ECG Blog #412 — Is Cardiac Cath Indicated?

The ECG in Figure-1 was obtained from a middle-aged man with known hypertension — who presented to the ED (Emergency Department) for CP (Chest Pain) over the preceding 2-3 days.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• Should you activate the cath lab?  If not — What next? 

Figure-1: The initial ECG in today's case — obtained from a middle-aged man with CP for the past 2-3 days. To activate the cath lab?

The Initial ECG in Today’s CASE:

The rhythm in ECG #1 is sinus at 65-70/minute. Intervals (PR - QRS - QTc) are all within normal limits. The axis is slightly leftward (at about -10 degrees — as suggested by slight negativity of the small amplitude QRS in lead aVF — but not negative enough to qualify as LAHB, because the QRS in lead II is all positive).

• Voltage for LVH is easily satisfied in many leads (Very tall R wave in lead I — R in lead aVL ~20 mm [given overlap with the S wave in lead aVR] — deep S waves in V1,V2 + tall R waves in V5,V6 ≥35 mm). 
• For more regarding ECG criteria for LVH — See the ADDENDUM below and/or ECG Blog #73 and ECG Blog #245.

Regarding Q-R-S-T Changes:

• Q Waves — Tiny normal septal q waves in leads I,aVL.
• R Wave Progression — Normal R wave progression — with appropriate transition (where the R wave becomes taller than the S wave is deep) occurring between leads V3-to-V4.
• ST-T Wave Changes — There is ~1 mm of lateral J-point ST depression, with coving of ST segments and deep symmetric T wave inversion (seen in leads I,aVL; V4,5,6). There is 1-2 mm of ST elevation in leads III,aVF and V1 — with the T waves in leads III and aVF being disproportionately tall and "bulky" (with a mirror-image opposite appearance to the J-point depression and deep T wave inversion seen in lateral leads). 

MY Impression of ECG #1:

As a single tracing in a patient with 2-3 days of CP — this is a difficult ECG to interpret. My thoughts were as follows:

• The rhythm is sinus. Marked LVH is suggested by greatly increased QRS amplitude in multiple leads in this patient with longstanding hypertension (See Figure-3 in the ADDENDUM below for the ECG criteria for LVH that I favor).
• My written interpretation on a tracing such as this one would read, "Marked LVH and 'strain' and/or ischemia — with need for clinical correlation." 
• Pure LV "strain" tends to produce downsloping ST depression with asymmetric T inversion in ≥1 of the lateral leads (ie, leads I,aVL; V5,V6). Although it is not uncommon in patients with marked hypertension to see deep, symmetric T wave inversion in lateral leads — pure LV "strain" is generally not associated with ST coving, as is clearly seen in lead V4 of ECG #1 (See Figure-4 below in the ADDENDUM for the ECG picture of typical LV "strain" ).
• In addition — the ST elevation in leads III and aVF, in association with the hypervoluminous T waves in these leads — is not expected with pure LV "strain".
• On the other hand — the ST elevation seen in lead V1 is perfectly consistent with LVH and LV "strain" (ie, The shape of this ST-T wave in lead V1, in association with the deep S wave in this lead — is a mirror-image opposite picture of the typical expected appearance of LVH with "strain" in a lateral chest lead).
• 
  
• BOTTOM Line: Today's patient presented with a 2-3 day history of chest pain and the ECG shown in Figure-1. While this initial ECG is not diagnostic of an OMI (ie, of acute coronary Occlusion) — there are enough findings present in ECG #1 that are not expected with simple LVH and "strain", such that further evaluation is clearly indicated.

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The CASE Continues:

The first 2 high-sensitivity troponin values returned slightly elevated. A prior ECG from 9 years earlier was found. For ease of comparison — I have put this patient's baseline tracing and his initial ECG in today's case together in Figure-2.

• Does seeing this patient's "baseline" ECG change your interpretation of ECG-1?

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

Comparison of the 2 ECGs in Figure-2:

Availability of a prior tracing on today's patient confirms that all of the ST-T wave abnormalities described above for ECG #1 — are new compared to this patient's baseline tracing done 9 years earlier.

• Limb lead QRS amplitudes have greatly increased since the ECG baseline done 9 years earlier.
• Given the large amplitude of the QRS complex in lead V2 of ECG #2 — I found it hard to determine if overall chest lead amplitude was changed.
• There was no ST elevation and no hypervoluminous T waves in leads III and aVF of ECG #2 that was done 9 years earlier.
• There was no J-point depression — no ST segment coving — and no T wave inversion on the prior ECG.
• 
  
• BOTTOM LINE: ECG changes of LV "strain" and/or ischemia that we see on today's initial ECG — were not present 9 years earlier. That said — We have no idea when during this 9-year interim period these abnormal ST-T wave findings may have developed.

CASE Follow-Up:

In view of this patient's CP at the time he was seen in the ED — the 2 slightly elevated troponin values — and the abnormal ST-T wave findings on the initial ECG (with all of these ST-T wave changes being new since the baseline ECG done 9 years earlier) — Cardiac cath was performed.

• Cardiac cath showed normal coronary arteries.
• Cath pictures and the formal Echocardiogram indicated apical HCM (Hypertrophic CardioMyopathy) as the probable etiology of the abnormal ECG in Figure-1.

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COMMENT:

To emphasize —  Cardiac catheterization was completely appropriate in today's case — as today's patient presented with ongoing CP over the 2-3 days before he arrived in the ED — troponin was elevated (albeit modestly) — and his initial ECG did show ST-T wave changes that suggested "something more" than simple LVH (albeit not being overly suggestive of acute coronary occlusion).

• Taking another LOOK at today's initial ECG (and secure with the knowledge from cardiac catheterization that today's patient does not have an acute OMI [ = Occlusion-based MI] — but instead has apical HCM) — the ECG in Figure-1 is completely consistent with this diagnosis! 
• ST-T wave changes in Figure-1 are localized to lateral leads (ie, leads I,aVL; and V4,5,6) — especially in leads with increased QRS amplitude. In contrast — with LAD occlusion, there is usually at least modest associated ST elevation in lead aVL (and often also in lead I).
• There is no loss of R wave in anterior leads in Figure-1 (as opposed to poor R wave progression that is commonly seen with LAD OMI).
• The ST-T wave picture in lead V1 of Figure-1 is typical of LVH with "strain" (ie, It is the mirror-image opposite picture of what lateral chest leads typically show with marked LVH).
• Rather than Wellens' T waves — the most abnormal appearing chest lead ( = lead V4) is much more suggestive of a transitional (repolarization) change from the positive ST-T waves in leads V1,2,3 — "on the way" to ST coving and deep T wave inversion seen in the remaining chest leads. Like recognition of a face that you know, but have trouble describing in words — this appearance does not suggest OMI.
• 
  
• P.S.: An additional reason justifying prompt cardiac cath in today's case — is how different the initial ECG in Figure-1 looked compared to the "baseline" ECG on file. It would be interesting to see what an Echo from 9 years earlier looked like — but we do not know if such a study was previously done. It therefore appears that this patient's apical HCM continued to evolve over this 9 year period (rendering it impossible to be certain that ST-T wave abnormalities in Figure-1 were all attributable to apical HCM and not acute ischemia).

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About HCM (Different Forms of this Entity):

I've excerpted what appears below from My Comment in the December 26, 2023 post in Dr. Smith's ECG Blog.

HCM is an "umbrella term" applied to the presence of LVH in the absence of "abnormal cardiac loading conditions" (Hughes et al — JAHA 9:e015294, 2020). 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 HCM — reverse septal — neutral — and apical HCM (initially known as Yamaguchi Cardiomyopathy — and sometimes abbreviated as ApHCM ).

• Clinically — Overall management of the above 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. Although T wave inversion in ECG #1 is prominent — it is not quite deep enough to qualify as true "Giant" T waves (See ECG Blog #276 and ECG Blog #309).

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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.

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).
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• ECG Blog #209 — and ECG Blog #254 — Reviews a case of marked LVH that results in similar ST-T wave changes as may be seen with Wellens' Syndrome.
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• ECG Blog #245 — Reviews the ECG diagnosis of LVH.
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• ECG Blog #276 — and ECG Blog #309 — Reviews the entity of Giant T waves.

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• ECG Blog #73 — Reviews "My Take" on the ECG Diagnosis of LVH. 
• ECG Blog #92 — Presents another perspective for ECG Diagnosis of LVH.
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• The November 4, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews 3 ECG Clues for rapid recognition of erroneous lead V1,V2 placement. 
• The March 31, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) illustrates the potentially misleading effect the pre-hospital ECG may have in patients with LVH, by cutting off S wave voltage in the anterior leads. 
• The March 29, 2019 post in Dr. Smith's ECG Blog — My Comment regarding Tracing A (at the bottom of the page) illustrates how LVH is a common mimic of acute ischemia. 
• The December 27, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) illustrates a case with anterior ST elevation from LVH that may falsely suggest acute anterior infarction.

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ADDENDUM (1/13/2024):

I've added below in Figure-3 and Figure-4 additional material to facilitate ECG diagnosis of LVH and LV "strain".

 

—  —

ECG Media PEARL #59 (9:10 minutes Audio) — Reviews the ECG diagnosis of LVH (and its impact clinically with both chronic and acute cardiac disorders).

Figure-3: The voltage and other criteria I favor for ECG diagnosis of LVH (Please see ECG Blog #73 for additional details).

Figure-4: ST-T wave appearance of normal (A) — vs "strain" (C) or a strain "equivalent" pattern (B) — vs ischemia (D). (Please see ECG Blog #73 for additional details).