly conducted beats most often manifest some known form of conduction block (ie, RBBB, LBBB, and/or left anterior or posterior hemiblock).

• The predominantly positive R wave in lead I — with predominant negativity of the QRS in each of the inferior leads — suggest that beat #7 in Figure-4 is conducted with LAHB (Left Anterior HemiBlock) aberration.

Figure-4: How do the measurements that I’ve added under beats #3-thru-7 in lead II explain why the QRS of beat #7 is wider and looks different than the QRS of beats #1-thru-6?

PEARL #8: It is important to appreciate that the run of reentry SVT that begins with beat #7 in Figure-4 — is initiated by a PAC! 

• In contrast to ATach (ie, an ectopic Atrial Tachycardia) that usually begins with gradual acceleration of the ectopic atrial focus ("warm-up" phenomenon) — SVT reentry rhythms often start abruptly after a PAC — because this early beat arrives at the AV Node when the faster AV Nodal pathway is still refractory.
• This may serve to set up a reentry circuit — IF as a result of the PAC, the impulse starts down the other pathway, and is then able to complete the formation of a reentry circuit (ie, IF the faster AV Nodal pathway that was blocked has recovered in time to allow return of the impulse via retrograde conduction — as shown in Figure-5). 

Figure-5: The mechanism of a reentry SVT rhythm can be seen from this schematic figure — in that each time the impulse completes its path over the reentry circuit — retrograde conduction (back to the atria) as well as forward conduction to the ventricles (through the His-Purkinje system) occurs. As discussed below (as well as in ECG Blog #240) — this retrograde conduction back to the atria can sometimes be seen on the ECG during the tachycardia in the form of retrograde P waves.
= = = = =
KEY Point: With a reentry SVT — the impulse continues to circulate over the reentry circuit until this circuit is either interrupted (ie, by AV nodal blocking drugs or a vagal maneuver or another PAC or a PVC) — or — until the reentry SVT stops spontaneously.
= = = = =
NOTE: The reentry circuit shown here in Figure-5 depicts the mechanism for AVNRT (in which the reentry circuit is completely contained within the AV Node). This differs from the situation with AVRT — in which the reentry circuit extends outside of the AV Node via participation of an AP = Accessory Pathway (See PEARL #9).

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NOTE: What follows below goes Beyond-the-Core. As an emergency provider — it is more than enough to recognize that the teenager in today's case is highly symptomatic with recurrent, rapid runs of a reentry SVT rhythm that merits referral to an EP cardiologist for EP study and probable ablation treatment.

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Beyond-the-Core:  Is there more Atrial Activity?

Take Another LOOK at Figure-4 that I've reproduced below ...

• Is there any evidence of atrial activity after beat #7?
• If so — What does this atrial activity suggest?

Figure-4: Take Another LOOK at Figure-4. Is there more atrial activity?

ANSWER:

There are a number of signs suggesting additional atrial activity that are seen after beat #7. I highlight some of these below in Figure-5:

• To Emphasize — I am not certain about all potential signs of additional atrial activity. That said — I thought this to be of less clinical importance, since this symptomatic teenager with recurrent runs of reentry SVT will need EP study regardless — to clarify the nature of his arrhythmia (and most likely for curative ablation).

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PEARL #9: Sinus P waves are upright in lead II (as well as in the other inferior leads). In contrast — retrograde P waves will be negative in the inferior leads. Other leads that commonly show retrograde atrial activity are leads aVR and V1 — in which retrograde P waves tend to be positive in these right-sided leads.

• As discussed in ECG Blog #240 — the 2 major types of reentry SVT rhythms are AVNRT (if the reentry circuit is completely contained within the AV Node) — and — AVRT (if an AP located outside of the AV Node is present and participating as the retrograde limb of the reentry circuit).
• The very sharp, negative deflections that are seen at the very end of the widened QRS complex for beats #8-thru-13 (highlighted by YELLOW arrows in Figure-6) look like retrograde P waves.
• I added yellow question marks highlighting possible retrograde P waves in the ST segment of beats #1 and 2, which are the last few beats of the narrow SVT rhythm that ends after beat #3.
• Perhaps the BLUE arrow that I added over the ST segment of beat #3 — represents another PAC that occurs with a very short coupling interval (180 msec.) but without a long preceding R-R interval, such that this PAC is blocked (therefore ending the SVT at the beginning of this tracing?).
• Perhaps the sharp, negative deflections seen in other leads during the widened SVT (ie, in lead aVF for beats #8-thru-13 — and at the very end of the QRS in leads V5,V6 for beats #14-thru-20) also represent retrograde P waves?

