ECG Blog #509 — The Computer Says, "Acute MI"

A 35-year old man had a witnessed cardiac arrest in a hotel. 

• EMS was called — and bystander CPR was promptly started. 
• VFib (Ventricular Fibrillation) was documented on arrival by the paramedic team. DC countershock was delivered — with ROSC (Return Of Spontaneous Circulation) and return of the patient to full consciousness.
• The ECG in Figure-1 was obtained following ROSC.

QUESTION:

• How would you interpret the ECG in Figure-1?
• Should the cath lab be activated?

Figure-1: The initial ECG in today's case — obtained following ROSC from witnessed cardiac arrest. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Today's CASE:

The "good news" about today's case — is that this previously healthy 35-year old man had a witnessed cardiac arrest at a site where bystander CPR was immediately started — and timely defibrillation by emergency responders resulted in restoration of a normal rhythm with full recovery and intact neurological status.

• The post-ROSC ECG shown in Figure-1 shows sinus tachycardia at 115/minute with a narrow QRS complex rhythm.
• My "eye" was immediately drawn to leads V1,V2 (within the RED rectangle in Figure-2). The marked ST elevation in these leads, with downsloping ST segment into terminal T wave inversion — is diagnostic of a Brugada-1 ECG pattern (See Figure-3 below).
• ST segment straightening, with a somewhat limited amount of ST elevation is seen in neighboring lead V3 (hard to define the J-point in this lead for judging the amount of ST elevation). 
• The remainder of this ECG is nonspecific, and surprisingly unremarkable. Small, narrow (and probably insignificant) q waves are seen in the inferior leads. ST segment coving is seen in lead aVL — and minimal J-point depression with an upsloping ST segment is seen in leads V5,V6.

Impression of ECG #1: 

• Sinus tachycardia. 
• Brugada-1 ECG pattern in the anterior leads. (I suspect the ST segment straightening with some ST elevation that is seen in neighboring lead V3 reflects a continuation of the Brugada-1 pattern). 
• This is not the ECG of acute infarction! (Apart than leads V1,V2 that fit perfectly with the Brugada-1 pattern illustrated in Figure-3 — other leads are nonspecific and non-diagnostic for acute MI).
• This is not the ECG of RBBB! (Not only is the QRS not wide enough — but terminal S waves that are wide in lateral leads are missing — and especially because QRS morphology in leads V1,V2 is so typical for the Brugada-1 pattern illustrated in Figure-3).
• Given that today's patient is now fully alert (and that there is no history of chest pain) — there is no indication for immediate activation of the cath lab. Instead, the management plan for this patient who at this moment is completely stable — should include full investigation for potential precipitating factors of his arrest (including genetic testing and family history assessment).
• Bottom Line: Given the occurrence cardiac arrest in association with a Brugada-1 pattern on ECG — an ICD (Implantable Cardioverter-Defibrillator) will almost certainly be recomended.

Follow-Up of Today's CASE: 

• Today's patient turns out to be of southeast Asian descent. As noted in the ADDENDUM below (See Figure-6) — this geographic area of the world has by far, the highest prevalence of Brugada Syndrome. 
• Work-Up of today's patient was negative (including normal CT angiography and normal cardiac MRI).
• An ICD was implanted — and the patient was discharged in excellent condition.

Figure-2: The ST-T wave appearance in leads V1,V2 is diagnostic of a Brugada-1 ECG pattern.  

 

Figure-3: Review of ECG Patterns in Brugada Syndrome (adapted from Brugada et al — in JACC 72(9):1046-1059, 2018) — (A) Brugada-1 ECG pattern, showing coved ST-segment elevation ≥2 mm in ≥1 right precordial lead, followed by a negative T-wave. 
(B) Brugada-2 ECG pattern ( = the “Saddleback” pattern) — showing concave-up ST-segment elevation ≥0.5 mm (generally ≥2 mm) in ≥1 right precordial lead, followed by a positive T-wave.
(C) Additional criteria for diagnosis of a Brugada-2 ECG pattern (TOP: The ß-angle; BOTTOM: A Brugada-2 pattern is present if 5 mm down from the maximum R’ rise point — the base of the triangle formed is ≥4 mm — as this ensures a ß-angle ≥58°).
= = = = = = = = = = = =
NOTE #1: Traditionally there have be 3 ECG Brugada patterns described. Newer criteria sometimes "combine" Type-2 and Type-3 into a single "Saddleback" classification for simplicity (which is the classification I favor — and which I show in this Figure). ST-T wave morphology looks similar for Type-2 and Type-3 patterns — but Type-3 Brugada manifests less ST elevation than Type-2 ( = less than 2 mm of J-point elevation — and less than 1 mm of ST elevation).
KEY Point: A Brugada-2 (Saddleback) pattern may be suggestive — but by itself, it is not diagnostic of Brugada Syndrome.
= = = = = = = = = = = =
NOTE #2: A Brugada-1 pattern may either be observed spontaneously (with leads V1, V2 positioned normally — or — positioned 1 or 2 interspaces higher than usual) — or — a Brugada-1 pattern may be observed as a response to provocative drug testing (ie, after IV administration of a sodium-channel blocking agent such as ajmaline, flecainide or procainamide).
= = = = = = = = = = = =
NOTE #3: In the past, the diagnosis of Brugada Syndrome required not only the presence of a Brugada-1 ECG pattern — but also a history of sudden death, sustained VT, non-vasovagal syncope or a positive family history of sudden death at an early age. This definition was changed following an expert consensus panel in 2013 — such that the only thing needed at present to diagnose Brugada Syndrome is a spontaneous or induced Brugada-1 ECG pattern (without need for additional criteria as long as there is no reversible cause of the Brugada-1 ECG, as would be the case with Phenocopy [which we describe a little bit further below]).

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What about the QT Interval?

Take another LOOK at the QT interval in Figure-2.

• Is the QTc too short? 

ANSWER: Is the QTc too short?

Among the potential precipitating etiologies for cardiac arrest in a previously healthy man — is the Short QT Syndrome (SQTS).

• As discussed in the review by Rudic et al (Arrhythm Electrophysiol Rev 3(2):76-79, 2014) — SQTS is an inherited cardiac channelopathy determined by the presence of symptoms (syncope, cardiac arrest), positive family history, and the ECG finding of an abnormally short QTc interval.
• SQTS has only been recognized as a distinct clinical entity since 2000. The disorder is rare — but its importance is as a potential cause of atrial and ventricular arrhythmias, including cardiac arrest. Treatment is by ICD.

NOTE #1: As implied by its name, identification of SQTS depends on finding a short QTc interval — which at times is easier said than done. This is especially true in a symptomatic patient when the heart rate in available ECGs is rapid — because formulas for estimating the QTc (QT interval corrected for rate) are less accurate when the rate is fast.

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What are minimum norms for the QTc?

• Males with a QTc ≤330 msec. (and females with a QTc ≤340 msec.) — are defined as having SQTS, even if they are asymptomatic.
• Males with a QTc ≤360 msec. (and females with a QTc ≤370 msec.) — are said to have a “short” QTc. Such patients may have SQTS if, in addition to the “short” QTc there is a history of cardiac arrest, unexplained syncope or atrial fibrillation at an early age.

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What is the QTc in Today's Case?

To facilitate estimation of the QTc interval at different heart rates — We've added a QTc Calculator in the menu of Tabs that can be found on the top of every page in this ECG Blog.

• In Figure-4 — I show the values instantly arrived at by our QTc Calculator once you plug in the heart rate (115/minute in today's case) — and once you add in the longest QT that you measure (which is 280 msec. in lead V5).
• As is typically seen — there is some variation in measurements by each of the 5 well-known and established formulas for QTc calculation (ie, Some of these formulas perform better at faster or slower heart rates). 
• Whereas in Figure-4 — None of the 5 formulas for QTc calculation come up with an estimated QTc ≤330 msec — both the Fridericia and Framingham methods come up with values below the <360 msec. cutoff for a QTc that is "short" (ie, 348 and 354 msec., respectively).
• Bottom Line: The QTc in today's case is shorter than usual — but is not short enough to qualify as SQTS (keeping in mind the range of QTc values calculated by the different methods — and, that accuracy by any method for QTc estimation is less precise as the heart rate becomes faster).
• P.S.: For discussion of a case of SQTS — Check out My Comment in the Sept 2, 2019 post in Dr. Smith's ECG Blog.

Figure-4: Estimation of the QTc in today's case. 
The GREEN arrow shows where to find my QTc Calculator in the TOP Menu of every page in this ECG Blog.
The lower RIGHT panel shows the values for ECG #1 (given the heart rate = 115/min. — and the measured QT = 280 msec.). Note the range for estimated QTc values (from 348 msec. to 388 msec.) — depending on which of the 5 most commonly used formulas is used.

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What then is Brugada Syndrome?

Full discussion of Brugada Syndrome is beyond the scope of this ECG Blog. Instead — I consider the basics regarding a number of selected concepts relevant to emergency providers.

• Among references I've used in my synthesis are: 
• El Sayed et al (StatPearls, 2023).
• Adytia & Sutanto (Current Prob Cardiol 49(6), 2024). 
• Batchvarov (Eur Cardiol 9(2):82-87, 2014). 
• Netsere et al (BMC Cardiovasc Dis 25, 638, 2025).  
• Nakano, Shimizu (JACC Asia 19:2(4):412-421, 2022).

First described in 1992 — the Brugada Syndrome is important to recognize because of an associated very high risk of sudden death in otherwise healthy young or middle-aged adults who in most cases have structurally normal hearts.

• The prevalence of Brugada Syndrome in the general population is ~1/2,000. The syndrome has become a leading cause of sudden death in young adults (under 40 years old).
• Brugada Syndrome is much more common in Southeast Asia compared to the rest of the world. When considering the possibility of this syndrome — demographics of the patient are important! (See Figure-6 in the Addendum below).
• Although the genetics of Brugada Syndrome are complicated — the gender of the patient is also important. There is a distinct male predominance to this syndrome.

Personal Reflection: I never learned about Brugada Syndrome in medical school (the syndrome had not yet been described). But especially in recent years, in which I've closely followed numerous international ECG internet forums — I've seen countless examples of the Brugada ECG patterns shown above in Figure-3.

• Clinical Irony: Once a medical entity is "discovered" — it begins to get noticed with increasing frequency (such that I always wonder how "common" it was before finally being recognized in the medical literature).

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What is PHENOCOPY? 

A number of conditions other than Brugada Syndrome may temporarily produce a Brugada-1 ECG pattern. A partial list includes the following:

• Certain drugs (antiarrhythmics; calcium channel blockers; ß-blockers; antianginals; psychotropic medications; alcohol; cocaine; other drugs).
• Acute febrile illness.
• Variations in autonomic tone.
• Hypothermia.
• Electrolyte imbalance (hypokalemia; hyperkalemia).
• Ischemia/infarction.
• Cardioversion/defibrillation.
• Bradycardia. 

 

KEY Point: Development of a Brugada-1 or Brugada-2 ECG pattern as a result of one or more of the above factors — with resolution of this Brugada ECG pattern after correction of the precipitating factor(s) — is known as Brugada Phenocopy.

• By far, the most common clinical situations I've encountered that are prone to induce Brugada Phenocopy are acute febrile illness and hyperkalemia (Acute ischemia, infarction and cardiac arrest are also common causes of Phenocopy — which is why it was important in today's case to make sure that the reason for this patient's Brugada-1 pattern was not underlying coronary disease).
• KEY Point: The importance of being aware of Phenocopy — is that correction of the underlying condition may result in resolution of the Brugada-1 ECG pattern — with usually an excellent longterm prognosis compared to patients with true Brugada Syndrome (ie, an ICD is unlikely to be needed — as it would be with true Brugada Syndrome).
• NOTE: To ensure a diagnosis of Brugada Phenocopy — the patient should have: i) A negative family history of sudden death; ii) Lack of a Brugada-1 ECG pattern in 1st-degree relatives; iii) No history of syncope, serous arrhythmias, seizures or nocturnal agonal respiration; and, iv) A negative sodium channel-blocker challenge test.
• P.S.: For more on Brugada Phenocopy with links to clinical case examples — Please scroll down to the bottom of the page for My Comment in the January 13, 2025 post in Dr. Smith's ECG Blog.

 

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Regarding the Need for Genetic Study: 

The reason for genetic study of patients suspected of having Brugada Syndrome — is the finding that certain gene mutations (the most common of which is the SCN5A gene) — may be responsible for altering transmembrane ion flow in a way that predisposes to malignant cardiac arrhythmias. This is in contrast to Phenocopy — in which there is no congenital abnormality — but instead a triggering condition (ie, fever, hyperkalemia) that if successfully treated, usually results in resolution of the Brugada-like ECG pattern without longterm predisposure to malignant ventricular arrhythmias.

• A positive genetic study in a patient with a Brugada-1 ECG pattern — makes the diagnosis of Brugada Syndrome!
• A negative genetic study however, does not rule out the possibility of Brugada Syndrome (since many patients do not have an identifiable gene pattern).

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Should an Athlete with a Type-2 Brugada Pattern play Sports? 

Clearly beyond the scope of this ECG Blog is the question of what to do when "routine" ECG screening of high school, college and/or professional athletes results in the incidental finding of a Brugada-2 (or Brugada-3) ECG pattern?

• Much (most) of the time — these highly conditioned, asymptomatic athletes can be allowed to safely participate in rigorous athletic activity — BUT — they should first be carefully assessed by clinicians experienced in the field to rule out increased risk. 
• Editorial Note: As primary care faculty responsible for interpreting the ECGs of 30+ medical providers — I was happy to send these occasional abnormal screening ECGs to my friendly cardiologists for their final decision.
• KEY Considerations: For clearance to actively participate in sports activities — the individual must be completely asymptomatic (ie, No syncope, presyncope, palpitations during exercise) — and have a negative family history. 
• Assessment Tools: Commonly used assessment tools may include provocative pharmacologic stress testing (to see if this induces a Brugada-1 pattern with exercise) — genetic testing — as well as testing to rule out underlying structural heart disease (consideration of Echo, cardiac MRI, etc.).

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Acknowledgment: My appreciation to Mubarak Al-Hatemi (from Doha, Qatar) for making me aware of this case and allowing me to use this tracing. 

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ADDENDUM (12/13/2025): Some extra material ...

 

 

Figure-5: 2-page Summary of the essentials of Brugada Syndrome (from my ECG-2014-ePub).

 

Figure-6: 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 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).

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.