Friday, March 27, 2026

ECG Blog #524 — A little bit of Jadwar ...


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NOTE: Today's post is from our publication in JACC Case Reports — 
(Nirdosh Rassani, MBBS & Ken Grauer, MD — Jan, 2026) (https://www.jacc.org/doi/10.1016/j.jaccas.2026.107164)
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The patient in today's case is a man in his late 20s — who presented to the ED about 6 hours after ingesting a finger-breadth piece of Jadwar (Figure-1).

Figure-1: Photograph of Delphinium denudatum (Jadwar). 


Details of today's case can be found in our JACC Case Reports article (available at the above link)
  • Suffice it to say that the patient's symptoms at the time of presentation were limited to mild flushing, increased sweating and palpitations
  • He was alert — with stable vital signs.

On seeing this patient's initial ECG (that I've reproduced in Figure-2) — it is easy to understand his chief complaint of "palpitations".


QUESTION:
  • How would you interpret this initial ECG?

Figure-2: The initial ECG in today's case — obtained from a man in his 20's who ingested Jadwar. (To improve visualization — I've digitized the original ECG using PMcardio).



MY Thoughts on the ECG in Figure-2:
This patient's initial ECG is extremely worrisome. That's because there is a constantly changing QRS morphology. It's hard to tell if there any "normal" beats.
  • To facilitate assessment in Figure-3 — I've numbered the beats in the long lead II rhythm strip.
    • Can you tell what is going on? (See below).

Figure-3: I've numbered the beats in today's initial ECG.


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

The Long-Lead II Rhythm Strip:
This is a complicated rhythm strip. I outline my stepwise "thought process" for assessment below:
  • The rhythm is irregularly irregular.
  • As noted — QRS morphology is constantly changing throughout the long lead II rhythm strip. Many of the beats are wide.
  • There are some narrow beats. Three of these narrow beats look similar and are upright in the long lead II (ie, beats #5,12,18). Presumably these 3 beats are supraventricular!
  • A short pause precedes beats #5 and 18 — but I see no sign of atrial activity. If P waves were present — I would expect to see them in the short pause that precedes beats #5 and 18. Given the overall irregularity with occasional narrow beats but no sign of P waves — I suspect that the underlying rhythm is AFib (Atrial Fibrillation).
  • There are multiple wide beats in the long lead II. Other than beats #5,12,18 — all of the other positive QRS complexes are clearly wide (ie, beats #1,2,3,4; #6; #9,10,11; #14; #19). Each of these beats look to be of ventricular etiology.
  • Fortunately — the long lead II rhythm strip is simultaneously recorded with the 12-lead tracing above it. The reason this is so helpful in this tracing — is that this allows us to view the QRS complexes that are negative in the long lead II in other simultaneously-recorded leads. For example — although beat #13 looks fairly narrow in the long lead II — it is actually a wide (presumably ventricular) beat when viewed in simultaneously-recorded leads V2,V3.
  • Beat #16 is all negative and appears to be slightly widened in the long lead II — but it looks much wider, and clearly of ventricular etiology in simultaneously-recorded leads V1,V2,V3.
  • Beat #15 in the long lead II looks intermediate in QRS morphology between beats #14 and #16. Is the intermediate QRS shape of beat #15 the result of fusion between beats arising from 2 different ventricular sites?
  • On the other hand — not only is beat #21 narrow in the long lead II — but it appears to also be narrow in simultaneously-recorded leads V4,V5,V6. This suggests that beat #21 may be supraventricular, with its negative QRS morphology in the long lead II explained by aberrant conduction. Perhaps other fairly narrow, negative complexes in the long lead II are also supraventricular with aberrant conduction?

My Impression of Figure-3: 
This is an extremely complicated tracing. My assessment:
  • The underlying rhythm appears to be AFib.
  • There are multiple wide beat QRS morphologies that most-likely represent non-sustained runs of PMVT (PolyMorphic Ventricular Tachycardia).
  • Those beats that are narrower in the long lead II exhibit beat-to-beat variation in QRS morphology, suggestive of aberrant conduction and/or fusion with ventricular ectopy.

  • PEARL #1: What counts in assessment of Figure-3 is the overall "Gestalt" of what is likely to be happening. It simply is not worth spending excessive time trying to "dissect" the etiology of every beat in this tracing — as this is a thankless, if not impossible task. Instead, our goal for interpreting the rhythm is to arrive at an overall assessment — and this appears to be underlying AFib with non-sustained runs of PMVT.

  • PEARL #2: As noted above — beat #21 is probably supraventricular with aberrant conduction. As a result, I looked closely at ST-T wave morphology and the QT interval for this beat. Note within the RED rectangle in Figure-3 — that there appears to be marked ST depression in leads V5,V6 for beat #21 (BLUE arrow) — as well as QT prolongation considering the overall rapid rate.

