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Does This Seem Like HCM....my cardiologist says no, without adequate explanation


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  • Does This Seem Like HCM....my cardiologist says no, without adequate explanation

    So here is my situation…..I’ve long suffered from severe, chronic lightheadedness and palpitations. My symptoms got really bad in 2012 and once again in late 2017, and each time I had some cardiac testing done. In 2012 my two echos didn’t show much, although there was suspicion that there might be some slight diastolic dysfunction due to a prolonged mitral valve deceleration on the first echo (362ms) time and symmetrical borderline hypertrophy of my left ventricular posterior wall and septum on the second echo (1.1cm/1.1cm).
    A cardiac MRI in January of 2018 was either some sort of colossal test error, imaging mix-up, or else a snapshot of some unrelated acute myocarditis that I have since fought off, for it showed all four chambers dilated (LVEDD was 6.0cm with LVEDV of 200mL, for example) with heavy volume overload, and thinned out LV walls (the septum and LVPW were 0.5cm each), with bizarrely perfectly preserved systolic function…. all of which suddenly disappeared when an echo was taken in March 2018. They were either looking at the wrong heart, misread the images, or I had a brief, unrelated infection that caused acute DCM that since recovered. Whatever the case with that MRI the March echo is much more in line with the echo I had back in 2012.

    This most recent echo showed that I now have evidence of grade 2 diastolic dysfunction.
    1.) My early diastolic mitral annular lateral velocity was slowed (11.1 cm/s) (age norm is more in the 15-18 range)
    2.) My mitral deceleration time is still mildly prolonged (216ms…..age norm is usually 160-200)
    3.) My E/e’ ratio was >8 (Peak early filling: 90.6cm/s, lateral e’: 11.1cm/s, E/e’: 8.16 (<8 ensures relatively normal LVEDP)
    4.) There was a b-bump on the M-mode doppler mitral readings
    -5.) Previously borderline/high-normal LV wall thickness (1.1cm apiece) and LA diameter (3.8cm) have now both progressed to being solidly mildly abnormal. My IVS and LVPW measure 1.59/1.52cm at end diastole. My left atrium measures 4.5cm in diameter.

    While I do run 60-70 miles per week (generally jog around 6:50/mile pace, PR in the 5k in the low 17’s) I do not display the results of an “athlete’s heart.”
    1.) There would be concurrent dilation with the hypertrophy (athlete’s heart has dilation in response to the volume overload in training and hypertrophy from the pressure overload in training), but my LV diameter has shrunk proportionally with increasing thickness over time. I went from 4.9cm LVEDD/0.88cm thickness to 4.6cm LVEDD/1.1cm thickness to 4.15cm LVEDD/1.5cm thickness.
    2.) Athlete’s heart also has normal or enhanced diastolic functionality, whereas mine is impaired.
    3.) Athlete’s heart has a normal or only very mildly dilated left atrium, whereas mine is solidly enlarged.
    4.) Athlete’s heart almost never exceeds 1.3cm, and especially in a smaller framed person whose exercise is all aerobic (as opposed to a tall/large weight lifter or something) it almost never gets beyond 1.1cm, whereas I’m already at 1.5cm.

    My doctor is insistent that these lines of evidence indicate that we need to accept two premises: 1.) That something pathological is causing diastolic dysfunction 2.) That I do not have evidence of “athlete’s heart” despite my training. Based on those two premises the goal would be to find a medical cause for the diastolic dysfunction. He says he cannot figure out what it would be, since I do not have any of the things which could cause such (hypertension, diabetes, aortic stenosis, thyroid disease, or even rarer things such as sarcoidosis, amyloidosis, various muscular dystrophies, etc). I do sometimes seem to have hypertension, although I've never known how much of that is white coat, because sometimes my BP is like 145-150/85, but other times it's more just like 125/80, so I don't know. This last time in his office it was almost 150/90. I kind of wonder if this is actually due to hypertension. I remember that first cardologist from 2012 was pretty convinced I had hypertension despite being 21 at the time and a college athlete, but he didn't put me on a beta blocker since my heart rate was already so low (like 40's at rest). So, with everything that could cause diastolic dysfunction as a secondary result supposedly being ruled out it would seem I ought to be diagnosed with HCM, right? Well not so fast. He is furthermore insistent that it can’t be HCM. His lines of reasoning are as follows….