PEARL #10: I thought the above suggestions of retrograde atrial activity during the runs of reentry SVT in Figure-6 were occurring relatively late in the cycle — which, as illustrated in ECG Blog #240 — suggests participation of an AP (Accessory Pathway) in the reentry circuit (therefore defining the rhythm as orthodromic AVRT). 

• NOTE: The presence and participation of an AP in the reentry circuit will result in a longer reentry circuit than what occurs with AVNRT, in which the reentry circuit is completely contained within the AV Node. This is why the RP' interval tends to be longer with orthodromic AVRT compared to AVNRT (in which the reentry circuit is shorter, given that it is completely contained within the AV Node).

Figure-6: I've highlighted some indications of retrograde atrial activity.

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More about AVRT (AtrioVentricular Reciprocating Tachycardia):

A nice review of AVRT by Jabbour et al appears in StatPearls, 2024.

• A significant percentage of patients with a reentry SVT rhythm will have a "silent" AP (Accessory Pathway) that only allows retrograde conduction — which is why delta waves are never seen on a 12-lead ECG in these patients.
• Sinus P waves in these patients are preferentially conducted in the forward direction over the normal AV Nodal pathway — which is why the QRS complex is narrow.
• If a PAC occurs in such patients — it will be conducted over the normal AV Nodal pathway and, if it occurs "at just the right moment" — it may find that the AP has recovered its ability to conduct retrograde, thereby completing the formation of a reentry circuit. If the "right timing" persists (ie, with recovery of AP ability to conduct retrograde each time an impulse conducted over the normal AV Nodal pathway arrives at the His-Purkinje junction) — this may perpetuate a run of orthodromic AVRT (as appears to be happening in Figure-6).

Miscellaneous additional notes re AVRT rhythms:

• Rarely (in only ~5% of AVRT episodes) — conduction of a supraventricular impulse may arrive in the ventricles via forward conduction over the AP — with retrograde conduction to complete the reentry circuit occurring over the AV Nodal pathway (ie, antidromic AVRT). In such cases, since the forward limb of the reentry circuit passes directly to the ventricles over the AP — the QRS complex will be wide, and antidromic AVRT may look identical to VT.
• On occasion — a patient may have more than a single AP (with this consideration relevant to the conclusion of today's case — as I discuss below).
• The ability of an AP to conduct retrograde (and participate in the reentry circuit of an AVRT rhythm) is not necessarily lifelong. Especially in children — the ability of a "silent" AP to conduct retrograde often resolves as the child becomes older.
• The abrupt switch of a reentry SVT that begins with QRS widening (ie, with either RBBB or LBBB conduction) — but then suddenly normalizes QRS duration without appreciable change in the R-R interval between wide vs narrow beats — suggests that an AP may be participating in the reentry cycle (This is seen beginning with beat #21 in Figure-6). 
• 
  
• Coumel's law may then help to predict localization of the AP:
• IF the R-R interval is slightly longer during the SVT with RBBB conduction than when the QRS is narrow — then the AP is right-sided. 
• IF the R-R interval is slightly longer during the SVT with LBBB conduction than when the QRS is narrow — then the AP is left-sided.

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CASE Follow-Up:

EP study was done on today's patient — and verified the presence of a participating AP in the reentry circuit (thereby confirming orthodromic AVRT as the mechanism of the arrhythmia).

• Noted in the EP report was that atrial stimulation induced orthodromic AVRT mediated by a concealed left lateral AP.
• Intermittent tachycardia was seen with RBBB conduction while maintaining the same cycle length — and with LBBB conduction manifesting a longer cycle length. This confirmed left-sided localization of the AP ( = Coumel's sign).
• The pathway was ablated — after which it was no longer inducible on EP study.

Unfortunately — The initial post-ablation Holter monitor done after the patient was discharged showed some recurrence of the SVT rhythm.

• As noted earlier — it is known that on occasion more than a single AP may be present. I suspect this may be the case with today's patient — as alternating participation by more than a single AP would seem the most logical explanation for recurrence of this patient's reentry SVT rhythm after ablation of only one of the APs.
• I suspect a 2nd EP study may be needed to identify one or more additional APs that may need to be ablated.

