How I Self-Diagnosed and Treated My Hypertrophic Cardiomyopathy

The skeptical cardiologist has been taking a beta-blocker, nebivolol, for the last seven years. Like all beta-blockers, nebivolol (brand name Bystolic), slows the heart rate and lowers the blood pressure, and can be used for cardiac rhythm problems (i.e. PVCs, PACs, VT, afib) and cardiomyopathies.

I put myself on the drug after diagnosing myself with a form of hypertrophic obstructive cardiomyopathy (HOCM) in 2015.

The treatment for exertional symptoms in patients with HOCM is typically a beta-blocker. Within a day of starting the nebivolol, I was able to run without chest pain or near-syncope.

Symptoms Developing During Exercise

I was about 2 years post extensive abdominal surgery for carcinoid tumors that were identified in my small intestine and was trying to get into better shape by running.

Shortly after starting the run I would notice a tightness in my anterior chest associated with a sensation that I was going to pass out

When I felt this sensation, if I continued running or even slowed down it would worsen to the point that I felt compelled to stop and sit down on the sidewalk in order to avoid the embarrassment of passing out.

What I experienced, feeling very faint, is termed near-syncope. If I had continued to worsen and lost consciousness I would have “passed out” and fallen to the ground and this would be termed syncope. The chest tightness on exertion is classic for angina, a symptom of severely blocked coronary arteries.

An Abnormal Echocardiogram Read As Normal

I knew that the major causes of exertional syncope are cardiac: aortic stenosis and hypertrophic obstructive cardiomyopathy (HOCM) being the most common.

I had experienced chest tightness without the near-syncope with exercise in 2012 but at that time a stress echocardiogram was performed on me and was read as normal.

The apparently normal echo interpretation meant that I didn’t have aortic stenosis which is much slower in onset and would likely not have been missed and/or developed in 3 years. The normal stress echo plus a subsequent coronary CT angiogram ruled out coronary artery blockages severe enough to cause my symptoms.

I went back and examined my echocardiogram in detail and noted that the basal portion of my ventricular septum bulged a little compared to the mid-portion. I reviewed the cardiac CT and this confirmed the basal septal thickening.

Echo view showing thickening of the base of the ventricular septum (white arrow). Whereas the basal septum measure 1.7 cm, the middle portion where standardized measurements are made is only 1.0 cm thick.

Neither the reader of the echocardiogram nor the reader of the cardiac CT made any note in their chart of the thickened area.

It is not uncommon for echocardiographic studies to be botched either by over or under diagnosis as I noted in an article entitled “Echocardiograms-Botched, Misread, or Overutilized.” You can read about my dad’s heart murmur and his botched echocardiogram here and read about the dangers of undergoing shoddy, mobile cardiovascular screenings including echos here and here,

Ultimately, I had another stress echocardiogram performed on me. This time I informed the sonographer performing the test to pay special attention to precisely measuring the mid and basal portions of the ventricular septum segments and to measure the development of obstruction within the left ventricle by Doppler immediately post-stress.

This stress echocardiogram confirmed the diagnosis of hypertrophic obstructive cardiomyopathy with severe obstruction developing with exercise. This, then, was the reason for my symptoms.

Continuous Wave Doppler recordings of the flow of blood out of my left ventricle showing marked obstruction (high gradient) post exercise. These kinds of recordings are not routinely made and have to be specified by the ordering doctor.

Research and a Paper

Ironically, I wrote a paper on hypertensive hypertrophic cardiomyopathy of the elderly in 1988, long before I had any signs or symptoms of the disease.

After diagnosing my specific form of cardiomyopathy, I spent a lot of my free hours researching the condition as it was clear that it was under-recognized in the general cardiology community.

Mild thickening or protrusion of the basal ventricular septum was identified in 1969 and initially termed a “sigmoid septum.” Initial studies suggested this was a benign finding related to hypertension and aging.

My research suggested otherwise and I decided to write an academic paper that would summarize the history of this entity, unify the diagnostic terminology, and make clinicians more aware of it.