  • PEARL #3: The unusual rhythm in Figure-3 is best interpreted in light of the clinical situation. This clinical situation is that today's patient ingested Jadwar prior to the onset of his symptoms! 
= = = = = = = = = = = = = = = = = = = = =

About Jadwar:
Jadwar (Delphinium denudatum) is a traditional medicinal herb widely used in South Asia as a "universal antidote" for treating a wide variety of neurologic, analgesic and gastrointestinal conditions. Among its attributed actions include pain relief, an anti-inflammatory effect, reduced fatigue, antidote properties (for snake or scorpion bites), addiction recovery (to help manage narcotic dependency) — as well as for treatment of URIs and other common infections.
  • Although Jadwar itself is generally considered safe and of low toxicity when used appropriately — Jadwar may sometimes be adulterated with aconite (which can occur if/when herbal medicines are improperly prepared).
  • Aconite ingestion may be highly toxic and even fatal. The mechanism stems from binding to and persistently activating voltage-sensitive sodium channels in excitable cells (including myocardial, nerve and muscular tissue). This results in sustained sodium influx with persistent sodium channel activation (Chan — Clin Toxicol 47(4):279-285, 2009).
  • Patients with aconite ingestion may present with a combination of neurologic features (paresthesias with facial or limb numbness) — motor effects (muscle weakness) — and cardiovascular effects that may be severe (hypotension, chest pain, palpitations from a variety of arrhythmias including refractory ventricular tachycardia and ventricular fibrillation).
  • Management of aconite poisoning is largely supportive until effects of ingestion have worn off. IV Lidocaine was successfully used in our case for its sodium-channel blocking effect that counteracts aconitine toxicity.
= = = = = = = = = = = = = = = = = = = = =

CASE Follow-Up:
Detailed description of today's presentation is covered in our JACC Case Reports article. In brief — laboratory evaluation of this patient was largely normal, with exception of low-normal serum Mg++ (treated with IV Mg++ replacement). Serum Troponins were negative and Echo showed surprisingly normal LV function despite the arrhythmia.
  • Within 30 minutes of administering IV Lidocaine (IV bolus followed by IV infusion) — there was a dramatic reduction in the frequency and duration of PMVT episodes — with complete suppression of ventricular ectopy achieved by 6 hours.
  • IV Lidocaine infusion was continued for 24 hours — followed by observation on telemetry for an additional 24 hours, after which the patient was discharged from the hospital.

To facilitate comparison in Figure-4 — I've added the discharge ECG below this patient's initial tracing. This discharge tracing reflects what was seen on telemetry during the last 40+ hours of observation.
  • Note return of normal sinus rhythm (RED arrow P waves in the long lead II of ECG #2) — and the complete absence of ventricular ectopy!
  • The lateral chest lead ST depression in ECG #2 is now minimal — with normalization of the QT interval.
  • PEARL #4: In support of my suspicion that beat #21 in the initial tracing was indeed a supraventricular beat — is the finding of similar QRS morphology for this beat in leads V5,V6 of ECG #1 — with QRS morphology in leads V5,V6 after restoration of sinus rhythm in ECG #2. This suggests that the reason beat #21 was negative in the long lead II of ECG #1 was indeed aberrant conduction.
  • The "PEARL" — is that sometimes the etiology of certain beats or rhythms of uncertain etiology in an initial tracing may become clear by careful comparison of morphology on subsequent tracings.

Figure-4: Comparison of today's initial ECG — with the discharge ECG recorded 48 hours later.


FINAL Thoughts (Addendum added on 3/29/2026):
Today's case proved satisfying by the complete recovery made by this patient who had ingested a potentially lethal dose of medicinal herb.
  • Technically — the rhythm in today's case should probably be classified as Torsades de Pointes — because, as highlighted in Figure-4 — the rhythm is PMVT with a preexisting long QTc (which we know is true — because after treatment the QTc normalizes, confirming that it was initially prolonged).
  • That said — I called this rhythm "PMVT" despite this initially prolonged QTc because Torsades typically manifests more of a "pattern", in the form of alternating predominant positivity transitioning to predominant negativity in a repetitive fashion (ie, "twisting of the baseline" — as per the French translation of its name). In contrast — I thought today's initial rhythm manifests more of a random variation in QRS morphology.

  • PEARL #5: Clinically — the semantics of whether today's initial rhythm is PMVT or Torsades is not important. This is because the KEY management concept for this rhythm is identification and treatment of the cause (which was successfully accomplished in today's case by Mg++ replacement + IV Lidocaine + a good dose of "luck", that with close monitoring the adverse effects from this toxic ingestion would wear off and the patient would recover).

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Related Material:

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Acknowledgment: My appreciation to Nirdosh Rassani (from Quetta, Pakistan) for the case and this tracing.
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Saturday, March 21, 2026

ECG Blog #523 — Is there a "Culprit"?


The ECG in Figure-1 was obtained from an older woman — who presents to the ED (Emergency Department) with CP (Chest Pain) that began ~2 hours earlier.


QUESTIONS:
  • How would you interpret the ECG in Figure-1?
    • Would you activate the cath lab?

Figure-1: The initial ECG in today's case.


MY Thoughts on Today's CASE:
Given the history of new CP — this is an extremely worrisome ECG:
  • The  rhythm is sinus at ~80/minute. Regarding intervals — the PR interval and QRS duration are both normal, with the QTc no more than of borderline duration. Regarding chamber enlargement — the S wave of >20 mm in lead V2 is consistent with voltage for LVH (See Figure-7 in the Addendum of ECG Blog #73).
Regarding Q-R-S-T Changes:
  • A small and narrow Q wave is seen in lead aVL.
  • R wave progression — is normal (Small but definite initial r waves are seen in both leads V1,V2 — with transition occurring normally between leads V3-to-V4).
The remarkable findings relate to ST-T waves:
  • My attention was immediately drawn to the ST-T waves in the 3 inferior leads — which show eyecatching straightened and downsloping ST segments (RED arrows in leads II,III,aVF in Figure-2). Each of these leads show terminal T wave positivity (upright YELLOW arrows) — with this down-up T wave appearance in a patient with new CP being an especially worrisome sign of hyperacuity.
  • Support for our concern is forthcoming from the hyperacute ST-T wave appearance in lead aVL (with ST segment straightening, subtle-but-real ST elevation given small size of the QRS — and a disproportionately "fattened" T wave with wide base).
In the Chest Leads: 
  • Lead V1 is notable for ST segment straightening — which is especially remarkable in light of the distinctly abnormal 1-2 mm of flat ST segment depression in leads V3,V4,V5,V6 (BLUE arrows in these leads). Each of these 4 chest leads show significant terminal T wave positivity — which in this patient with new CP strongly suggests hyperacuity.
  • I found lead V2 especially interesting as a "transition" lead — in that it shows neither J-point depression or elevation. This is most probably because lead V2 is situated between lead V1 (which is remarkable for its hyperacute-looking ST segment straightening) — and leads V3,V4,V5,V6 (each of which show unmistakeable ST segment flattening and depression with terminal T wave positivity).
  • Finally — there is slight-but-real ST elevation in lead aVR.

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

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Putting It All Together:
  • I'd immediately activate the cath lab. The history of new-onset CP in this older woman whose initial ECG shows significant ST-T wave abnormalities in no less than 11/12 leads indicates an acute cardiac event until proven otherwise.

The question arises as to what the "culprit" artery might be? 
  • The only lead showing ST elevation is lead aVL. In the absence of ST elevation in other lateral leads — I thought acute LCx (Left Circumflex) occlusion to be less likely.
  • ST elevation is commonly seen in multiple chest leads with proximal LAD (Left Anterior Descending) occlusion — but there is no anterior lead ST elevation in today's initial ECG..
  • Instead, we see the ST segment straightening in lead V1 — with the predominant findings in Figure-2 being the very acute-looking ST depression with terminal T wave positivity in 7 leads (leads II,III,aVF — and in V3,V4,V5,V6) — with transition lead V2 — and with ST elevation in lead aVR.

  • PEARL #1: The most logical explanation for this series of acute-looking ST-T wave abnormalities without suggestion of a specific "culprit" artery — is that there is severe multi-vessel disease.
  • I suspected acute LAD occlusion given findings of ST straightening in V1 + transition lead in V2 with lateral chest lead ST depression suggesting a Precordial "Swirl" pattern in a patient with significant multi-vessel disease (See ECG Blog #380). Supportive findings of ST elevation in aVL with reciprocal inferior lead ST depression is consistent with proximal LAD occlusion — with the diffuseness of the ST depression reflecting impossible-to-account-for attenuation effects from multi-vessel involvement.
  • Bottom Line: None of this matters. What counts is simply that prompt cath with PCI is needed. Specific anatomy to be revealed by cardiac cath.

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The CASE Continues:
  • Cardiac cath was performed — and revealed severe multi-vessel disease (with an 80% ostial LMain lesion — a 95% "culprit" mid-LAD lesion + RCA disease).
  • The initial hs-Troponin-I came back with borderline elevation. The repeat Troponin was clearly elevated.

