ECG Blog #486 — Unusual Coupling

The ECG in Figure-1 is from a middle-aged man — who presented to the ED (Emergency Department) with on-and-off CP (Chest Pain). The patient was hemodynamically stable at the time this ECG was recorded.

QUESTIONS:

• How would you interpret this ECG in Figure-1?
•    — What is the rhythm?
•       — Would you activate the cath lab?

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

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My Initial Thoughts on Today’s CASE:

This is a challenging case — in that both the rhythm and the 12-lead tracing manifest complexities, which are important to resolve in time-efficient fashion in this patient who presents to the ED with new CP.

• In time-sensitive cases such as this one — I favor beginning my interpretation with a quick look at the long-lead rhythm strip (ie, that appears at the bottom of Figure-1). 
• To Emphasize: Precise interpretation of the rhythm is not initially needed. But it is helpful to establish if the underlying rhythm is sinus — and to determine if any initial management measures might be needed for the rhythm.
• After this quick look at the rhythm (and after verifying that the patient is hemodynamically stable) — I focus my attention on a quick survey of the 12-lead (ie, In today’s patient who presents with new CP — we want to determine as rapidly as possible IF prompt cath, thrombolytics or other emergency treatment measures are needed).
• NOTE: Although I describe my initial thoughts in "slow motion" — in most cases, the total time I spend for my initial Survey of the rhythm and 12-lead — should be less than 1 minute (and often less than 30 seconds).

The Cardiac Rhythm in Today’s Tracing:

The underlying rhythm in today’s tracing, as seen in the long lead II rhythm strip — is sinus (RED arrows in Figure-2 that highlight upright P waves in this lead).

• There are frequent PVCs ( = beats #3,5; 8,10; 13,15; and 18) — but no repetitive PVC forms are seen (ie, There is never more than 1 PVC in a row).
• NOTE: There is more to see in today’s rhythm — but since this patient is hemodynamically stable, we do not need to assess any more than the above for our initial Survey of the rhythm (that should have taken no more than seconds to complete).

Figure-2: I've labeled sinus P waves with RED arrows. 

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The 12-Lead ECG:

At this point — I turn my attention to the 12-lead ECG. Given today’s clinical presentation (ie, New CP in a middle-aged man — who manifests sinus rhythm with frequent uniform PVCs) — our principal task with initial Survey of the 12-lead ECG is to determine if prompt cath is needed.

• PEARL #1: Given the frequent PVCs — we need to focus our attention on ST-T wave appearance in the sinus-conducted beats ( = beats #2,4,6; 7,9,11; 12,14,16; and 17 — in Figure-3).
• My attention is immediately drawn to the 3 leads within the RED rectangle in Figure-3 ( = leads V2,V3,V4). Note that ST depression is maximal for sinus-conducted beats in these 3 leads — compared to ST depression seen in other chest leads (large BLUE arrows in leads V2,V3,V4).
• PEARL #2: In a patient with new CP — the finding of ST depression that is maximal in leads V2 and/or V3 and/or V4 indicates acute posterior OMI until proven otherwise!
• PEARL #3: Although it is always more difficult to assess the clinical significance of ST depression in PVCs — there are times in which the morphology of ST depression in PVCs is clearly abormal. I thought this was the case for the PVCs within the RED rectangle in Figure-3 ( = beats #13, 15, 18) — which show even more ST depression than is seen for sinus beats #11,12,14,16,17.
• PEARL #4: Because of a common blood supply — acute posterior OMI is often associated with acute inferior MI. And although there is no ST elevation in the inferior leads in Figure-3 — there is straightening of the ST segment takeoff in leads II,III,aVF (angled BLUE lines above the ST segments in these leads). There is also reciprocal ST depression seen in lead aVL (BLUE arrow in this lead) — such that these subtle hyperacute signs of acute inferior OMI serve to confirm my impression of the marked ST depression that immediately caught my "eye" in the chest leads (within the RED rectangle).
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• BOTTOM Line: Within less than 1 minute — I knew this middle-aged man with new CP and frequent PVCs — was evolving an acute infero-postero OMI — for which prompt activation of the cath lab was clearly indicated!

