Continuous prolonged generalized weakness, lightheadedness, and presyncope. What might you suspect from the ECG?

A young man presented with continuous prolonged generalized weakness, lightheadedness, and presyncope.  There was some dyspnea but no chest pain.   

Here is his ECG.  

This shows LVH, with high voltage.

LVH can have very thick-walled ventricles and a correspondingly small LV cavity.  LVH is a common etiology of heart failure with preserved ejection fraction, as it may results in a stiff ventricle with poor diastolic relaxation.

See this articles: Heart Failure with Preserved Ejection Fraction (NEJM review)

One etiology of LVH on the ECG is Hypertrophic Cardiolmyopathy (HOCM), and sometimes ECGs in patients with HOCM are specific for HOCM.  

But this ECG is NOT specific for HOCM.

However, it is atypical for LVH: most ECGs with LVH that manifest as precordial high voltage have deep S-waves in V1-V3.  This one has very early transition: the only lead with a deep S-wave is lead V1.

See Ken's excellent tutorial on the ECG in HOCM below.

Case continued

We did a chart review and, indeed, this patient had known HOCM and an implanted ICD.  It was present during sinus rhythm with normal heart rate; therefore, the ICD not interrogated.

We did a bedside echo (original quality was not so good, and this is moreover an iPhone video of the screen -- but it is good enough):

Notice how small the LV cavity is.  It is only a slit.  This is because of the large LV myocardial mass due to HOCM.  There is very little filling, and thus very poor stroke volume.  

The heart rate is too fast for this poor filling. 

Preload must be increased and the heart rate slowed in order to allow more LV filling.

Further ultrasound showed no B-lines (no pulmonary edema).  

These patients are often on beta blockers to prevent such a scenario.  So we looked into the chart and this patient was indeed prescribed a beta blocker, and also verapamil.  He stated he had stopped taking them.

We gave him IV fluids and metoprolol, and his pulse normalized, after which he felt completely well.

See this even more interesting and more dramatic and fascinating case:

History of Hypertrophic Cardiomyopathy (HOCM), with Tachycardia and High Lactate

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My Comment by KEN GRAUER, MD (10/28/2023):

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QUESTION: 

For clarity in Figure-1 — I've reproduced today's ECG without the long lead rhythm strip. 

• Can you diagnose HCM (Hypertrophic CardioMyopathy) from today's ECG?  

Figure-1: The ECG in today's case. 

ANSWER: 

The answer is NO. We can not diagnose HCM solely from the ECG in Figure-1:

• All we can say about the ECG in Figure-1 — is that the rhythm is sinus with a normal axis (about +45 degrees), and essentially normal intervals (perhaps a borderline QTc given the heart rate).
• Small and narrow q waves are seen in lateral leads I and aVL.
• The zone of transition in the chest leads occurs normally between leads V2-to-V4 — but as per Dr. Smith, R wave amplitude abruptly increases to a 20 mm R wave already by lead V3!
• Overall QRS amplitude is dramatically increased (even for a young adult) — easily satisfying voltage criteria for LVH (Left Ventricular Hypertrophy).
• There is ST-T wave depression consistent with LV "strain" in no less than 8/12 leads! In addition — the tall ST-T wave in lead V1 is also a manifestation of LV "strain" in an anterior lead with a very deep S wave (that measures 28 mm in V1!).
• The only reason we don't see LV "strain" in lead V2 — is that this is a "transition lead" that separates lead V1 with a huge S wave (and large upright T wave) — from lead V3 which has a very tall R wave (and marked ST-T wave depression).

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).

Regarding Today's Patient:

The bedside echo performed by Dr. Smith in today's case is truly impressive! As per Dr. Smith — the LV cavity is tiny! As compensation for greatly reduced LV filling — heart rate increases, which perpetuates the vicious cycle of further reducing the time for LV filling. No wonder today's patient presented with symptoms of dizziness and weakness (ie, essentially presyncope).

• The diagnosis of severe HCM, presumably with a significant obstructive component is obvious from the above bedside Echo. 
• The clinical severity of many cases along the large "spectrum" of HCM disorders may not be nearly as easy to evaluate without a more formal Echo study.
• 
  
• As per Dr. Smith — Today's patient may clearly benefit from the rate-slowing and negative inotropic effect of the beta-blocker he was prescribed, but stopped taking.
• That said — Given severity of this patient's presenting symptoms and the extreme reduction in LV cavity size (with presumed obstruction in systole) — I suspect additional measures will soon be needed.

Recommended Treatment Measures for HCM:

In Figures-2, -3 and -4 below — I've reproduced the concise review by Jacoby et al on management measures for HCM (ACC.23/WCC — 2/21/2020).

• In addition to beta-blocker therapy — Verapamil (sometimes combined with a beta-blocker) may be helpful.
• The presyncopal symptoms of today's patient are potentially life-threatening, given the severity of his HCM. Referral to a center with special interest and expertise in the management of this complex and potentially life-threatening disorder is probably advised at this point.
• Unless there is a dramatic response to being put back on beta-blocker therapy — consideration of Septal Reduction Therapy (SRT), in the form of either surgical myomectomy or alcohol septal ablation, performed at a center with experience in this area may soon be needed. 

Figure-2: Part 1 — from the Review of HCM Treatment by Jacoby et al (ACC.23/WCC — 2/21/2020).

Figure-3: Part 2 — from the Review of HCM Treatment by Jacoby et al (ACC.23/WCC — 2/21/2020).

Figure-4: Part 3 — from the Review of HCM Treatment by Jacoby et al (ACC.23/WCC — 2/21/2020).