Sunday, February 4, 2024

ECG Blog #415 — The Cath showed NO Occlusion!

Today’s patient is an older woman who experienced a number of fainting epiodes over the previous week. No CP (Chest Pain). Shortly after arrival in the ED (Emergency Department) — she suffered a cardiac arrest. The ECG in Figure-1 was obtained following successful resuscitation.
  • Stat Echo — obtained shortly after successful resuscitation revealed anterior wall akinesis.
  • BUT — Cardiac catheterization done a little later did not reveal any significant stenosis.

  • In view of the above history — How would YOU interpret the ECG in Figure-1?
  • How can you explain that no “culprit” artery was found on cardiac catheterization?
  • What is T-QRS-D? Is this ECG finding present in today’s initial ECG? 

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

MY Thoughts on Today’s CASE:
Fortunately — Today’s patient was successfully resuscitated following her cardiac arrest. Despite the absence of significant coronary stenosis on her post-arrest cath — the ECG in Figure-1 is clearly diagnostic of an extensive anterolateral STEMI (presumably from acute LAD [Left Anterior Descending] coronary artery occlusion).
  • The rhythm in ECG #1 is regular and supraventricular at a rate of ~75/minute. Although I do not clearly see sinus P waves in lead II (ie, only the 1st beat seems to have an upright P wave in lead II) — the QRS complex is narrow in all 12 leads, and a small, upright P wave with fixed PR interval is seen in lead V1 (RED arrows in Figure-2).
  • There is marked LAD (Left Axis Deviation) — with predominant negativity in lead II, consistent with LAHB (Left Anterior HemiBlock).
  • No chamber enlargement.

Regarding Q-R-S-T Changes:
  • Q Waves — A very small, but somewhat widened Q wave of uncertain significance is seen in lead aVL. Tiny-but-present initial R waves are seen in each of the inferior leads (consistent with LAHB — but not indicative of inferior infarction).
  • R Wave Progression — Although an initial R wave is seen in anterior leads V1,V2,V3 — there is loss of R wave amplitude between lead V1-to-V2.
  • ST-T Wave Changes — The most dramatic change is the marked ST elevation that begins in lead V2 — and which remains substantial throughout the rest of the precordial leads. T waves in the inferior leads look more-peaked-than-expected given QRS amplitude in these leads — and there is reciprocal ST-T wave depression in lead aVL.
  • There is T-QRS-D (Terminal QRS Distortion) in leads V4,V5,V6 (BLUE arrows in Figure-2as discussed in detail below).

As emphasized above — the post-arrest ECG in Figure-2 is clearly diagnostic of an extensive anterolateral STEMI.
  • As best we can tell from the history we are given — this patient had syncope but no CP prior to her acute event. As discussed in detail in ECG Blog #228 — this seemingly qualifies as a Silent MI (Approximately half of those MIs not accompanied by CP — have some other associated symptom such as syncope, which substitutes as a “chest pain equivalent”).
  • The fact that cardiac cath performed shortly after cardiopulmonary resuscitation failed to reveal any significant coronary stenosis (ie, No evidence of any “culprit” artery)qualifies today's case as MINOCA ( = MI with Non-Obstructive Coronary Arteries — which I discuss in detail below).

Figure-2: I've labeled sinus P waves in lead V1 — and T-QRS-D in leads V4,V5.

What is T-QRS-D?
The concept of Terminal QRS Distortion (T-QRS-Dwas unknown to me prior to becoming an Associate Editor in Dr. Smith's ECG Blog. Since then I've seen many clinical cases that validate this ECG finding promoted by Dr. Stephen Smith.
  • T-QRS-D — is defined as the absence of both a J-wave and an S-wave in lead V2and/or lead V3and/or lead V4 (T-QRS-D may be seen in leads other than V2,V3,V4 — but its clinical significance when T-QRS-D is only seen in other leads is less certain)
  • NOTE: T-QRS-D is simple to define. That said — this ECG finding may be subtle! I fully acknowledge that it has taken me some time to become comfortable and confident in its recognition.

  • Clinical Significance: When present — T-QRS-D may provide invaluable assistance for distinguishing between a repolarization variant vs acute OMI. When true T-QRS-D is present in a patient with new symptoms — it is virtually diagnostic of acute OMI ( = of an acute coronary Occlusion Myocardial Infarction).

A picture is worth 1,000 words. I illustrate the ECG finding of T-QRS-D below in Figure-3, which I've excerpted from My Comment in the November 14, 2019 post in Dr. Smith's ECG Blog. I’ve taken thlead V3 examples in Figure-3 from previous cases posted on Dr. Smith’s ECG Blog:
  • TOP in Figure-3 — Despite the marked ST elevation in this lead V3 — this is not T-QRS-D, because there is well-defined J-point notching (BLUE arrow). This patient had a repolarization variant as the reason for ST elevation.
  •  BOTTOM in Figure-3 — This is T-QRS-D, because in this V3 lead there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline to form an S wave).

Figure-3: Comparison between ST elevation in lead V3 due to a repolarization variant (TOP — from 4/27/2019— vs acute OMI (BOTTOM — from 9/20/2015), which manifests T-QRS-D (See text).

What is MINOCA? 
I suspect the entity known as MINOCA (MI with Non-Obstructive Coronary Arteries) — is not fully appreciated by many clinicians.

  • I was surprised to learn that an estimated 5-15% of patients (depending on the studied population) who are diagnosed with either STEMI or NSTEMI — turn out to have MINOCA, in which cardiac catheterization fails to reveal any infarct-related artery (ie, no "culprit" vessel with at least 50% stenosis) — and no clear systemic etiology is found to explain the patient's presentation to the hospital (Tamis-Holland et al: AHA Scientific Statement on MINOCA — Circulation 139:e891-e908, 2019 — Broncano et al — RadioGraphics 41:8-31, 2021 — and — Sykes et al — Interventional Card Review 16:e10, 2021).

I was therefore intrigued by today's case — in which an older woman presented with syncope and cardiac arrest (but no chest pain) — with the ECG shown in Figure-2 (as well as anterior wall akinesis on Echo) — but without any obstructive coronary disease on cardiac catheterization.
  • Because all emergency providers will periodically encounter MINOCA (ie, the 5-15% estimated incidence of MINOCA that I cite above in patients initially diagnosed as having a STEMI or NSTEMI) — I've added Figure-4, which summarizes the more common entities associated with MINOCA (This Figure previously published in My Comment in the November 30, 2022 post in Dr. Smith's ECG Blog).
  • An all-too-common misconception is that the absence of obstructive coronary disease on cardiac catheterization rules out acute coronary occlusion as the cause of the patient's acute event. This is not the caseNon-obstructive coronary disease at the time cardiac cath is done does not necessarily imply there was no plaque rupture with thrombus. This is because non-obstructive plaques can fissure, thrombose, totally (or near totally) occlude, have autolysis (spontaneous lysis of thrombus with reperfusion) — yet have less than 50% obstruction at angiography. 
  • Such plaques will often not be recognized as "culprits" — because no fissuring or ulceration is seen. As a result — determination of plaque disruption in such patients can only be diagnosed by use of intracoronary imaging — with either higher-resolution OCT (Optical Coherence Tomography) or IVUS (IntraVascular UltraSound).

  • KEY Clinical Point: Despite lack of obstructive coronary disease on cardiac catheterization — the most common cause of MINOCA is still probably an acute OMI that has spontaneously reperfused (but which is simply no longer evident by the time cardiac cath is performed).

Additional Points about MINOCA:
I found it surprising to learn that the initial description of acute MI despite normal coronary vessels is not a new concept — having been first described ~80 years ago (with eventual adoption of the term, "MINOCA" in 2013).
  • The 3 most common Causes of ACS (Acute Coronary Syndrome) without coronary disease are: i) Myocarditis (up to 1/3 of these patients); ii) Takotsubo cardiomyopathy; and, iii) MINOCA.
  • There is a trend toward these patients being younger — with a greater relative percentage of women — and fewer traditional cardiac risk factors.
  • Longterm prognosis of patients with MINOCA clearly depends on the underlying etiology. That said — it's important to appreciate that this entity is not benign, with similar mortality as for patients with obstructive coronary disease following their infarction.

  • Cardiac MRI — provides an answer to the etiology of patients with MINOCA in more than 2/3 of cases. 
  • Cardiac MRI successfully identifies ~80% of patients with acute myocarditis by picking up evidence of inflammation — with the distinct advantage of being noninvasive compared to endomyocardial biopsy.
  • Use of LGE (Late Gadolinium Enhancement) — is routinely recommended with cardiac MRI to increase diagnostic yield, as a means to identify fibrosis and other abnormalities in cardiac tissues.
  • Cardiac MRI (especially with the addition of LGE) provides insight to longterm prognosis of patients with MINOCA.

Figure-4: Classification of Underlying Diagnoses in Patients with MINOCA (Adapted from Table-1 in Sykes et al: Interventional Cardiology Review: 16:e10, 2021)

NOTE: As per Sykes et al — The entities listed under "Other Etiology" may be diagnosed following further investigation and should be considered separately (because they are typically associated with myocardial injury but not considered an MI by the 4th universal definition of MI). This is an important indication for cardiac MRI in patients suspected of MINOCA. 

KEY Clinical Point: 
Despite lack of obstructive coronary disease on cardiac catheterization — the most common cause of MINOCA is still probably an acute OMI that has spontaneously reperfused (but which is simply no longer evident by the time cardiac cath is performed).


Acknowledgment: My appreciation to Arlind Dragoshi (from Tirana, Albania) for the case and this tracing.



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
  • ECG Blog #183 — Reviews the concept of deWinter T-Waves (with reproduction of the illustrative Figure from the original deWinter NEJM manuscript).

  • ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 

  • ECG Blog #193 — Reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and — reviews the basics on how to predict the "culpritartery.
  • ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.

  • ECG Blog #228 — Reviews the concept of "Silent" MI.

  • ECG Blog #215 and ECG Blog #318 — Review of cases with T-QRS-D.

  • The November 14, 2019 post in Dr. Smith’s ECG Blog (Please scroll down to the BOTTOM of the page for My Comment and illustration of the phenomenon of T-QRS-D = Terminal QRS Distortion).
  • The November 15, 2023 post in Dr. Smith’s ECG Blog (See My Comment at the bottom of the page regarding MINOCA).

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