Figure-3: My attention was immediatey drawn to the maximal ST depression in sinus-conducted beats within the RED rectangle (BLUE arrows in leads V2,V3,V4). 

PEARL #5: Note that there is ST segment flattening, but no more than minimal ST depression of sinus-conducted beats in lead V1 of Figure-3. Given how much ST depression we see for sinus-conducted beats in neighboring leads V2,V3,V4 — the most logical explanation for not seeing more ST depression in lead V1 (that typically also manifests ST depression with posterior OMI) — is that there is associated acute RV involvment (RV MI often manifests ST elevation in right-sided lead V1 — which will attenuate any ST depression that otherwise would have been seen in lead V1 from posterior OMI).

• Clinically — It's important to be aware of acute RV MI because of its different hemodynamics (See ECG Blog #190 — for more on ECG diagnosis and clinical implications of acute RV MI).
• The way to confirm if acute RV MI is (or is not) present — is to obtain right-sided leads (which will show ST elevation in leads V2R,V3R,V4R).
• Anatomically — detection of acute RV MI localizes the "culprit" artery to the proximal RCA (Right Coronary Artery) — since the LCx does not supply the RV.

PEARL #6: Taking another "overview look" at ST-T wave morphology for sinus-conducted beats in Figure-3 — there are ST-T wave abnormalities in virtually all leads in this tracing. As a result, in addition to a proximal RCA "culprit" artery that I'd predict on cardiac cath — I would not be surprised if the patient also had significant underlying multi-vessel coronary disease.

• To Emphasize: Specific findings on cardiac cath will be interesting to learn — but are not needed for my rapid initial Survey decision-making — that as described above, should allow recognition of the need for prompt cath with PCI in this patient with new CP, frequent PVCs — and clear evidence of acute infero-postero OMI.

CASE Follow-Up:

Cardiac catheterization was performed in timely fashion. It revealed proximal RCA occlusion.

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Beyond-the-Core: The fascinating aspect of today's case for me — relates to the coupling intervals for the PVCs that we see in ECG #1.

• Because of our focus on treatment — We often ignore consideration of the mechanisms of cardiac arrhythmias. But awareness of these mechanisms (that although there is overlap, tend to fall within the 3 categories of increased automaticity — reentry — and "triggered" activity) — will at times provide important insight for optimal treatment selection. (Please check out my ADDENDUM below — in which I've excerpted the brilliant brief review of these concepts from Dr. S Venkatesan's website on Expressions in Cardiology — Nov. 2, 2020).
• As per Dr. Venkatesan — the usual mechanism for most ischemic VT rhythms is increased automaticity (especially when the ECG shows a polymorphic morphology with variable coupling intervals). This is in contrast to scar-related and idiopathic VT rhythms, that tend to circulate through the ventricles over a constant path, because they originate from a well defined site (ie, scar) — or in the case of idiopathic VTs (fascicular VT; RVOT VT) — from a specific anatomic location. It follows that QRS morphology will usually be monomorphic — the coupling interval tends to be constant (a result of the repeating re-entry pathway) — and there is generally less chance of deteriorating to VFib. 
• As a result, I find it helpful to look at coupling intervals (ie, the distance from sinus QRS complexes to the onset of the PVC) — with awareness that deterioration to VFib seems to be less common with isolated, monomorphic PVCs that manifest fixed coupling intervals (Hamon et al — Circulation: Arrhythm & Electrophysiol 10(4):XXX, 2017) — and — deVries et al — J Interv Card Electrophysiol 51(1):25-33, 2018).
• With the exception of parasystole (an uncommon independent focus ventricular arrhythmia that is often benign) — many (most) uniform PVCs that I see manifest fairly fixed coupling.
• Today's ECG is an exception ...  