Latest Follow-Up (11/30/2025):

• I have just heard that a 2nd post-discharge Holter monitor showed clinical improvement, with marked reduction in the number of PACs without recurrence of tachycardia.
• 
  
• PEARL #11: On occasion — the positive effect from ablation may be delayed for days, or even weeks after ablation is performed! (Zeljkovic et al — Eur Hear J Case Rep, 2021). This may be due to "thermal latency" (in which heat continues to exert an effect on ablated tissue even after the energy source has been turned off) — or — it may be due to a delayed inflammatory response from initial ablation on neighboring tissue that ultimately affects conduction properties. 
• As a result — EP cardiologists often adopt "watchful waiting" after an initial failed ablation procedure for a period of weeks, to see if the desired effect is ultimately achieved. 
• Unfortunately (for the same reasons) — significant AV block necessitating a pacemaker may also be delayed in its appearance. Close follow-up post ablation is essential!

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Acknowledgment: My appreciation to Amelia Aria (from Bucharest, Romania) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs & 3Rs Approach to systematic rhythm interpretation.
• ECG Blog #240 — and ECG Blog #345 — Atrial activity in reentry SVT Rhythms.

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ADDENDUM #1 (11/29/2025): Included below is the following:

• The Every-other-Beat Method for rapid estimation of fast rates.
• More on aberrant conduction.

ECG Media Pearl #27 (3:00 minutes Video) — ECG Blog #210 — Reviews the Rule of 300 for estimating heart rate — and — @ 1:25 minutes in the video, the Every-Other-Beat Method for Estimating Rate with fast rhythms (4/2/2021).

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ECG Media PEARL #28 (4:45 minutes Video) — Reviews WHY some early beats and some SVT rhythms are conducted with Aberration (and why the most common form of aberrant conduction manifests RBBB morphology).

• NOTE: I have excerpted a 6-page written summary regarding Aberrant Conduction from my ACLS-2013-ePub. This appears below in Figures-7, -8, and -9).
• CLICK HERE — to download a PDF of this 6-page file on Aberrant Conduction. 

Figure-7: Aberrant Conduction — Refractory periods/Coupling intervals (from my ACLS-2013-ePub).

 

Figure-8: Aberrant Conduction (Continued) — QRS morphology/Rabbit Ears.

 

Figure-9: Aberrant Conduction (Continued) — Example/Summary.

ECG Blog #506 — What did the Repeat ECG Show?

This case was sent to me by an anonymous follower.

• If told that this patient was having new CP (Chest Pain) — How would YOU interpret this tracing?

Figure-1: The initial ECG in today's case — obtained from a patient with new chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

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MY Thoughts on the ECG in Figure-1:

In view of the history of new CP — I was extremely concerned by this tracing. To emphasize — that the ECG findings are extremely subtle, but they often are on an initial tracing.

• In Figure-2 — I have highlighted within the RED rectangle the single lead that most caught my "eye".
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• Why do I say this?

Figure-2: I've highlighted the lead that most caught my "eye".

My Concern about Lead V1:

The QRS complex in lead V1 is tiny.

• Normally — the ST-T wave in this lead is isoelectric, or slightly negative. In a patient who does not have LVH or QRS widening — the ST-T wave in lead V1 should virtually never show the amount of disproportionate ST segment coving and elevation that we see in Figure-2.
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• Given the history of new CP — the abnormal appearance of the ST-T wave in lead V1 prompted me to look extra carefully at the other 11 leads on this tracing.

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MY Thoughts on the Other 11 Leads:

As stated earlier — the ECG findings on today's tracing are extremely subtle. But they often are on the initial tracing of an acute cardiac event. I've labeled KEY findings below in Figure-3.

