EXTRA COPY — Epigastric Pain — EXTRA COPY

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

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Figure-2: I've labeled today's ECG.

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DeWinter T Waves:

In 2008 — Robert J. deWinter and colleagues (Drs. Verouden, Wellens, and Wilde) submitted a Letter to the Editor to the New England Journal of Medicine (N Engl J Med 359:2071-2073, 2008) — in which they described a “new ECG pattern” without ST elevation that signifies acute occlusion of the proximal LAD (Left Anterior Descending) coronary artery.

• The authors recognized this pattern in 30 of 1532 (~2%) patients with acute anterior MI. Cardiac cath confirmed LAD occlusion in all cases — with ~50% of patients having a "wraparound" LAD. Left mainstem occlusion was not present.
• This was the authors’ original description of the new ECG pattern: “Instead of the signature ST-segment elevation — the ST segment showed 1-3 mm of upsloping ST depression at the J point in leads V1-to-V6 — that continued into tall, positive symmetrical T waves”.
• The QRS complex was usually not widened (or no more than minimally widened).
• Most patients also manifested 1-2 mm of ST elevation in lead aVR.
• NOTE: I’ve adapted Figure-2 from the original de Winter manuscript, published in this 2008 NEJM citation.

 

Figure-2: The de Winter T Wave Pattern, as first described by Robbert J. de Winter et al in N Engl J Med 359:2071-2073, 2008. ECGs for the 8 patients shown here were obtained between 26 and 141 minutes after the onset of symptoms. (See text).

In their original 2008 manuscript — de Winter et al went on to describe the following additional features:

• “Although tall, symmetrical T waves have been recognized as a transient early feature that changes into overt ST elevation in the precordial leads — in this group of patients, this new pattern was static, persisting from time of the 1st ECG until the pre-cath ECG.”
• Hyperkalemia was not a contributing factor to this ECG pattern (ie, Serum K+ levels on admission were normal for these patients).  

 

NOTE: Technically speaking — the de Winter T wave pattern as described in 2008 by de Winter et al differs from the finding of simple “hyperacute” anterior T waves — because ECG findings with a strict de Winter T wave pattern persist for an hour or more until the “culprit” LAD vessel has been reperfused. 

• As I note above (and as illustrated in the example ECGs taken from the de Winter manuscript that are shown in Figure-2) — there should be involvement in all 6 chest leads with the strict de Winter pattern, with most leads showing several mm of upsloping J-point ST depression and giant T waves.

MY Observations regarding De Winter T Waves: 

Over the past decade — I have observed literally hundreds of cases in numerous international ECG-internet Forums of deWinter-like T waves in patients with new cardiac symptoms.

• Many (most) of these cases do not fit strict definition of “de Winter T waves” — in that fewer than all 6 chest leads may be involved — J-point ST depression is often minimal (if present at all) in many of the chest leads — and, giant T waves are limited.
• ECG changes in many of these cases are not “static” until reperfusion, as was initially reported in 2008 by de Winter et al. Nevertheless, cath follow-up routinely confirms LAD occlusion.
• 
  
• MY "Take": I believe there is a spectrum of ECG findings, that in the setting of new-onset cardiac symptoms is predictive of acute LAD occlusion as the cause. What will be seen on the ECG depends greatly on when during the process the ECG was obtained. While many of these patients do not manifest “true de Winter T waves” (because their ECG pattern does not remain static until reperfusion by coronary angioplasty) — for the practical purpose of promptly recognizing acute OMI — I don’t feel ( = my opinion) that it matters whether a “true” de Winter T wave pattern vs simple “hyperacute” T waves (that are deWinter-like) is present.

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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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ADDENDUM (345/XXX/2026): 

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—  —

TODAY’s ECG Media PEARL #1 (3:00 minutes Audio): — relates to the phenomenon of deWinter-like T waves.

Nirdosh Rassani

Nirdosh sent me an email on 5/13/2024

Dr. Nirdosh Ashok Kumar, MBBS, MRCEM

Chief Resident, Emergency Medicine

24/7 Emergency & Acute Care

Mobile. +92 332 7468542

—  — Epigastric Pain and this ECG —  — 

                                    

The Aga Khan University Hospital
Stadium Road, P.O.Box 3500, Karachi 74800, Pakistan

 

THE CASE (5/13/2024):

Dear Dr. Ken — I hope you are doing well. I want to discuss an EKG of a young male who presented to ED with epigastric pain.

History: 37-year-old male with previous 2 PCIs in 2020-2021, non-compliant to meds for last 10 days. He presented to ED with severe pain in the epigastrium, not responding to any medications.
On arrival, he was vitally stable

 

Cardiology was rushed with the suspicion of OMI, Fellow wasn't convinced about OMI.
To me, it's obvious anterolateral OMI with obvious Hyperacute T waves in anterolateral leads.
What do you think about it?  — Thanks

MY REPLY:

Hello Nirdosh.

 

In a patient with KNOWN CAD ( = 2 PCIs in the past) and new symptoms (even though not chest pain — this is “severe epigastric pain” so HAS to be taken as a “chest pain equivalent symptom” !!! — this ECG HAS TO BE interpreted as deWinter T waves suggestive of acute proximal LAD OMI until proven otherwise. Prompt cath is clearly indicated!

• It would of course help to see a prior ECG (to prove to that cardiologist fellow that this is new) — but hard to conceive that this amount of huge T waves (and actually STEMI criteria ARE met by 2 mm of ST elevation in V4,V5!).
• The limb leads prove beyond doubt that this is acute (ie, ST elevation in aVL; hyperacute T in lead I — and clearly abnormal ST flattening in leads III & aVF = reciprocal depression.

 

I’d love to use this as an ECG Blog if you can get follow-up on this case. It is an important case — since in my opinion, there is no way that the Cardiology Fellow should have decided not to do prompt cath …

 

I would be happy to acknowledge you OR I could make this submission anonymous.

Hope the above is helpful. Just let me know. — Take care. — Ken

 

NIRDOSH REPLY:

Dear Dr. Ken — Thank you for the prompt response. Yeah, you can use this ECG for your blog, and you can use my name. The patient was rushed to the cath lab later on due to unresolved pain and low EF on focused bedside echo, CAG showed 90% occluded LAD. PCi was done and the patient is doing well now. — Regards

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ECG Blog #341

https://ecg-interpretation.blogspot.com/2022/10/ecg-blog-341-why-are-t-waves-peaked_29.html 

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ECG Blog #183

https://ecg-interpretation.blogspot.com/2021/01/ecg-blog-183-repolarization-variant.html

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NOTE: SEE BELOW for today’s ECG Media Pearl — which is an audio message relating to the phenomenon of deWinter-like T waves.

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The patient whose ECG is shown in Figure-1 is a middle-aged man who presented to the ED with new-onset chest pain.

Which 2 of the following 5 choices are most correct?

• Extra Credit: WHY are the remaining 3 choices either less correct or wrong?

 

CHOICES to Consider:

• Choice A: The T waves in anterior leads may reflect a repolarization variant.
• Choice B: The anterior T waves and inferior ST-T waves suggest possible ischemia.
• Choice C: The cath lab should be immediately activated with an “OMI alert”.
• Choice D: The “classical” deWinter T wave pattern is present in the anterior leads. 
• Choice E: Although a “classical” deWinter T wave pattern is not seen in ECG #1 — clinical implications are essential the same as if one was present.

Figure-1: ECG obtained from a middle-aged man with new chest pain (See text).

MY THOUGHTS on ECG #1:

As always — it BEST to begin by systematic assessment of the ECG in question before moving on to clinical implications.

• NOTE: It could be easy to overlook that the rhythm in ECG #1 is not regular if one didn’t start by reviewing the long lead II rhythm strip at the bottom of the tracing. The mechanism of the rhythm is sinus — and all QRS complexes are preceded by similar-looking P waves with a constant PR interval. Variation in the R-R interval during the first half of the tracing is consistent with sinus arrhythmia — which then regularizes to normal sinus rhythm at ~80-85/minute toward the end of the rhythm strip.
• All intervals (PR, QRS, QTc) and the axis are normal. There is no chamber enlargement.

 

Regarding Q-R-S-T Changes:

• There are no Q waves.
• The R wave in anterior leads V1, V2, V3 is a bit slow to develop until transition occurs between V3-to-V4 (but there are no anterior Q waves or QS complexes).
• The most remarkable finding is the presence of hyperacute T waves that are seen in leads V2, V3 and V4. This is most marked in lead V3 (especially given relatively small S wave amplitude in this lead) — albeit there is no ST elevation in this lead. T waves in these 3 chest leads are clearly taller-than-they-should-be and overly “voluminous” (ie, fatter-at-their-peak and wider-at-their-base than would be expected given QRS amplitude in each respective lead).
• There is slight ST elevation in leads V1 and V2. 
• Of note — there is subtle-but-definite J-point ST depression in leads V4, V5 and V6.
• There is some ST segment scooping, with slight depression in the inferior leads (including terminal T wave positivity after the ST-T depression).

 

Clinical IMPRESSION of ECG #1: This is not a repolarization variant (Choice A). Much more than “possible ischemia” (Choice B) — there are definite ECG abnormalities on this tracing in this patient with new-onsetchest pain. Given this history — ECG #1 should be interpreted as acute proximal LAD OMI (Occlusion-based MI) until proven otherwise — and the cath lab should be immediately activated (Choice C).

• PEARL #1: There are a number of findings in ECG #1 that suggest LAD occlusion is at a proximal location in this vessel. These include: i) ST elevation begins as early as in lead V1 — with hyperacute T waves also beginning early (in lead V2); and, ii) Reciprocal ST-T wave changes are seen in the inferior leads. Proximal LAD occlusion is usually also associated with at least slight ST elevation in lead aVL — but that is not present here.
• PEARL #2: Did YOU notice the lack of R wave progression until lead V4? The presence of a tiny-but-real initial r wave in leads V1 and V2 suggests that the septum remains intact — but lack of any increase in R wave amplitude until lead V4 may be indication of ongoing anterior infarction (ie, loss of anterior forces).

 

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NOTE: SEE BELOW for today’s ECG Media Pearl (#1) — which is an audio message relating to the phenomenon of deWinter-like T waves.

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Regarding Today’s Case: Comparing the chest lead ST-T wave appearance in ECG #1 with the 8 example tracings from the original de Winter et al manuscript shown in Figure-2 — ECG #1 is lacking in several features:

• Hyperacute T waves are not nearly as prominent in ECG #1 as in the 8 examples shown in Figure-2.
• The chest lead in ECG #1 that shows the most prominent T wave ( = lead V3) does not show any J-point ST depression.
• Only a single lead in ECG #1 shows both J-point ST depression and a hyperacute T wave ( = lead V4).
• BOTTOM LINE: ECG #1 does not satisfy criteria for a “STEMI” — because there is not enough ST elevation. It does not quite meet the original 2008 description for de Winter T waves. That said — it should still be obvious in this patient with new-onset chest pain that acute proximal LAD occlusion must be assumed until proven otherwise!

 

 The 2nd ECG in Today’s Case:

A follow-up ECG was obtained about 3 hours after ECG #1. For purposes of comparison — I have put this ECG #2 under the initial tracing in Figure-3.

• How would YOU describe the ECG changes that have occurred since the initial tracing?

 

Figure-3: Comparison of the initial ECG in today’s case — with the follow-up ECG done about 3 hours later (See text).

MY THOUGHTS on the Follow-Up Tracing:

ECG #2 shows that there has been extensive evolution during the 3 hours since the initial tracing was done:

• A significant Q wave is now seen in lead aVL of ECG #2, with suggestion of a tiny q wave in lead I. This is associated with loss of R wave amplitude (compared to ECG #1) in both of these high lateral leads.
• The poor R wave progression in leads V1, V2, and V3 persists — with loss of this initial r wave in lead V4 — leading to prominent Q waves in leads V4 and V5.
• There is now frank ST elevation in multiple leads, including leads I, aVL and V2-thru-V6.
• Inferior lead reciprocal changes of ST depression have deepened since ECG #1.
• Cardiac Cath was performed after ECG #2. It confirmed acute proximal LAD occlusion. Underlying multi-vessel disease (with ~50-60% stenoses) was present.

 

In CONCLUSION: Based on my experience over the past decade in commenting on hundreds of ECGs posted on various ECG internet forums — there are many “variants” of the original de Winter T wave pattern. 

• Often, there won’t be J-point ST depression in anterior leads that also manifest overly large positive T waves — and, “deWinter-like” T wave patterns such as the one in today’s case may not necessarily persist until coronary reperfusion is accomplished. 
• That said — despite not quite satisfying strict criteria for the de Winter T wave pattern described in the original 2008 NEJM manuscript — clinical implications of the findings in ECG #1 are essentially the same as if those strict criteria were present = acute proximal LAD occlusion until proven otherwise (Choice E).

 

EXTRA COPY- ECG Blog #525- Another Wide Tachycardia- EXTRA COPY

The ECG in Figure-1 was obtained from an older woman who presented with new-onset palpitations. She was hemodynamically stable in association with this tracing.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• How specific can you be with your interpretation?
• What is the treatment of choice? 

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

MY Thoughts on this Tracing:

The ECG in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at a rate of ~185/minute without clear sign of atrial activity.

• QRS morphology is consistent with LBBB conduction in the chest leads (ie, predominantly negative QRS in the anterior leads — with an all-positive QRS in lateral chest leads) — with an inferior frontal plane axis (as determined by the all-positive QRS in inferior leads — with an equiphasic QRS in lead I).

Impression:

The above description is virtually diagnostic of RVOT VT (Right Ventricular Outflow Track Ventricular Tachycardia).

• PEARL #1: Once you are familiar with the entity of RVOT VT — You should be able to make this diagnosis with high accuracy within seconds of seeing an ECG that looks like today’s tracing. 
• As we’ve shown on multiple posts on this ECG Blog — RVOT VT is one of the two most common forms of idiopathic VT (See ECG Blog #489 — Blog #346 — Blog #323 — among many others). This term “idiopathic” VT simply refers to the ~10% of patients who present with VT without underlying heart disease.

I review the KEY distinguishing points of the idiopathic VTs in the ADDENDUM to today’s post (See my summary info sheet in Figure-4 — and my 8-minute Audio Pearl below).

• Many (admittedly not all) of the idiopathic VTs are readily recognizable by their QRS morphology (described in Figure-4).
• Because the QRS complex in idioventricular VT is typically not overly wide — and because of the resemblance to QRS morphologic features of known conduction blocks (ie, RBBB + Hemiblock for fasicular VTs — and LBBB for outflow track VTs) — there is a tendency to misdiagnose the idiopathic VTs as some form of reentry SVT with aberrant conduction (instead of recognizing them as VT).

PEARL #2: One of the most helpful clues that a regular WCT without P waves is likely to be idiopathic VT (and not some form of reentry SVT with aberrant conduction) — is that there are subtle atypical features that are not consistent with any known form of conduction block. For example — in Figure-1:

• Although the predominant negativity of the QRS complex in leads V1,V2 is consistent with LBBB conduction — with typical LBBB, transition tends to occur later than what is seen in Figure-1 (ie, with simple LBBB — no more than a tiny r wave usually persists past lead V3 — and this R wave does not become predominant until at least lead V5). Instead, as we look at Figure-1 — the R wave is already enlarging in lead V3, and it is predominant in lead V4.
• With LBBB — septal depolarization moves right-to-left (instead of left-to-right) — followed by slow, progressive leftward depolarization of the left ventricle (that overwhelms electrical activity arising from the much smaller right ventricle). As a result — the QRS vector in left-sided leads V6 and in lead 1 manifest an all-positive widened R wave. The small, isoelectric QRS complex in lead I of Figure-1 should not be seen with LBBB (unless there has been prior infarction and/or extensive scarring or myocardial infiltration). The fact that this small isoelectric complex in lead I begins with a negative deflection — and the finding of an all negative QRS in high-lateral lead aVL are especially atypical for LBBB conduction.
• To Emphasize: It’s impossible from Figure-1 alone to be 100% certain that this ECG represents VT. But the findings of LBBB-like conduction in the chest leads with an inferior frontal plane axis are completely typical for RVOT VT — and — the atypical QRS morphology features described in this PEARL #2 strongly suggest VT until proven otherwise.

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The CASE Continues:

Today's patient was successfully cardioverted — but the WCT rhythm in Figure-1 returned. Lasting conversion to sinus rhythm was finally achieved after a 2nd cardioversion (as shown in Figure-2).

QUESTIONS:

• Does the ECG in Figure-2 solidify the diagnosis of VT for the initial ECG that was seen in Figure-1?
• What other interventions might have been considered?

Figure-2: The repeat ECG, recorded after the 2nd cardioversion.

My Thoughts:

The repeat ECG in Figure-2 shows restoration of a normal sinus rhythm (RED arrows in Figure-3 highlighting upright sinus P waves in the long lead II) — with the exception of a single early wide beat toward the end of the tracing ( = beat "X").

• PEARL #3: We know with 100% certainty from Figure-3 that beat X is a PVC (Premature Ventricular Contraction) and not an aberrantly conducted supraventricular beat — because underlying "on time" sinus P waves continue thoughout this long lead II rhythm strip (ie, The PINK arrow P wave shows continuation of these "on time" sinus P waves — and this can only happen if the wide beat originates "from below", since a supraventricular beat would have delayed the next sinus P wave).
• 
  
• PEARL #4: Note that QRS morphology in Figure-3 of the PVC is identical in simultaneously-recorded leads V4,V5,V6 (within the BLUE rectangle) — to QRS morphology in leads II,V4,V5,V6 during the WCT rhythm in ECG #1. This finding highlights the utility of the post-conversion ECG for retrospectively making a definitive diagnosis of the etiology of a WCT rhythm if one or more similar QRS morphology PVCs are seen.

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

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Final Thought: Regarding treatment of the WCT rhythm in ECG #1: 

• There is no single "correct" answer for how best to treat the regular WCT rhythm that today's patient presented with. And, the treatment path chosen in today's case was successful.
• Synchronized cardioversion is clearly the intervention of choice if there is any concern about hemodynamic stability in association with a WCT rhythm. Sometimes, "Ya just gotta be there" to judge when to go ahead with synchronized cardioversion.
• That said — today's patient was stable on presentation, so options are available. As noted below in Figure-4 — RVOT VT often responds to Adenosine, which could have been tried.
• Recurrence of the WCT after the 1st synchronized cardioversion in today's case was a signal that a longer-acting intervention (ie, perhaps IV Amiodarone) might be needed to maintain sinus rhythm, rather than repeat cardioversion.
• I do not have further follow-up as to whether or not this patient was referred for EP evaluation. 

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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/XXX/2026):

• Below — More on idiopathic VT:

Figure-4: Review of KEY features regarding Idiopathic VT (See text).

—  —

ECG Media PEARL #14 (8 minutes Audio) — What is Idiopathic VT? 

— WHY do we care? Special attention to the 2 most common forms 

= RVOT (Right Ventricular Outflow Track) VT and Fascicular VT. 

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EXTRA COPY — ECG Blog #524: A little bit of Jadwar — EXTRA COPY

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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:

Today's case proved satisfying by the complete recovery made by this patient who had ingested a potentially lethal dose of medicinal herb.

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Related Material:

• ECG Blog #231 — reviews the various types of VT terminology.
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• See Viskin et al (Circulation 144:823-839, 2021) — for an in-depth review of PMVT.