Wenckebach Coupling?

The frequent PVCs that we see in ECG #1 in today's case are monomorphic (similar QRS morphology in each of the 12 leads for beats #3,5; 8,10; 13,15; and 18 — with the exception of minor differences due to artifact).

• As shown below in Figure-4 — a pattern of group beating is seen for these PVCs (repetition of this pattern showing 2 PVCs within each 5-beat grouping for beats #2-thru-6; 7-thru-11; and 12-thru-16).
• As shown by the colored double-arrows — the coupling interval increases within each group (YELLOW double-arrow — to PINK double arrow) — until there is a pause without any PVC (ie, within the R-R intervals between beats #6-to-7; 11-to-12; and 16-to-17) — after which the cycle (with the next YELLOW double arrow) begins again. 
• This timing of group beating with PVCs in today's tracing — to me suggests that the reentry cycle for coupling intervals of these PVCs manifests Wenckebach periodicity (Hansom et al — Curr Cardiol Rev 17(1):10-16, 2021). I have not previously observed this phenomenon of Wenckebach timing for PVC coupling intervals.
• My Theory: Whereas fixed coupling (reentry mechanism) of PVCs tends to be associated with somewhat lesser risk of deterioration to VFib — the obvious acute ischemia in today's ECG predisposes to other arrhythmia mechanisms (increased automaticity; "triggered" activity) which manifest here in the form of Wenckebach periodicity for PVC coupling intervals. The concern is potentially higher risk from these PVCs (therefore, all the more reason in today's case for prompt cath with PCI reperfusion).

Figure-4: I've highlighted what appears to be PVC coupling with Wenckebach periodicity!

Today's final Beyond-the-Core Concept: Did YOU Notice the increase in PR intervals for sinus-conducted beats within the 5-beat groupings in today's long-lead II rhythm strip?

• I illustrate this finding in Figure-5 — in which I focus solely on the long lead II rhythm strip. Baseline artifact in the 1st grouping (for beats #2-thru-6) renders assessment of this phenomenon difficult. But an increase in the PR interval of conducted beats is evident in the last 2 groupings (this increase in PR interval being highlighted as we move from the RED — to PINK — to YELLOW arrows in these last 2 groups).
• As per the laddergram illustration in ECG Blog #68 — this increase in PR interval for the next sinus-conducted beat that occurs after a PVC is not the result of Wenckebach. Instead, it reflects the phenomenon of "concealed" conduction — in which retrograde conduction from the preceding PVC, while not enough to block forward conduction of the next sinus beat — is enough to slightly prolong the ensuing PR interval.
• The term "concealed" is used, because we cannot explain this effect on the ensuing PR interval from what is seen on the actual ECG — but instead must infer there is retrograde conduction from the PVC that impedes forward conduction of the next sinus impulse.

Figure-5: The reaon for the increasing PR intervals (PINK and YELLOW arrow P waves) — is the result of "concealed" conduction from the preceding PVCs.

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Acknowledgment: My appreciation to Narveen Sharma (from India) for the case and this tracing.

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ADDENDUM #1 (7/5/2025):

• Review on basic mechanisms of cardiac arrhythmias:

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Figure-6: Mechanisms of Arrhythmias- Part 1 (from Dr. S Venkatesan's website on Expressions in Cardiology — Nov. 2, 2020).

Figure-7: Mechanisms of Arrhythmias- Part 2 (from Dr. S Venkatesan's website on Expressions in Cardiology — Nov. 2, 2020).

Figure-8: What is "Triggered Activity" with respect to arrhythmia mechanisms? (from AI Internet Summary- 2025).

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ADDENDUM #2 (7/5/2025):

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

Figure-9: 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).
• In 'My ECG Videos" — Check out near the top of that page 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.
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• 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.
• The Clinical Reality: Many acute coronary occlusions 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.

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