• The rhythm is sinus arrhythmia at a rate slightly over 60/minute. Intervals (PR-QRS-QTc) and the frontal plane axis are normal. There is no chamber enlargement.
• There is low voltage in the limb leads (None of the 6 limb leads exceed 5 mm in amplitude).
• Transition occurs early (ie, The R wave in lead V2 is already equal to the S wave in this lead — whereas "transition" usually does not occur until later).
• There is ST segment straightening in lead V3. Given my heightened concern about anterior ST elevation, prompted by the history of new CP and the abnormal ST-T wave appearance in lead V1 — I thought the ST-T wave in lead V3 looked "bulkier" than-it-should-be (ie, "fatter"-at-its-peak and wider-at-its-base than I'd expect given modest R wave amplitude in this lead).
• I was uncertain what to make of the ST-T wave appearance in neighboring leads V4,V5 — but there is definite ST segment flattening and subtle-but-real ST depression in lead V6.
• That the above-noted ST-T wave findings in leads V1,V3,V6 are "real" — is supported by the subtle ST segment flattening and depression in each of the inferior leads (BLUE arrows in these leads).

MY Impression of Today's Tracing:

Based on the above findings (and before I was told what happened in this case) — I wrote back that my concern was that the ECG picture in Figure-3 could represent the early appearance of Precordial "Swirl".

• As described in detail in ECG Blog #380 — the colorful term, "Swirl" facilitates recognition of a unique ECG pattern strongly suggestive of a very proximal site of acute LAD occlusion (usually proximal to the 1st septal perforator) — with resultant septal ischemia, in addition to anterior wall and apical involvement.
• KEY features of "Swirl" are: i) Abnormal ST elevation and an usual ST-T wave appearance in lead V1 (especially when there is no LVH and no QRS widening); — and ii) Reciprocal ST depression in lead V6 (if not also in lead V5) — with the shape of this lateral chest lead ST depression being flatter than that seen with simple LV "strain" from LVH (Check out ECG Blog #380 for a much more detailed description!).
• To emphasize — that other anterior leads in addition to lead V1 often manifest hyperacute T waves with "Swirl" — but that in an early pattern, ST-T wave abnormalities in other chest leads might not be obvious. It is for this reason that my concern regarding leads V1,V3,V6 was heightened in today's case because this patient had new CP — and especially because each of the inferior leads showed definite ST segment flattening and depression (as they often do with a proximal site of LAD occlusion).

Figure-3: I've labeled KEY findings on today's tracing.

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CASE Follow-Up:

Today's patient died suddenly — a short while after today's ECG was recorded (before a repeat tracing could be recorded). Providers were appropriately concerned about abnormal findings on the initial ECG.

• Presumably — the ECG in Figure-3 is the result of a very proximal acute LAD occlusion that rapidly evolved into an extensive acute infarction with cardiogenic shock before treatment to open the "culprit" vessel could be initiated.

Learning Points:

Sometimes the evolution of acute infarction is extremely rapid — with dramatic ECG changes and clinical deterioration of the patient occurring over a period of minutes (See ECG Blog #459 — as well as many other cases in this ECG Blog).

• Today's case serves as reminder that: i) A history of worrisome new chest pain immediately places your patient at increased risk of an acute evolving event — therefore the need for close attention to subtle ECG findings that might not otherwise be important in an asymptomatic patient; — ii) When we see 1 or 2 leads that clearly manifest abnormal ECG findings in a higher-risk patient with new CP (as was the case for leads V1 and V6 in today's tracing) — We need to pay extra close attention to other leads that may show subtle supportive findings (as per the inferior lead ST depression in today's tracing); — and, iii) When there is any doubt about whether an acute process is evolving — Repeat the ECG within 10-20 minutes of the 1st tracing (which in today's case was not possible given the rapid demise of this patient).

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P.S.: And the Patient had Low Voltage ...

As I've often noted in this ECG Blog — there are many potential causes of low voltage (See ECG Blog #272 — for full discussion of this entity).

• The above said — among the potentially relevant causes of low voltage in today's case is myocardial "stunning" — that may be the result of a large acute infarction associated with cardiogenic shock that presumably resulted in the sudden demise of today's patient.

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Acknowledgment: My appreciation for the anonymous submission of today's case.

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ADDENDUM (11/22/2025): 

• For More Material — regarding the ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-5: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.

• In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion). NOTE: The timed-contents of this Podcast #2 facilitate quickly finding whatever key concepts you wish to review.
• Check out near the top of the "My ECG Videos" page, those videos from my MedAll ECG Talks that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
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• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.

• As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
• BUT — because the cath lab was activated within 1 hour of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlier) was clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
• The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.
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• KEY Clinical Reality: Many of the acute coronary occlusions that we see never develop ST elevation (or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases.