An elderly patient with stuttering chest pain. Don't jump to conclusions.

I was reading ECGs on the system and saw this one, and instantly knew the probable ECG diagnosis:

What do you think?

I went to the patient's chart:

Elderly woman with stuttering chest pain and SOB, and dizziness.

What do you think now?

This is a very typical ECG for Hypertrophic Cardiomyopathy. 

I sent it to our EKG Nerdz group and Jesse McLaren replied: "Apical HOCM"

It reminded me of many other cases I have seen, such as this one: Left Bundle Branch Block with Less Than 1 mm of Concordant ST Elevation (in the Setting of Hypertrophic Cardiomyopathy)

HOCM that mimicked LBBB with OMI (concordant STE in V5)

Case continued

So I went to the chart and this is what I found:

She indeed had a history of hypertrophic cardiomyopathy (HOCM).  

The first troponin was 52 ng/L (URL = 16 ng/L, so this is slightly elevated.  The most recent previous was 4 years prior, and was in the normal range)

Elderly patients, and patients with cardiomyopathy (including HOCM), may have troponin values in this range chronically ("chronic myocardial injury").  I suspected this was the case, and that in 4 years time she had developed some chronic injury.  She had serial troponins in the ED that remained constant.

Here is what The Queen of Hearts thought of this ECG:

The telegram version of Queen of Hearts only gives an output of OMI or Not OMI, with various confidence levels.  

The full PM Cardio app (see below) gives the full range of EKG diagnoses.

Explainability

Notice it is the wide, large R-wave which catches her attention and leads to the "Not OMI" diagnosis.

The full PM Cardio application, which is available in Europe but not in the U.S. (not yet FDA approved) gives other diagnoses.

Notice the PM Cardio app covers the whole gamut of diagnoses.  Interestingly, this time she gave a diagnosis of OMI with low confidence.  She sees the T-wave inversion and thinks it is a reperfused OMI. 

Version 1 has output of "OMI" whether she knows it is reperfused or actively occluded.

This will be fixed in Version 2, coming soon.

So she has a true negative on the Telegram app and a false positive on the PM Cardio app, both with low confidence.  Why?  Because this is a difficult ECG and she is on the fence, undecided.  

But we humans have more data at our fingertips.

We can use bedside echo:

Here is a Bedside Echo, short axis:

Severe hypertrophy

long axis

 

Again, severe hypertrophy

We can find previous ECGs:

Not much different

Here is an ECG 1 hour later

Not much different

Next AM before Angiogram

Not much different

Because of symptoms and elevated troponins, the patient had a next day angiogram.  It was normal.

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MY Comment, by KEN GRAUER, MD (12/26/2023):

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It's always rewarding to encounter an ECG that allows you to make an instant clinical pathophysiologic diagnosis. And so it is with today's tracing — that Dr. Smith instantly recognized as indicative of the apical form of HCM (Hypertrophic CardioMyopathy) — until proven otherwise. Among the ECG findings suggestive of this diagnosis include the following:

• Giant T waves (See the initial tracing in today's case that I've reproduced in Figure-1).
• The unique "shape" of the prominent ST-T wave abnormalities in this tracing — that are much more suggestive of some significant form of LVH (Left Ventricular Hypertophy) rather than ischemia.
• Voltage for LVH (the R wave in lead aVL easily surpassing 12 mm).
• Accompanying LAA (Left Atrial Abnormality) — in the form a widened, notched P wave in lead II (≥0.12 second in duration) — with a deep and wide negative component to the P wave in lead V1.
• An unusual form of QRS widening — that just does not look like LBBB.

Figure-1: I've labeled the initial ECG in today's case.

Taking a Closer Look:

• There is something unique about the "shape" of chest lead ST-T wave appearance. Unlike acute LAD OMI — the deep T wave inversion is localized primarily to all of the lateral leads (ie, leads I,aVL; and V4,5,6). Rather than Wellens' T waves — the prominent biphasic T wave in lead V3 is much more suggestive of a transitional/repolarization change "on the way" to the deep T wave inversion seen in the remaining chest leads. And the ST segment in leads V4,V5,V6 actually slants upward before becoming coved, on its way to that deep T wave inversion. Like recognition of a face that you know, but have trouble describing in words — this appearance does not suggest OMI.
• 
  
• Technically — the QRS does not measure to be "wide" (ie, Not >0.10 second in duration). But — the QRS "looks" like it is wide ... This is because the near vertical QRS complexes in each of the lateral leads would look "normal" if there was less space between the ascending and descending limbs of the R waves.
• PEARL: Among the causes of a widened QRS appearance are hemiblocks (LAHB, LPHB — each of which may widen the QRS by ~0.01 second) — and LVH (which usually does not widen the QRS by more than 0.01 second). A thicker left ventricle takes more time to traverse. And a much thicker LV may take even more time for the LV depolarization vector to traverse (as seems to be the reason for this lateral lead QRS appearance in today's case). 

But the KEY finding in ECG #1 that provides the immediate "tip off" to apical HCM — is the presence of “Giant” T wave inversion in leads V4 and V5.

• Although some T wave inversion is common in many conditions — the term “Giant" T waves is reserved for a select number of clinical entities that produce truly deep (ie, >5-10 mm amplitude) T wave inversion. Depth of the inverted T waves in leads V4 and V5 in Figure-1 attains this range. (For more on Giant T waves — See My Comment at the bottom of the page in the June 22, 2020 and September 19, 2022 posts in Dr. Smith's ECG Blog).
• 
  
• PEARL #1: Truly “giant” T waves are not overly common. When you see them — it is worthwhile to consider the diagnostic entities listed in Figure-2. When you are not provided with any history — it may be difficult to know WHICH of the entities in this list is most likely. Once you know the history — Simply consider these diagnostic possibilities!
• PEARL #2: In today's case — the 5 bullets I include at the beginning of my comment are the reason for instant suspicion of apical HCM until proven otherwise.

Figure-2: List of diagnostic entities to consider when giant T waves is seen.

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Types of HCM:

As per Hughes et al (JAHA 9:e015294, 2020) — HCM is an "umbrella term" applied to the presence of LVH in the absence of "abnormal cardiac loading conditions". These are often felt to be the result of autosomal dominant mutations in sarcomeric protein genes — and may present with a number of distinct LVH forms including the "classic" = asymmetric septal hypertrophy form (which is the type most commonly referred to when the abbreviation "HCM" is used) — concentric — reverse septal — neutral — and apical HCM (initially known as Yamaguchi Cardiomyopathy — and sometimes abbreviated as ApHCM ).

• Clinically — Overall management of these different morphological forms of HCM is similar for the emergency provider. That said — distinction between "classic" HCM vs the apical HCM form may be useful because: i) ECG findings tend to be different (Lyon et al — Europace 20:102-112iii, 2018); — ii) Echo appearance is different when hypertrophy localizes to the apex; and, iii) There is a significantly greater incidence of AFib with apical HCM.
• 
  
• Beyond the scope of this ECG Blog — specific formal Echo findings may help to sort through the large "spectrum" of HCM disorders — encompassing "lower risk" HCM (in those with modest or moderate hypertrophy — but without obstruction) — vs higher-risk obstructrive forms of HCM.

ECG Findings with HCM:

Most patients with HCM do not have a normal ECG. Among the many ECG findings that may be seen in patients with "classic" HCM are the following: 

• Increases in QRS amplitude.
• Large septal Q waves (Sometimes known as "dagger" Q waves — because these are deep but narrow Q waves seen in lateral leads). 
• Tall R wave in lead V1 and/or early transition in the chest leads (reflecting increased "septal" forces).
• Abnormal ST-T wave abnormalities.
• Conduction defects (ie, LBBB, IVCD).
• WPW
• Cardiac arrhythmias (including AFib). 
• 
  
• The Problem: None of the above ECG findings are specific for HCM. The variety of potential ECG findings with "classic" HCM is great — which poses problems when contemplating whether or not to use the ECG as a screening tool in athletes.

ECG Findings with Apical HCM:

Apical HCM makes up a minority of patients who qualify as having "HCM" (ie, less than 10% in the non-Asian population). 

• With the exception "dagger" Q waves (which are typically a result of a thickened septum) — any of the other ECG findings listed above for "classic" HCM may be seen with apical HCM.
• The ECG finding that is most characteristic of apical HCM is the presence of Giant T waves — as are seen in today's tracing.

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NOTE: For more on HCM, with a summarizing Table on the treatment approach to this group of disorders — Please check out My Comment in the October 28, 2023 post in Dr. Smith's ECG Blog.