Monday, May 6, 2019

A Middle-Aged male with Chest Pain and an Unusual ECG

This ECG was sent from South Asia.




The patient presented with chest pain.

Here is the ECG:
What do you think?


I frankly did not know what to think.  Is it Brugada pattern?  Probably.  If it is STEMI, it would have to be RBBB with STEMI.  But in a very unusual pattern.

This physician thought it was an anterior MI and gave thrombolytics.

All troponins were negative.

No angiogram was done.


Followup ECG:

No Change
Absence of evolution is the best evidence against ischemia as the etiology.



This is probably an unusual Brugada pattern.



Here are some questions from readers:

Question. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chest pain for the ischemia and potential syncope for brugada. Could this be a coincidence that the patient was experiencing chest pain and upon ECG capture the atypical brugada pattern was found? 

Answer: History is insensitive and nonspecific.  It helps a little bit.  Only 5-18% of ED patients with chest pain have a myocardial infarction of any kind.  Only 1-5% have OMI.  Anyone with a baseline Brugada pattern ECG can have esophageal pain, or chest wall pain, and then be thought to be having an MI based upon a false positive ECG.


Question: This has reciprocal STD in inferior leads. How can this be 'Not MI' ? What about his pain ? Did it subside?
Answer: I don't know about the pain, but the ECG did not evolve at all. In all myocardial infarctions which manifest on the ECG, there is some evolution over time as the infarct progresses and completes, or reperfuses.


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Comment by KEN GRAUER, MD (5/7/2019):
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This case by Dr. Smith raises the question as to whether this patient’s tracing represents: iBrugada-1 ECG patterniiBrugada SyndromeiiiAcute Anterior STEMI (with or without RBBB)and/orivSome combination of these findings. The patient in question presented with new-onset chest pain — and was from South(east) Asia.
  • 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 have structurally normal hearts.
  • The fact that the patient in this case is from South(east) Asia is relevant! This is because of how much more common Brugada Syndrome is in Southeast Asia compared to the rest of the world (See Figure-1).
  • We are not told if this patient is male or female. This also is relevant — because of the male predominance of Brugada Syndrome. The syndrome displays autosomal dominant transmission (ie, potentially only 1 gene is needed for clinical expression — which means ~50% of children receive the gene from affected parents). Genetics are complicated … (ie, >160 mutations have been discovered in the SCN5A gene — but “penetration” varies, so not all persons with the gene have the syndrome). Bottom Line: Despite equal genetic transmission — the clinical phenotype is 8-10X more common in males (ie, much higher “penetrance” in males — perhaps due to different sodium channel properties).
Figure-1: 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).
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Distinction is made between 2 types of Brugada ECG patterns:
  • Brugada-1 ECG pattern — shows ≥2 mm coved ST elevation with sharp downslope plus T wave inversion in ≥2 anterior leads. This is not RBBB (TOP LEFT in Figure-2). This ECG pattern may be diagnostic of Brugada Syndrome IF seen in association with: ia history of cardiac arrest; polymorphic VT; or of non-vagal syncope; and/or iia positive family history of sudden death at an early age; and/or iiia similar ECG in relatives.
  • Brugada-2 ECG pattern — is not diagnostic of Brugada Syndrome unless the saddleback anterior ST elevation with positive T wave at some time later converts to a Brugada-1 tracing (TOP RIGHT in Figure-2).
CAVEAT: A Brugada-1 or Brugada-2 ECG pattern may be induced by a variety of factors. 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.
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.
  • In most cases — clinical implications of a transient Brugada ECG pattern that promptly resolves after the underlying condition is corrected are much less ominous than spontaneous occurrence of a Brugada-1 ECG pattern.
Figure-2: TOP: ECG Brugada-1 and Brugada-2 patterns (from Bayés de Luna et al: J. Electrocardiol 45:433-442, 2012). BOTTOM: The initial ECG in this case (See text).
=================
The ECG in this Case: It is completely understandable why the treating physician in this case was concerned enough about an acute anterior STEMI that he/she gave thrombolytics (Figure-2):
  • The ST-T wave appearance in lead V1 looks typical for a Brugada-ECG pattern — as there is substantial ST elevation (4mm), with slow descent of the ST segment from its the r’ peak (light BLUE line in lead V1).
  • The ST-T wave appearance in lead V3 resembles a Brugada-2 (saddlebackECG pattern — albeit the ß-angle (RED line in V3) is not quite wide enough from the r’ at 5 mm to qualify as a Brugada-2 pattern (the GREEN line base of the triangle in V3 is <3.5mm).
  • The ST-T wave appearance in lead V2 looks intermediate between what we see in leads V1 and V3. Descent from the r’ peak is rapid (YELLOW line in V2) — which is atypical for either a Brugada-1 or Brugada-2 ECG pattern.
  • There is an “elbow” of ST elevation in leads V2 and V3 (RED arrows in these leads) — which to me suggested anterior ST elevation in addition to the apparent Brugada-1 pattern seen in lead V1.
  • I thought the very sharp decline from the r’ peak in lead V2 suggested RBBB, especially with the presence of terminal S waves in leads I and V6.
  • Although the J-point in each of the 3 inferior leads appears depressed below the baseline — the duration of the depressed ST segment in these leads seemed much shorter to me than what is usually seen with reciprocal ST depression in association with an anterior stemi. Similarly, the duration of the elevated ST segment in lead aVL looked overly brief. This argued against acute MI.
BOTTOM LINE: I thought the ST-T wave pattern in lead V1 for the ECG in the BOTTOM of Figure-2 was clearly consistent with a Brugada-1 ECG pattern. But — one of the causes of Brugada Phenocopy is acute infarction — so I didn’t know how to distinguish between a preexisting Brugada-1 ECG pattern vs a Brugada ECG pattern developing as a result of acute ongoing anterior STEMI.
  • As per Dr. Smith — troponins were negative, and lack of ECG evolution in serial tracings argued against an acute ischemic etiology.
  • I would have favored cardiac catheterization prior to patient discharge.
  • I agree with Dr. Smith that the ECG in Figure-2 may simply be an unusual Brugada pattern. Then again, given the greatly increased prevalence of spontaneously-occurring Brugada-1 and Brugada-2 ECG patterns in the Southeast Asian population — this seemingly unusual ECG pattern may not be so “unusual” in that part of the world.
  • Finally — a detailed family history (for early sudden death) + a careful personal history (for syncope/presyncope; malignant arrhythmia) is in order. Almost regardless, the patient whose ECG is shown in Figure-2 merits EP referral for full evaluation and risk assessment.
====================
CLICK HERE — for more on assessment of Brugada ECG Patterns (my 29-minute ECG video on this topic)
  • Click on SHOW MORE below the video on the YouTube page — and you’ll see a linked Contents to all in the video.
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13 comments:

  1. Question. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chest pain for the ischemia and potential syncope for brugada. Could this be a coincidence that the patient was experiencing chest pain and upon ECG capture the atypical brugada pattern was found?

    Thank you! - a lowly paramedic

    ReplyDelete
    Replies
    1. History is insensitive and nonspecific. It helps a little bit. Only 5-18% of ED patients with chest pain have a myocardial infarction of any kind. Only 1-5% have OMI. Anyone with a baseline Brugada pattern ECG can have esophageal pain, or chest wall pain, and then be thought to be having an MI based upon a false positive ECG.

      Paramedics are not lowly!!

      Steve Smith

      Delete
    2. As per My Comment (above; added after you asked your question) — the fact that this patient is from Southeast Asia greatly increases the prevalence of having a preexisting Brugada ECG pattern. Added to this — we have to remember that acute ischemia may of itself precipitate appearance of a Brugada ECG pattern ( = Brugada Phenocopy) — such that sometimes (ie, in this case) — it is difficult to distinguish between Brugada ECG patterns vs an acute ischemic event (or both)!

      Delete
  2. This has reciprocal STD in inferior leads. How can this be 'Not MI' ? What about his pain ? Did it subside ?

    ReplyDelete
    Replies
    1. I don't know about the pain, but the ECG did not evolve at all. In all myocardial infarctions which manifest on the ECG, there is some evolution over time as the infarct progresses and completes, or reperfuses.

      Delete
    2. In addition to lack of evolution of this ECG — in my opinion, the VERY short duration of inferior lead ST depression (and of lead aVL ST elevation) just doesn’t look like the true reciprocal changes seen with acute anterior stemi (See My Comment above — added after you asked this question).

      Delete
  3. Hyperkalemia is a well known cause of acquired Brugada ECG pattern. Brugada syndrome is due to a congenitally defective sodium channel. Hyperkalemia can also disable the sodium channel causing acquired Brugada ECG pattern at times.
    K. Wang.

    ReplyDelete
    Replies
    1. Thanks for your comment K! I agree completely. I've added hyperkalemia, and have listed some other potential causes of Brugada Phenotype to my Caveat in My Comment above — :)

      Delete
  4. if u see same pt or pt in similar presentation what u will do , for thrombolysis or not ??

    ReplyDelete
    Replies
    1. I would not. I would do bedside ultrasound and serial ECGs and check troponins, then thrombolyse if more evidence emerged. It does not look like STEMI.

      Delete

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