Hypertrophic Cardiomyopathy with dehydration and chest pain

A middle-aged man with a history of HOCM presented with 24 hours of chest pain, still active.  He stated that he had been dehydrated for a day as well.  The pain was not at all severe, and localized to the left sternal border, without radiation.  The patient was in no distress and had normal vital signs.

Here is his presentation ECG:

What do you think?

I thought it just looked like HOCM.  But because there were the dramatic HOCM findings, I did not look closely enough.

We did a bedside ultrasound:

This shows very thick LV walls and VERY small LV chamber, with high ejection fraction but low stroke volume. 

My impression was that the patient was dehydrated, which can cause poor LV filling in HOCM, and that might result in chest pain and type 2 MI, with minimally elevated troponin.  So we ordered troponins:

The first troponin I returned at 30,000 ng/L!  This troponin is most consistent with acute coronary occlusion, or in this case, subacute occlusion (because the symptoms are so prolonged and the first troponin so high).

I went back to look at the first ECG, and found an old one to compare with:

Can you see anything?

How about if we put the inferior leads and aVL side-by-side:

You can see now that the T-wave in lead III is far larger in the presentation ECG.  In aVL, although the inverted T-wave is the same size in both, the QRS is far larger in the historical ECG.

Therefore, I thought that this must be an inferior OMI.  The 24 hours of pain and the very high initial troponin show that this is a subacute OMI.

I put this through the PMCardio Queen of Hearts AI model, and she did not see OMI. However, she does not have the advantage of seeing an old EKG.  She did say that the ejection fraction was less than 40%. I wonder if she can see low stroke volume, which this patient definitely had due to low chamber volume?

I asked the patient if he still had chest pain and he confirmed that he did. Therefore, Cath Lab activation was indicated. 

I activated the cath lab 88 minutes after ED arrival.  The patient was in the Cath Lab at approximately 114 minutes after arrival.  

Such a delay is not nearly as detrimental as it would be if the OMI was acute (as opposed to subacute).   Almost all of the damage is already done. 

A 100% distal circumflex occlusion was found, opened, and stented.

A formal echo later showed no wall motion abnormality.  EF was 72%.

Learning point:

When the ECG at baseline is very abnormal, it can be very difficult to make an OMI diagnosis on the ECG. One must scrutinize the ECG, even more closely, and always find an old one to compare with.  Fortunately, my Miss, in this case, did not result in more myocardial damage, because it was such a prolonged myocardial infarction. Moreover, we do not know what the ECG would've shown in the acute phase. 

Outcomes of acute myocardial infarction in patients with hypertrophic cardiomyopathy.

I could not find any data on troponin levels in acute myocardial infarction in hypertrophic cardiomyopathy.  But because there is so much more myocardial mass, one might expect that Peak troponins could be much higher. This would not necessarily translate into a worse outcome, however, because there's so much myocardial mess to begin with.  This increased baseline, myocardial mass may explain why, in the above paper, they did not find worse mortality in patients with hypertrophic cardiomyopathy. 

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MY Comment, by KEN GRAUER, MD (6/7/2025):

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We've illustrated the difficulty of recognizing acute OMI in patients with marked LVH (Left Ventricular Hypertrophy) on a number of occasions (See My Comment at the bottom of the page in the February 6, 2020 post, among many others).

• Today's case is perhaps the most challenging that I have seen in regard to appreciating an acute OMI in the presence of marked LVH.

For clarity in Figure-1 — I've reproduced side-by-side the initial ECG and the prior ECG of today's patient.

• As per Dr. Smith — the patient in today's case is a middle-aged man with known HOCM (Hypertrophic Obstructive CardioMyopathy) — who presented with ongoing severe CP (Chest Pain) for the previous 24 hours. 
• ECG #1 ( = the initial ECG in today's case = TOP tracing in Figure-1) shows obvious marked LVH, with greatly increased R waves in all lateral leads and very deep S waves in leads V1,V2.
• In addition — ECG #1 shows deep, symmetric T wave inversion in multiple leads, as well as marked J-point ST depression (WHITE arrows) in virtually all leads manifesting increased R wave amplitude. But this patient has known HOCM — so the above remarkable findings could be completely appropriate for a nonischemic ECG in a patient with HOCM (See my discussion below Figure-1).

In the absence of a prior tracing for comparison — I examined today's initial ECG knowing that none of the above findings were necessarily diagnostic of acute OMI given the known diagnosis of HOCM.

• PEARL: In cases such as this, in which no definite abnormality is seen in most of the 12 leads — I look for 1 or 2 leads that I know look abnormal. Doing so — my "eye" was drawn to the ST-T wave in lead III (within the RED rectangle) — which I thought clearly manifested a "bulkier"-than-expected T wave, given tiny amplitude of the QRS in this lead.
• NOTE: I did not initially think that lead aVL was diagnostic of acute OMI. It was only after I recognized the above definite abnormality in lead III — that I thought the ST-T inversion in lead aVL was more-marked-than-expected given modest amplitude of the R wave in this lead.
• Acknowledgment: I was not at all certain of the diagnosis of acute OMI based on my initial impression of ECG #1, because only 2/12 leads showed changes suggesting acute OMI. But given the history — I thought ECG #1 was clearly suspicious of a hyperacute inferior lead T wave, with reciprocal changes in lead aVL.
• As per Dr. Smith's discussion above — finding a prior ECG on today's patient confirmed the diagnosis of acute OMI, proven and treated by timely cardiac cath.

Figure-1: Comparison of today's initial ECG — with a prior ECG on this patient.

As review — I've excerpted the following from My Comment in the October 28, 2023 post of Dr. Smith's ECG Blog:

ECG Findings in HCM — vs Echo?

The question of what ECG findings to look for when in search of HCM arises often. HCM is estimated to occur in ~1 in 500 young adults, making it among the most common inherited cardiac disorders. It is the most common underlying cause of sudden cardiac death (SCD) in asymptomatic young individuals — which raises the question of whether to screen those involved in regular (high performance) athletic activity? If so — WHO to screen? College and professional athletes? High school athletes? Others?

• Echocardiography is diagnostic. With formal echo — accurate measurement of septal and chamber size can be obtained and followed on a serial basis. Echo also helps 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 obstructive forms of HCM.
• Obtaining formal Echo is expensive. It's easier and cheaper to do screening ECGs in athletic individuals — reserving Echo for when ECG reveals any findings potentially suggestive of HCM.

Most patients with HCM do not have a normal ECG. Among the many ECG findings that may be seen in patients with 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 (especially AFib). 
• 
  
• The Problem: None of the above ECG findings are specific for HCM. It is also interesting (if not confusing) — how much of a variety one may see on the ECG of a patient with HCM (ie, While QRS amplitude and ST-T wave findings of LV "strain" are marked on today's ECG — large septal Q waves are no where to be found).

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NOTE: For readers interested in treatment recommendations for HCM — this October 28, 2023 post adds information on this subject.

• For more on distinction between the apical form of HCM vs other HCM forms — See My Comment in the December 26, 2023 post.