    1.) My hypertrophy is too mild to be HCM. Yet my research indicates that amongst those in my age bracket who definitely have HCM (i.e. tested positive for a known HCM mutation), 10-15% still have thickness of 15mm or less, and another 30% are in the 16-19mm range (I’m at like 15.9 and 15.2 septum/posterior wall to be exact).
    2.) My hypertrophy is too symmetrical. Yet, my research indicates hat while the 1.3:1 septumosterior wall ratio is the most common HCM presentation about 20% have concentric hypertrophy (others yet also have the apical form).
    3.) My LVOT gradient was normal (2.49mmHG peak, 1.3mmHg mean), suggesting no obstruction. Yet my research indicates 30% of HCM cases are non-obstructive and of the other 70% the obstruction is very transient, with average LVOT gradient variability in the course of hour long studies being around 45mmHg, and some patients ranging as much as 200 plus mmHg during the study.

    I tend to think that further investigation into whether or not I have HCM is very warranted.
    - I have a long history of symptoms, and those symptoms predate my current degree of hypertrophy.
    -I had lightheadedness and palpitations back when my walls were 0.88/0.82cm.
    - I had signs of grade 1 diastolic dysfunction at that time (MV DT of 362ms) at that time.
    -My walls have grown over time, now reaching the 1.5-1.6 range.
    -This is no viable alternative explanation for my hypertrophy nor the diastolic dysfunction
    -Growing up I was always relatively more easily short of breath than others (despite being an athlete), had waves of childhood chest pain, the palpitations, lightheadedness, etc
    -My current severe lightheadedness is greatly exacerbated by activities such as eating, showering, exercise, etc, all of which either reduce preload (via peripherial or splanchnic dilation) or increase contractility, both of which are said to provoke and exacerbated transient LVOT obstruction

    I feel like it matters whether or not I have HCM, because if it is HCM wouldn’t they want to put me on precautionary antiarrhythmic drugs, do an EP study (and perform ablation if necessary) or even consider the eventual move towards an ICD, especially given how active I am? Or maybe it doesn’t matter. I mean, if someone has HCM and their septum/walls are 1.5-1.6-ish and they have no history of NSVT, no family history, no fainting, etc do they basically just say, “stay hydrated and don’t push it too hard and we’ll keep an eye on it over time,” without providing any drugs and/or surgical treatments? If that’s the case then I guess it’s almost irrelevant to even pursue finding if it is or isn’t HCM.

    Right now the guy says he just wants to run a repeat echo in a year to see if anything got worse, but that I don't have HCM. He also seems to indicate that HCM or no HCM he doesn't feel my situation warrants any treatments or restrictions. He basically just told me to live my life. Should I feel confident in all this? I mean, based on what I've looked up, plugging my stats into those HCM risk calculators it says I wouldn't be a candidate for an ICD and that my sudden death risk is like barely 2%, so do I just go on and do whatever and hope I land in the 98%?
    Last edited by djd1990; 03-25-2018, 01:05 AM.

  • #2
    Hi djd,
    And welcome!

    You've asked a lot of questions. Perhaps the best thing would be for you to call the HCMA office and make an appointment to talk with them as a new patient. They can answer a lot of your questions, and make suggestions as to what you should be asking - and of whom.

    In the meanwhile, a comment or two.

    1. In general, antiarrhythmic drugs aren't used unless patients actually have arrhythmias. While they can be lifesavers, they have their problems too - in particular, many of them can also promote certain arrhythmias. So they're not used prophylactically.

    2. EP studies aren't informative with HCM patients. While you'll find some EPs who recommend them, a consensus statement by the leading associations of those treating heart patients (including the Heart Rhythm Society) agrees with this.

    3. Commonly, people are treated with beta blockers.

    4. There are a series of criteria used for recommending (or not) an ICD. The degree of activity isn't one of them. That said, recommendations are (in general) to be active but avoid certain kinds of activities.

    5. In general, alcohol septal ablations are not recommended for most of those who are obstructed. Myectomy, a surgical procedure, has a better success and safety record, and so ablations are recommended mainly for those who are poor surgical candidates (e.g., very old or infirm people). I know, it sounds more severe, but many of us have had great success with myectomies.

    6. We strongly recommend getting evaluated at one of the recognized Centers of Excellence for HCM. Even very good local cardiologists are typically not up to date on important details of diagnosing or treating HCM.

    So -- you can see that there's a lot to learn! Besides calling the HCMA, I'd strongly recommend purchasing the HCM book, available on this site.

    Myectomy on Feb. 5, 2007.


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