I forgot to mention I also have LV outflow tract gradient of 35 mm Hg, and Grade 2 diastolic LV dysfunction with normal LA pressure. Don't know if this is any help.
You need say no more. You have HCM based on what you have written on here. AND you have a strong family history of it. Concentric Hypertrophic Cardiomyopathy means that you have more than one wall affected which is a rarer form of the disease. HCM is generally genetic in nature, but can be sporadic. You need to see a doctor who deals with HCM patients. Cleveland Clinic, the Mayo Clinic, the NIH (National Institutes of Health in Maryland) the University of Michigan those are a few places who see patients with this disease. A BP of 130/whatever, is not high enough to cause your walls to thicken. Get yourself an appointment with a doctor who will take this seriously; it's a serious disease.
QUOTE: My mitral valve is elongated and I understand that this may be the reason for the MR.and the LAE. This is my question. Is concenteric left ventricular hypertrophy any indication that I may have HCM".
"I forgot to mention I also have LV outflow tract gradient of 35 mm Hg, and Grade 2 diastolic LV dysfunction with normal LA pressure. Don't know if this is any help"
The pressure your doctor may be refering to is the intraventricular pressure caused by tract gradient pressure. The Left ventricle systolic (pumping) pressure elevation can cause concentric hypertrophy leading to diastolic (filling phase) dysfunction with preserved pumping functionality.
Hypertrophy in medical terms means enlargement of the size and concentric means all round. In terms of heart, concentric LV hypertrophy means that the muscle of the left sided pumping chamber of the heart has increased in size and thickness. This usually occurs because of either high blood pressure or any obstruction to the outflow of blood from the left heart chamber (causing high LV pressure). Commonest example of latter is narrowing of the aorta valve (aortic valve...output tract). I suppose only your doctor can tell you as to the real reason of this LV hypertrophy. Remedial measures can only be taken once you know the cause of LV hypertrophy.
Hope this helps, and if you have any further questions you are welcome to respond. Thanks for sharing and take care.
"In terms of the heart, concentric LV hypertrophy means that the muscle of the left sided pumping chamber of the heart has increased in size and thickness".
It has been our experience with our daughter, having a Concentric form of cardiomyopathy, that they referred to it as being 'concentric' because ALL of the heart walls, in both left and right ventricles were hypertrophied. LVH is not always referred to as being the same as having the concentric form of the disease. Most people do not have the concentric form.
Ken you have listed some reasons for the hypertrophy, however in true hypertrophic cardiomyopathy, genetics are generally the reason for the presents of this disease. Sometimes it's sporadic as in my own daughter's case, but that's rare. My daughter did not have high blood pressure, hers always ran low to normal, although her diastolic levels were always low. She also had no obstructions even though her walls were 4+cm thick at the time of her transplant and all of her valves leaked, but that only became severe in the very end. HCM in the truest sense is really genetic in nature and therefore treatments are only geered toward relieving symptoms with about 5% of patients needing to be transplanted. maybe I'm missing something here but these were the things we were told for years about the Concentric form of this type of cardiomyopathy.
I have LV concentric hypertrophy with midwall obstruction HOCM. It`s been a while but I think they called mine symmectrical meaning one side of the heart. The other term was asymmetrical meaning both sides, I may have them confused. I may be totally wrong but there is a term to separate the two.
With your family history I would want a second and third opinion. You show some classic signs of HCM and As grendslori mentions HCM can be very serious and something you need to stay on top of. You may even want to talk to the HCMA to help you. If there is anything I can do to help let me know.
From Wikipedia, the free encyclopedia:
Unhealthy cardiac hypertrophy (pathological hypertrophy) is the response to stress or disease such as hypertension, heart muscle injury (myocardial infarction) or neurohormones. Valvular heart disease is another cause of pathological hypertrophy.
Chronic hypertension causes pathological ventricular hypertrophy. This response enables the heart to maintain a normal stroke volume despite the increase in afterload. However, over time, pathological changes occur in the heart that lead to a functional degradation and heart failure.
In the case of chronic pressure overload (as through anaerobic exercise, which increases resistance to blood flow by compressing arteries), the chamber radius may not change; however, the wall thickness greatly increases as new sarcomeres are added in-parallel to existing sarcomeres. This is termed CONCENTRIC hypertrophy. This type of ventricle is capable of generating greater forces and higher PRESSURES, while the increased wall thickness maintains normal wall stress. This type of ventricle becomes "stiff" (i.e., compliance is reduced) which can impair filling and lead to diastolic dysfunction.
For those interested in EKG...The axis of the heart shifts towards the hypertrophied ventricle for two reasons: 1. far more muscles exist on the hypertrophied side, which allows excess generation of electrical potentials on this side. 2. more time is required for the depolarization to travel to the hypertrophied ventricle compared with the normal. Can cause arryhthmia.
It seems to me the issue discussed is patholological hypertrophy, and to fine tune the discussion one would go to the sarcomere heart cells. When heart cells are injured they lose there ability to expand and contract (hypokineses). The cells line up differently for patholgical hypercardiomyopathy when compared to an athlete's heart (non-pathological.
It is true there is a genetic component for concentric cardio enlargement and that would/may have a different pathological impact to the sarcomere heart cells of the wall tissue but I believe the heart's dysfunction and limitations would be the same. Also, treatment options may differ, etc..
Thanks for sharing your view point...