PEARL #2:
 It does not matter what Troponin shows in today's case. This is because regardless of what the 1st and 2nd Troponin assays show — prompt cath with PCI will be needed given the history of new-onset CP and today's initial ECG showing diffuse acute-looking ST-T wave changes in 11/12 leads!

  • The initial hs-Troponin may be negative or non-diagnostic in up to 25% of acute STEMI patients (Wereski et al — JAMA Cards 5(11):1302, 2020).
  • "Time is Muscle (myocardium)". As repeatedly shown in Dr. Smith's ECG Blog (See My Comment in the February 8, 2026 post) — The most benefit from reperfusion occurs within the first 4 hours after acute coronary occlusion (and every 2-hour delay results in 60% more myocardium infarcted).
  • Serum Troponin values provide a rear-view mirrow of what has already happened — and not of what is about to happen.
  • PEARL #3: The decision to perform cardiac cath in today's case can be made as soon as the initial ECG is seen.
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A 2nd ECG was recorded ~3 hours after ECG #1 (shown in Figure-3):
  • ECG #2 was obtained prior to cardiac cath — at a time when the patient's symptoms had decreased. Dual antiplatelet therapy (DAPT) and Heparin were ongoing.

QUESTIONS:
  • Given that the patient's CP was less at the time ECG #2 was recorded — How would you interpret this repeat ECG?

Figure-3: Comparison between the 2 ECGs in today's case.


MY Thoughts on ECG #2:
Compared to ECG #1 — the repeat ECG in Figure-3 shows reperfusion changes in virtually all leads that previously looked acute:
  • Most remarkable in ECG #2 is the anterior lead ST segment coving, now with deep, symmetric T wave inversion in lead V2.
  • The horizontal ST depression previously seen in leads V3,V4,V5,V6 has essentially resolved.
  • Reciprocal reperfusion changes are now seen in the inferior leads — in which downsloping ST depression has been replaced by tall, "bulky" positive T waves.
  • Deep symmetric T wave inversion is seen in lead aVL.
  • PEARL #4: Especially in view of reduced CP — I interpreted the evolutionary changes in ECG #2 as confirming acute LAD occlusion as the "culprit" artery in this patient with underlying multi-vessel disease.

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Acknowledgment: My appreciation to Chun-Hung Chen (from Taichung City, Taiwan) for the case and this tracing.
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Saturday, March 14, 2026

ECG Blog #522 — What is the "Other" Diagnosis?


The ECG in Figure-1 is from a middle-aged man who presented to the ED with new-onset severe CP (Chest Pain). His symptoms lasted ~30 minutes — but his CP had totally resolved by the time this ECG was recorded.


QUESTIONS:
  • How would you interpret the ECG in Figure-1?
    • What would you do? 

Figure-1: The initial ECG in today's case — obtained from middle-aged man with new CP. His CP had resolved by the time this ECG was recorded (To improve visualization — I've digitized the original ECG using PMcardio).


CASE Follow-Up:
Providers on the case interpreted the ECG in Figure-1 as consistent with Brugada Phenocopy (ie, a BrugadaType-1 ECG pattern as a result of "something else" — but not a true Brugada Syndrome).
  • Because providers were certain ECG #1 was a manifestation of Brugada Phenocopy — serum Troponin was not ordered.

QUESTION: 
  • Do you agree with the above approach?

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NOTE: I review Brugada ECG Patterns in the ADDENDUM below:
  • A summary of Brugada Syndrome vs Phenocopy appears in Figure-6 — with more depth exploration in the 2-part ECG Video below (Total view time ~17 minutes).
  • For more of an update on Brugada Syndrome — See below!
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MY Thoughts on the CASE:
As is often the case — today's History is KEY ==> a middle-aged man who presents with new CP — but who was asymptomatic by the time today's initial ECG was recorded.

My interpretation of the ECG in Figure-1:
  • The rhythm is sinus.
  • The QRST complex in lead V1 (within the RED rectangle in Figure-2) — is diagnostic of a Brugada-1 ECG pattern.
  • That said — the shape of the ST segment coving in neighboring leads V2,V3,V4 differs from the very steep downsloping ST segment seen in lead V1.  
  • Deep, symmetric T wave inversion persists in leads V3 and V4.
  • More subtle ST-T wave changes are seen in the limb leads (ST segment straightening in leads I,II,III,aVF — and ST segment coving with slight elevation and T wave inversion in lead aVL). Given small size of the QRS in the limb leads (especially tiny in leads III and aVL) — these changes are subtle indeed!