After months and months of crawling through the peer review process with multiple revisions, it was finally published in 2017 in the journal, Echocardiography.

In my introduction, I give references for each of the 12 different terms that have been used in the imaging literature to describe this anatomic/echocardiographic finding.

Localized thickening of the basal portion of the ventricular septum has been identified by necropsy and imaging studies for decades, but there is no consensus on its significance and a remarkable lack of consistency in terminology. This anatomic finding has been termed:

  • localized hypertrophy of the upper portion of the ventricular septum
  • disproportionate ventricular septal hypertrophy,
  • disproportionate upper septal thickening (DUST)
  • sigmoid or sigmoid-shaped (interventricular) septum (typically felt to be benign)
  • localized septal hypertrophy,
  • basal ventricular septal hypertrophy
  • ventricular septal bulge
  • discrete upper septal thickening 
  • upper septal knuckle/discrete upper septal thickening,
  • basal septal hypertrophy
  • sigmoid (sic) hypertrophy of the ventricular septum, characterized by the knob-like prominence of its basal subaortic segment
  • isolated hypertrophy of the basal septum
  • isolated basal septal hypertrophy (sigmoid septum) in elderly people

Unfortunately, although my paper has been cited 8 times since then, it hasn’t had the earth-shattering (or at least echocardiographic earth-shattering) effects I had hoped for and I still see the diagnosis completely missed or given a benign-sounding name like “sigmoid septum.”

I’m still running and not collapsing. And I’m still reading echos and findings lots of previously undiagnosed basal septal hypertrophy.

Disproportionately Yours,



8 thoughts on “How I Self-Diagnosed and Treated My Hypertrophic Cardiomyopathy”

  1. I remember reading your paper on BSH and LVOTO, it was a great read, I was curious after reading your post if you were the patient in the paper?

    LVOTO from BSH seems to be exacerbated by exercise from SAM and MV leaflet obstruction, do you think BSH can be reversible in your case? I would guess based on your conscientiousness of managing HTN that this is not a case of HCM BSH but maybe genetic, I am speculating but do you know the cause of your BSH? I know you are against unnecessary testing but I was curious if you ever did a follow echo up to see if BSH resolved or lessened with the addition of the beta blocker (I wasn’t sure if it would have an impact like reduction of HTN on LVH)?

    Also I think you are short selling yourself, it appeared to me that Wiley had you listed as 9 citations! Woohoo

    • Christian,
      The case report in that paper that serves as a launching pad for the review of BSH looks remarkably like my case. The advantages of the author utilizing their own case is the ability to have all the information including precise symptoms and symptom response at hand.
      Your first question about reversibility is a great one and one I’ve pondered.I had planned on a follow up stress echo last year to look at the current situation but had to reschedule it. It is conceivable that with more aggressive BP control (perhaps enhanced by the beta-blocker BP independent effects) if the BSH was hypertension-related it might regress.
      I’m glad to be up to 9 citations. I’m most pleased to see that a European consensus document on post-mortem imaging of patients with sudden death cited me.
      Dr. P

  2. I always to do a couple simple valsalva challenges with these prominent sigmoid basal septums during the echo (ED Wigle influence).
    Shame on the reader for not at least describing the morphology.

    • Rick,
      Yes, the Valsalva is helpful when BSH is identified. I have one outstanding sonographer at my current facility who routinely recognizes BSH and performs CW Doppler with Valsalva to look for a provocable gradient. It should be the norm.
      Dr. P

  3. Nice job. I self-diagnosed chronic atrial fib. I didn’t want to take a strong blood thinner, so I take high dose omega-3 to keep my AA/EPA ratio between 1 and 3. This has been reported to prevent thrombus formation. I’ve had the a. fib. for many years and so far, so good!

  4. Thank you so much for sharing your own personal experience with this condition. When someone in the healthcare field shares their own health conditions rather than only experiences with patients, I believe it greatly adds to their credibility.


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