  • BOTTOM Line for Figure-2: Although the QRST complex in lead V1 is typical for a Brugada-1 ECG pattern — the other findings described above are not expected with Brugada Phenocopy in the absence of ongoing ischemia. Instead, in this patient who presents for new-onset CP — We have to suspect that in addition to the typical Brugada-1 ECG pattern that we see in lead V1 — the neighboring chest leads also suggest there may be an ongoing acute infarction!

Figure-2: I've labeled KEY findings in ECG #1 (and added an insert with illustration of Brugada-1 and Brugada-2 ECG patterns).


The CASE Continues:
As noted above — serum Troponins were not obtained because the provider attributed all ECG findings in Figure-2 to Brugada "Phenocopy".
  • A short while later — the ECG in Figure-3 was recorded. 

HINT: The changes in the chest leads of ECG #2 are extremely subtle.
  • Do you see them?

Figure-3: Repeat ECG done a short while after ECG #1.


Comparison of the ECGs in Figure-3:
As noted above — the changes between the 2 ECGs in Figure-3 are extremely subtle:
  • The R' that was seen in ECG #1 has thinned out — with subtle-but-real reduction in the ß-angle in ECG #2 (See the insert in the upper right of Figure-2 regarding calculation of the ß-angle).
  • In neighboring leads V2,V3,V4 of ECG #2 — the ST segment coving is less pronounced, and there is narrowing with slight reduction in the depth of T wave inversion that was seen in the initial ECG.
  • Bottom Line: Although subtle indeed — ECG #2 suggests ongoing evolution of reperfusion T waves.

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Figure-4 shows the final ECG done the next day ( = ECG #3):
  • Unfortunately — I lack details on this case beyond knowing that the patient had no more chest pain — that Troponins were never done — and that there was no cardiac catheterization.

QUESTION:
  • How would you explain the ECG changes seen in Figure-4?

Figure-4: Comparison between the initial and the final ECGs that were recorded in today's case. How best to explain these changes?


MY Thoughts on the ECGs in Figure-4:
Whereas the changes in Figure-3 (between ECGs #1 and #2) were extremely subtle — the changes now seen in Figure-4 (between ECGs #1 and the final ECG #3) are obvious.
  • The Brugada-1 ECG pattern in lead V1 of ECG #1 has now almost completely resolved in ECG #3.
  • ST segment coving without ST elevation persists in neighboring chest leads of ECG #3 — with marked deepening of symmetric T wave inversion.
  • In the limb leads of ECG #3 — there has been slight axis shift, with marked increase in the now widened and tall inferior T waves (essentially the reciprocal opposite ST-T wave picture that is now seen for leads V2 and V3 in ECG #3).
  • Deep, widened T wave inversion is now seen in leads I and aVL of ECG #3.
  • Bottom Line: Even without Troponin values and without cardiac catheterization — the ECG evolution that is now obvious in ECG #3 confirms reperfusion changes following extensive infero-antero MI (presumably following acute LAD occlusion in a patient with multi-vessel disease).

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Final Editorial NOTE:
I initially hesitated using today's case because I lacked follow-up. Efforts to contact today's patient were unsuccessful. He lived remotely, away from health care facilities — and apparently flew back to the island where he lived without returning calls.
  • Today's case is insightful — because it illustrates that among the causes of a transient Brugada-1 ECG pattern are acute LAD occlusion, which may superimpose on the ST-T wave changes of acute infarction.
  • In my experience — the most common precipitants of a Brugada-1 ECG pattern in patients who do not have Brugada Syndrome (ie, Brugada "Phenocopy" ) — are acute febrile illness and hyperkalemia. I've seen cases in which there is complete resolution of the Brugada-1 ECG pattern after resolution of the febrile illness and hyperkalemia.
  • But — acute ischemia and/or infarction and/or S/P cardiac arrest may also be causes of a Brugada-1 ECG pattern, as was seen in today's patient whose presenting complaint was new chest pain.
 

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Acknowledgment: My appreciation to Kianseng Ng (from Kluang, Johore, Malaysia) for making me aware of this case and allowing me to use this tracing.

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ADDENDUM (3/13/2026): 

I've added below material relating to Brugada ECG Patterns — beginning with my 2-part ECG Video:

  • NOTE: Although I recorded this 2-part ECG Video in 2021 ( = 5 years ago) — with the exception of a few changes in approach (that I highlight below) — this 2-part video remains current, and hopefully facilitates recall of Brugada ECG patterns.
  • I introduced the concept of Brugada Phenocopy in my ECG Blog #238 (published in July, 2021). This distinction between true Brugada Syndrome — vs a transient Brugada ECG pattern attributable to some other precipitating condition (ie, febrile illness; hyperkalemia; acute ischemia/MI, etc.with resolution of the ECG pattern once the precipitating condition resolves — remains critical for risk assessment, as well as for optimal management (Adytia and Sutanto — Current Prob in Card 49(6), 2024).  


What's NEW?
I'll preface the 2-part Video below with select updates from the following comprehensive newer references:

Brugada ECG Patterns: 
  • As per the above JACC Review — for practical purposes, the only ECG pattern that is diagnostic of BrS (Brugada Syndrome) is Type-1 (as shown below for A in Figure-5 — when this ECG pattern is present in ≥1 of the anterior leads = V1,V2,V3).
  • I had not been distinguishing between a Type-2 vs Type-3 pattern (as per my illustration in Figure-2 above). For investigators who do favor distinction between Type-2 ( = B in Figure-5) and Type-3 ( = C in Figure-5) — the shape of the ST-T wave is similar, with the difference being that with Type-3, there is <2mm of ST elevation. 
  • My Preference: I still favor use of only 2 Types ( = Brugada Types-1 and -2) — but whatever your preference, it’s good to be aware that some investigators employ the use of 3 Types (as shown below in Figure-5).
  • Neither Type-2 nor Type-3 Brugada ECG patterns alone are diagnostic of BrS. That said — BrS can be diagnosed in these patients IF provocative testing with a SCB (Sodium Channel Blocker) converts a Type-2 or Type-3 pattern into a Brugada-1 ECG. 

Figure-5: The 3 Brugada ECG Patterns (Adapted from Krahn et al — JACC: Clin Electrophys 8(3):386-405, 2022).


Additional Considerations:
The KEY to optimal management of BrS lies with Risk Assessment (To Emphasize: Risk assessment is best performed by cardiologists well versed in the many manifestations of BrS — with current accepted concepts explored in the above 2 references).
  • SAEs (Serious Arrhythmic Events) — are rarely the 1st symptom in patients with BrS (which emphasizes the importance of identifying Brugada ECG Patterns — and determining which of these patients are at highest risk for SAEs, and therefore in need of preventive treatment).
  • Aside from a malignant arrhythmia — highest risk of SAEs are in: i) Patients with a history of cardiogenic syncope; — ii) The presence of a spontaneous Brugada-1 ECG; — and/oriii) Association with Other Factors (ie, Excessive alcohol consumption — hypo-/hyperKalemia — Acidosis — Febrile Illness — have all been shown to facilitate Brugada-1-induced SAEs).

  • The sensitivity for ECG recognition of a Brugada-1 pattern is increased by ~50% including high-lead positions (ie, Recording of leads V1 and V2 not only in the 4th IC space — but also in the 2nd and 3rd IC spaces, so as to account for anatomic variation in the position of the vulnerable RV Outflow Track).
  • Be aware of intermittent, spontaneous fluctuations in the presence and potential sudden resolution of a Brugada-1 ECG pattern, especially in response to potential precipitating factors such as febrile illness, hyperkalemia, and/or certain drugs. As a result — Provocative Testing with a SCB (Sodium-Channel Blocking agent), is an important adjunct in risk assessment of the patient with a Brugada-1 ECG pattern (NOTE: Not all SCBs used in provocative testing are created equal — but this concept extends well beyond the scope of this ECG Blog).
  • Genetic Testing is an important part of Brugada-1 risk assessment (especially since such testing may facilitate identifying family members at risk).

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In Part 1 of this ECG Video (9 minutes) — the essentials of Brugada Syndrome are reviewed.




Int Part 2 (8:00 minutes) — these essentials are applied clinically. 

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Figure-6: 2-page Summary of the essentials of Brugada Syndrome (from Grauer K: ECG-2014-ePub, KG/EKG Press, 2014).



 

Figure-7: World prevalence map of Brugada Syndrome. The overall worldwide prevalence of Brugada Syndrome is ~0.5/1,000 in the population. This prevalence is highest in Southeast Asia (at least 5 times more common than in North America). The country with highest prevalence of Brugada Syndrome is Thailand, with ~15 times higher prevalence than for the worldwide average. Brugada-2 patterns (ie, "Saddleback") are also much more prevalent in Southeast Asia than elsewhere in the world. (Excerpted from Vutthikraivit et al: Acta Cardiol Sin 34:267-277, 2018).


 

Figure-8: Summary of KEY concepts reviewed in the above ECG Video.




 




 



 



Saturday, March 7, 2026

ECG Blog #521 — Inferior MI? — Anything else?


The ECG in Figure-1 was obtained from a middle-aged man with a long history of smoking — who presents with severe new-onset CP (Chest Pain).
  • The patient reports having 2 episodes of severe CP — each of which spontaneously resolved. He then presented to the ED (Emergency Department) several hours after the 2nd episode (ie, He was not having CP at the time ECG #1 was recorded).
  • The initial Troponin level was negative for acute infarction.

QUESTIONS
  • How would you interpret the ECG in Figure-1?
    • Should you activate the cath lab?

Figure-1: The initial ECG in today's case — obtained from a middle-aged man with CP — but who was asymptomatic at the time this ECG was recorded. (To improve visualization — I've digitized the original ECG using PMcardio).



MY Thoughts on Today's ECG:
The ECG in Figure-1 shows a regular sinus rhythm at ~80/minute. Intervals (PR, QRS, QTc) and the axis are normal. There is no chamber enlargement.

Regarding Q-R-S-T Changes:
  • Q Waves: There are q waves in the lateral leads (ie, leads I,aVL; and leads V4,V5,V6). These have the appearance of normal septal q waves — in that all of these q waves are narrow and small in size.
  • R Wave Progression: Normal (ie, R wave amplitude progessively increases as we move across the chest leads — with transition occurring normally between leads V2-to-V4).

Regarding ST-T Wave Changes:
  • In this patient with new CP — My "eye" was immediately drawn to the "scooped" ST depression in lead V2 (within the RED rectangle in Figure-2)
  • This ST depression continues in neighboring leads V3,V4 (RED arrows in these chest leads— but has largely resolved by lead V5.

  • ST-T wave changes in the inferior leads are more difficult to evaluate (See below).


Figure-2: I've labeled the ECG in today's case.

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ANSWERS: Putting It All Together . . .
There are a number of reasons why assessment of today's case is challenging. Unfortunately, we lack many details and only have limited follow-up. That said, my purpose in presenting this case — is that the following points can still be made from the brief history we are given, and from today's initial ECG:
  • The history of several episodes of new-onset and severe CP in this middle-aged man with a longterm history of smoking immediately place him in a higher-risk group for having an acute cardiac event. Awareness of this clinical situation should lower our threshold for accepting ST-T wave findings as abnormal.
  • Availability of a prior ECG for comparison would have made it much easier to determine if the ST-T wave changes that we see in ECG #1 are acute.
  • Repeating the ECG within 10-20 minutes of the initial tracing is advisable when symptoms are new and there is uncertainty about whether ST-T wave findings are acute — as diagnostic "dynamic" ST-T wave changes may sometimes be seen within minutes (See ECG Blog #115 — and ECG Blog #459)
  • Obtaining a bedside Echo may sometimes be diagnostic if it shows a localized wall motion abnormality. (While Echo may be diagnostic if positive — a normal Echo does not rule out an acute event if the patient is not having CP at the time the Echo is done).
  • The initial normal hs-Troponin in today's case in no way rules out an acute cardiac event (See ECG Blog #508). In addition to infarct size, whether or not Troponin will be elevated depends on how long the "culprit" artery is occluded for — which we do not know in today's case. But if the duration of time that the "culprit" artery is occluded is very brief — there may not be any Troponin elevation at all (and on occasion — the first 2 Troponin values may come back normal despite the patient going on to develop a STEMI).

Consider the following additional points:
  • The patient was not having CP at the time ECG #1 was recorded. This suggests that spontaneous resolution of acute coronary occlusion may have occurred — in which case acute ST-T wave abnormalities that were present during CP may signficantly improve (and even resolve).
  • That said — there normally should be slight, gently upsloping ST elevation in leads V2 and V3. This is why in a patient with new CP — the finding of ST depression that is maximal in leads V2,V3,V4 (as is seen in ECG #1) — is diagnostic of acute posterior MI until proven otherwise! (See ECG Blog #351 — and ECG Blog #298, among many others).
  • NOTE: Because of a common blood supply to the inferior and posterior walls of the left ventricle — I always look for acute inferior lead changes whenever I suspect acute posterior OMI. Unfortunately, the inconsistent ST-T wave appearance in the inferior leads of ECG #1 makes it all-but-impossible to assess the inferior leads (ie, Whereas complex B within the BLUE rectangle suggests a straightened, hyperacute ST segment with terminal T wave inversion — complexes A and C do not look acute).

BOTTOM Line:
 Maximal ST depression in leads V2,V3,V4 in this patient with a history of new CP suggests acute posterior OMI until proven otherwise. Knowing that this patient's CP had completely resolved at the time ECG #1 was recorded may account for relatively modest ST-T wave changes in the remaining leads.
  • Ideally — the cath lab would be activated on seeing ECG #1.
  • If the interventionist was reluctant to catheterize the patient at this point — then the following actions might serve to expedite acceptance to perform this procedure: i) Repeating the ECG within 10-20 minutes — and if this initial repeat tracing failed to show dynamic changes — follow-up with a few more repeat tracings within the hour; — ii) Immediately repeating the ECG if at any time the patient's CP returns; — iii) Searching for a prior ECG on this patient (that most probably would confirm that the ST depression in leads V2,V3,V4 is acute); — iv) Performing bedside Echo, looking for a localized wall motion abnormality; — and, v) Looking for any elevation in the 2nd Troponin value (which in a patient with new worrisome symptoms is indication for prompt cath — even when ECG changes are less than diagnostic).
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CASE Follow-Up: 
My follow-up is limited — but the results that I have reinforce the above clinical points:
  • The repeat Troponin was elevated at ~60 (I'm not sure of units or norms — but a value of 60 is clearly elevated).
  • A repeat ECG done many hours later seemed to show less acute changes compared to ECG #1.
  • Bedside Echo done the next day showed a wall motion abnormality localized to lateral and posterolateral segments.
  • Cardiac cath done the next day confirmed the LCx (Left Circumflex) as the "culprit" artery (I do not know about additional cardiac cath findings).

Lessons to Be Learned:
  • Waiting for ST elevation before activating the cath lab misses a substantial percentage of acute coronary occlusions. Acute posterior OMI is most easily recognized in a patient with new CP by maximal ST depression in leads V2,V3,V4 — which is much easier to recognize and more reliable than than trying to assess the dampened amplitudes obtained with posterior leads (See ECG Blog #80). Posterior OMI is the best example of how we can make a presumptive diagnosis of acute coronary occlusion without insisting on ST elevation
  • The diagnosis of acute OMI could have been made significantly earlier in today's case.
  • Delay in diagnosis (and therefore in reperfusion treatment of acute coronary occlusion) comes at a price. The most benefit from reperfusion occurs within the first 4 hours after acute coronary occlusion (Every 2-hour delay results in 60% more myocardium infarcted). Documentation of these Lessons-to-be-Learned is forthcoming in these 3 posts from Dr. Smith's ECG Blog ( = the February 8, 2026 post — the January 15, 2026 post — and the October 23, 2025 post with My Comment appearing at the bottom of the page in each of these posts).

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Acknowledgment: My appreciation to Hisham Alshamekh (from Egypt) for the case and this tracing.
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ADDENDUM (3/7/2026)
For more regarding the concept and ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria):
  • Check out ECG Blog #337 — that reviews a case with focus on distinction between a "NSTEMI" vs an OMI.
  • Consider the 2 Audio Pearls at the bottom of this page.
  • Consider Figure-3 — which reviews some ECG findings to look for when you suspect an acute OMI in a patient who does not satisfy the millimeter-based STEMI criteria that I review below this Figure.

Figure-3: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG.
= = = = =
KEY Note #1: Insistence in satisfying millimeter-based STEMI criteria before considering prompt cath with PCI (or thrombolytic therapy when access to 24/7 cath-capability is not available) — will miss at least 1/3 of all acute coronary occlusions. In a patient with new CP — attention to the ECG findings in Figure-3 may allow you to identify these patients with an acute OMI despite lacking STEMI criteria.
= = = = =
KEY Note #2: Loss of potentially viable myocardium is actually much greater than that implied in Key Note #1 — because even for patients in whom a "STEMI" is eventually recognized — by waiting until millimeter-based criteria are finally satisfied, the needed reperfusion therapy (PCI or thrombolytic therapy) is all-too-often delayed (often by many hours!)Time is critical! — as the greatest amount of potential myocardial-saving benefit occurs when reperfusion therapy is provided within the first few hours! (with the self-fulfilling prophecy that the outdated and inferior "STEMI-paradigm" gets perpetuated in the literature — because data will be recorded saying PCI was delivered "within minutes" of STEMI elevation [neglecting the clinical reality that OMI-criteria will often have been present hours earlier! ).
= = = = =
Note #3: See ECG Blog #318 — for clarification of T-QRS-D (Terminal QRS Distortion = my 2nd bullet in Figure-4).



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How a "STEMI" is Defined:

I've excerpted the following Akbar and Mountfort's citation in StatPearls, 2024 — of ECG Guidelines for defining a "STEMI" from the AHA (American Heart Association)ACC (American College of Cardiology)ESC (European Society of Cardiology), and the WHF (World Heart Federation):
  • New ST-segment elevation of ≥1 mm at the J point in 2 contiguous leads (except in leads V2 and V3).

  • In leads V2 and V3:
    • ST elevation ≥2 mm for men >40 years of age.
    • ST elevation ≥2.5 for men ≤40 years of age.
    • ST elevation ≥1.5 mm for women.


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ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MIshould replace the more familiar term STEMI — and, reviews the basics on how to predict the "culprit" artery.



ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria.