Why should take Metoprolol if symtoms are better without

[the search for moderation]

When taking Metoprolol I find that sob is extremely unbearable when i try to do cardio. My (mayo) doc gave me a HR max of 140.

Whether I take 50 mg of extended release once a day or 2 - 25's (Lopressor) twice a day or cut the 25's in half and do 2 - 12 1/2's a day...my sob is much worse when taking this med. Against doctors orders I stopped it once for a month and almost immediately i noticed a world of difference. I could do cardio with no problems. Had a flutter or two and wife and I both decided to be safe so I started back with the med and in no time the sob was back.

They discovered my HOCM by way of a required physical from my job. I wasn't having symptoms. I had in the past complained over the past 10-12 years of chest pains, dizziness and shortness of breath but the sob came only after local doc put me on metoprolol for blood pressure. I took myself off after six month and this is when i first discovered that this med was the culprit of my extreme sob. The doc at mayo wanted me to try it again and said that if it still causes sob then cut in half and if still there then cut it again. All the way down to 12.5 mg per day total.

Is this amount doing me any good at all??? other than causing sob?

Why do i even need the med if it is causing more harm than good...or am i wrong about that?

I am so frustrated about this med. Hopefully someone can shed some light on this.

[Toogoofy317]

Well, from explanations to me it is to relax the heart to keep it from overworking itself. I can only tolerate 12.5mg due to hypotension. Even with that I've passed out and wondered why I should keep taking a menial amount when it seemed that the negatives outweighed the positives. They said my heart needed all the help it could get.

Maybe they can try another BB though and see if you have less symptoms.

Mary

[Reenie]

I agree with Mary. There are other medications out there that might work better for you. Even some in the same class (beta blockers) might have a totally different affect on you. Please let your doctors know how bad the metoprolol makes you feel and tell them you would like to try a different medication. I'm sure they'll be willing to work with you.

[Jillmgk]

My son basically has the same issue. He was prescribed Atenolol but it causes him chest pain. We ended up in the ER the first day he took it, were told to continue then cut it in half. He took it 3 more days with chest discomfort from it every day, then he refused it. They said they did not want to try Toprol or anything else yet, and since he has no symptoms right now, that was okay. The local cardiologist saw him a few weeks ago and said that he does have low BP anyway, so that is probably the issue. He was supposed to see Dr Lever this week, but it has been rescheduled to March 1st, so we will see what he says. In the meantime, he is not taking anything. he also has them heart rate limit of 140.

[jancer121]

I am seeing my doctor today and have the same question. I felt so much better and had more energy before taking Metoprolol. I was first put on 50mg for a week and then increased to 100mg. I work part-time and would come home so exhausted I had to nap each day. Because I complained so much, my doctor then cut the dosage in half to 50mg per day. At first I noticed some improvement but the symptoms have returned. I'm still just as fatigued as I was when I took 100mg, requiring the need to rest daily. This medication is really affecting my life and I've been told the same thing by the doctors - that it's doing my heart good. Yet, I felt better without it. Has anyone else experienced this with this drug or any other BB?

[Jillmgk]

Could you take the medication at night so you sleep through the worst of the fatigue (is it extended release?) I take Toprol (generic) for my BP- not HCM- and it wears me out. I can take mine at night and it works well for me that way. I too found that it just flat knocked me out midday and made work very difficult, even on the low dose I take.

[Darth Lefty]

I've had the same problem but I didn't think to blame it on the meto. I figured it was loss of cardio tone from stopping hard exercise.

[bberk1]

140 HR. Dang I wish I could get mine there. Lever said he want's me to stay at 110 and below. I had the same problem and switched to metro. and it was better. So def. try a different med.

[the search for moderation]

140 HR. Dang I wish I could get mine there. Lever said he want's me to stay at 110 and below.

Before I went to Mayo and reading all info I could I was thinking my exercising days were over. After diagnosis, I am not sure doc believed me that I was asymptomatic during exercise (i wasn't taking any meds). He ordered exercise test and I did well. I feel very blessed that I am able to get my heart rate up to 140. He still wanted me to start back on Metoprolol. I still have about 30 pounds that I need to lose so it is definitely helping...but...i have been fighting against the meds. Without it, it's easy to get my hr up to 140 but with the amount i was taking i struggled to get hr up to 125-130.

Three days ago I cut the halves in half again. Now I am taking 12 1/2 mgs a day. Going to see how that works. I am already feeling a difference.

I just don't know how that little amount could even help???

Thanks for all the posts.

[Pam Alexson]

Why use medications :( some reasons are about the POTENTIAL effect of taking them)

http://emedicine.medscape.com/article/152913-overview

Medication

The purpose of pharmacologic therapy is to reduce the pressure gradient across the LV outflow tract by reducing the inotropic state of the left ventricle, improving compliance of the left ventricle, and reducing diastolic dysfunction. To date, only one pharmacologic agent, amiodarone (Cordarone), has been shown to reduce the incidence of arrhythmogenic sudden cardiac death.24,25

Beta-adrenergic blocking agents

Reduce inotropic state of left ventricle. Decrease diastolic dysfunction and increase LV compliance, thereby reducing pressure gradient across LV outflow tract. Decrease myocardial oxygen consumption, thereby reducing myocardial ischemia potential. Decrease heart rate, thus reducing myocardial oxygen consumption and reducing myocardial ischemia potential.

[the search for moderation]

Why use medications :( some reasons are about the POTENTIAL effect of taking them)

Medication

Beta-adrenergic blocking agents

Reduce inotropic state of left ventricle. Decrease diastolic dysfunction and increase LV compliance, thereby reducing pressure gradient across LV outflow tract. Decrease myocardial oxygen consumption, thereby reducing myocardial ischemia potential. Decrease heart rate, thus reducing myocardial oxygen consumption and reducing myocardial ischemia potential.

What does that mean in English. I wish i could understand all that!!!

My biggest question is this, "Has this medication been proven to PREVENT sudden cardiac death or prolong my life in any way"? If not, then if my symptoms are worse with the med than why take it?

[Pam Alexson]

Reduce inotropic state of left ventricle.=

An inotrope (pronounced /ˈaɪnɵtroʊp/) (from Greek in-, meaning fibre or sinew) is an agent that alters the force or energy of muscular contractions. Negatively inotropic agents weaken the force of muscular contractions. Positively inotropic agents increase the strength of muscular contraction.
Most commonly, the inotropic state is used in reference to various drugs that affect the strength of contraction of heart muscle (myocardial contractility). However, it can also refer to pathological conditions. For example, enlarged heart muscle (ventricular hypertrophy) can increase inotropic state, while dead heart muscle (myocardial infarction) can decrease it.

Decrease diastolic dysfunction=

Diastolic dysfunction refers to an abnormality in the heart's (i.e., left ventricle's) filling during diastole. Diastole is that phase of the cardiac cycle when the heart (i.e. ventricle) is not contracting but is actually relaxed and filling with blood that is being returned to it, either from the body (into right ventricle) or from the lungs (into left ventricle).

In optimal left sided performance of the heart, blood mass loads forward in an unobstructed manner from the lungs, into the pulmonary veins, into the left atrium, through the mitral valve, and finally into the left ventricle. When the left ventricle cannot be normally filled due to deterioration of preload,compliance and E/A Ratio during diastole, blood regurgitates into the left atrium and, eventually, in a backward gradient into the lungs. Physiologically this results in a higher than normal [mismatch] pressure gradient of blood within the vessels of the lung. As a result of hydrostatic forces, this pressure mismatch leads to leaking of fluid (i.e. transudate) from the pulmonary blood vessels into the air-spaces (alveoli) of the lungs. The result is pulmonary edema, a condition characterized by difficulty breathing, inadequate oxygenation of blood, and, if severe and untreated, death. Pulmonary edema developed as a result of diastolic dysfunction is not fully imparted by failing pump function of the left ventricle. Indeed, it may result from the left ventricle's inability to readily accept blood trying to enter it from the left atrium.
Pathophysiology

Diastolic dysfunction is characterized by elevated diastolic pressure in the left ventricle despite normal or sub-normal diastolic volume. Histologic evidence supporting diastolic dysfunction demonstrates hypertrophy of the cardiomyocytes, increased interstitial collagen deposition and/or infiltration of the myocardium. These influences collectively lead to a downhill spiral in distensibility of the myocardium. The ventricle then behaves as a balloon made from abnormally thick rubber. Despite filling with high pressure, the volume cannot expand adequately. If the heart cannot fill with blood easily, either the cardiac output becomes diminished or compensation ensues to increase the ventricular diastolic pressure to higher levels. When the left ventricular diastolic pressure is elevated, venous pressure in the lungs must also become elevated to maintain forward flow. Increased pulmonary venous pressure results in alveolar edema causing the patient to be short of breath. Phrased differently, left ventricular stiffness makes it more difficult for blood to enter from the left atrium. As a result, pressure rises in the atrium and is transmitted back to the pulmonary venous system thereby increasing its hydrostatic pressure and thus promoting pulmonary edema.
It is crucial to note that a normal heart that is overfilled with blood may demonstrate increased stiffness and decreased compliance characteristics. This is analogous to a balloon that is over-filled with air. Blowing more air into the balloon becomes difficult because the balloon acts stiff and non-compliant at a filling volume it wasn't designed to hold. It is wrong to classify the volume overloaded heart as having diastolic dysfunction just because it is behaving stiff and non-compliant. The term diastolic dysfunction should therefore not be applied to the dilated heart. The term diastolic dysfunction is often erroneously applied in this circumstance when increased fluid volume retention causes the heart to be over-filled.

In simple words over time this process translates to many risks for the hCM heart.. some will get secondary pulmonary hypertension some will get atrial fib, some will progress to end stage and even dilate. Who the "some " are is impossible to predict as there are many unique compensatory mechanisms in each of us that sets us apart from the whole HCM common denominator. It is important to consider that without intervening with medication to assist the overworking HCM heart, serious and irreparable damage may take place. Far better to consider discomforting side effects then to risk damaging the HCM heart further. The process can be very slow and then again it can turn and change quickly with deterioration quite rapidly. All this and what is known and even theorized needs to be considered carefully and with the advice of an HCM expert before opting out.

...and increase LV compliance= the meds make the LV perform more accurately,

thereby reducing pressure gradient across LV outflow tract= the meds will reduce the obstructive gradient that we refer to with some HCM hearts.Obstructive gradients are bad.

Decrease myocardial oxygen consumption,= simply stated that if the myocardium ( heart muscle) can consume or use less oxygen to do its job thereby in the bigger picture .... reducing myocardial ischemia(scarring is reduced)... potential= the theory that this all works when we are given beta blockers.
Decrease heart rate( this is what BB's do), thus reducing myocardial oxygen consumption( this is what will happen with a decreased heart rate from taking the BB) and therefore again reducing myocardial( heart muscle) ischemia ( scarring) potential.

OVERALL it is a good thing to give beta blockers or if found to be more effective calcium channel blockers to those with HCM hearts and sometimes irregardless of symptoms that these drugs cause. In time the nervous system will adjust to the effects that are not so pleasant.

You must understand that all these things listed above effect the heart negatively if not intervened in on a timely basis. WEAR and TEAR takes place as in many adverse changes that cannot be universally assigned to all. EACH person with HCM is unique. Risk stratifications for your particular HCM needs to be assessed individually for you. It is hoped that during an expert assessment risk of sudden cardiac death and overall HCM health will reveal itself to the practioner who learns about you and your HCM. The word potential often found in the literature about treatment is just that.. potential. HCM knowledge is NOT an exact science and still so much is being determined from those that have come before you , those who live a full life, those who do not and those who have such a varied course of their disease.
Because there have been a good amount of individuals over history who were missed in diagnosis and therefore not treated early .. some conclusions can be theorized; made. There are HOWEVER NO guarantees that treatment and interventions will change the course of ones unique expression of HCM.

[the search for moderation]

Thank you so much for taking the time to respond the way you did. So thorough, you have been at this a while, haven't you.

If I can bore you, my story goes kinda like this:

In April of last year, my wife and I started on a path to better health. I weighed in at 256 lbs on a 5-9 frame. I set a goal to lose 2 lbs a week, I cut my calories to 1500-1800 per day and started going to the gym 5-6 days a week with a mix of weightlifting and cardio. My diet consisted of all the things healthy eating are made of. At the time I started this new way of life, my local family doctor had me taking Metoprolol for my blood pressure which by the way made me very short of breath. I couldn't hardly do any cardio unless I was "med free". So, I quit taking it and my blood pressure was doing well and I could breath and do cardio no problem. My health was improving and I felt like a million bucks.

About 8 weeks later at the end of May I was 30 lbs lighter and felt better than I had in years. The company I work for decided all of a sudden that OSHA says that all of the employees that are on the "First Responder" Team need to start having an annual required physical. (I do realize now that this was a gift from God, without the company required physical I never would have known of my HOCM and my weightlifting would have gotten more intense and I may be dead now)

The company doctor told me I had a heart murmur as well as an abnormal EKG and told me I needed to go to my family doc and get it checked out. I went to my regular doctor and his EKG came back abnormal as well. He sent me to a local cardiologist who ran several test and told me I had an obstruction and a rare heart disease that he knows as IHSS. After he consulted with a few more cardiologists, they referred me to the Mayo Clinic in Rochester, MN. He told me I needed to start on a Beta Blocker and Toprol was the med of choice. I told him my experience with that med and he put me on Atacand for my BP which was a little high probably due to white coat syndrome. He shut me down on the exercise other than walking. He told me that I could lift no more than five pounds until I was seen by a specialist. This devastated me, "how could this be"? I felt fine!!!

At the end of July, I went to Mayo and they confirmed that I had HOCM. My wife are very impressed with the Mayo, the whole experience was great. They put me through a series of tests and the last day of testing I had and exercise test and I did well enough on it that they allowed me to do cardio and get my heart rate up to 140 max (I don't think results would have been as favorable if i was on toprol). I could still lift weights but only up to 50 lbs. It was determined that my SCD risk was high due to undetermined sudden death in several members of my family members. HCM was never confirmed but a possible suspect. My family history was somewhat unclear. My holter monitor showed a three beat run of 130 the night i wore it. It was highly recommended that I receive an ICD. So, August 3, I got one implanted in my chest.

They told me to stop taking the Atacand, that it makes my obstruction worse. They wanted to start me back on the Toprol XL. I told them my experience with the med and they told me that they would really like to see me try it again that it would help. The doc told me if SOB was a problem then cut pills in half and if it was still bad then cut 'em in half again. They prescribed 50 mgs a day (2-25's)

It wasn't long before my SOB came back. I cut the pills in half then...not much better and just a couple of weeks ago I cut them in half again. So...I am now taking approx 12.5 mg's a day. I am feeling like I can breath again. I do worry that I am not taking enough. But...I feel great. That shortness of breath in my chest that I was feeling is all but gone. Is this amount enough to help me???

Looking at my schedule, my yearly checkup at the Mayo will be at the end of Sept or First week in October. I guess I will keep taking the 12.5 mg's a day and see how my check up comes out.

Will taking less medication possibly effect my yearly checkup and make me worse? Will it make my obstruction worse or my septum get bigger?

I have so many questions. I do feel blessed that this was found. At first I had the big question of "if this was genetic and I have always had this then why is it just now showing up"? I was just starting to get active again and this really stunted me. I am currently going to the gym 5-6 days a week again. My weightlifting has gotten a whole lot lighter, I am trying to be smart with it. Since I am only taking 12.5 mg's a day of Metoprolol I feel so much better.

Could the weightlifting have caused this to be detected?

Will lifting too much weight now cause it to get worse or is the weightlifting thing just higher risk of SCD?

Thanks again for being patient with me and answering my questions.

I will be 40 next month and this really knocked me down. How could this be??? I was feeling a whole lot younger until this happened. My struggle is in my user name. That is why i chose "the search for moderation". That is what I search for now that I have this "disease" (ouch, that is hard to say).

All my life I have been an "all or nothing" kind of person. Maybe this is God's way of teaching me how to slow down and have moderation in my life.

Thanks again.

[Pam Alexson]

Thank you... your story answers some questions .. Yes I have been at this for some time. I was a nurse working at the time I first became ill, working in home care as a psychiatric coordinator of a home care unit , also setting up and directing and running an adult assessment center for people over 55 at a local hospital clinic, and managing a team of medical surgical nurses seeing patients in the community. I had more hats then heads to put them on and was crashing and burning health wise. I understand all about working at full throttle and achieving lots of goals. I also was a single parent of 3 children and the bread source. It seems hard for me to think that this was almost 10 years ago now.
So I decided to use my skills as a nurse and my then young son's skills in computer technology to find out what it was that was making me so ill. I soon zeroed in on the words hypertrophic cardiomyopathy and figured out it was obstructed type. No one believed me.. my co- workers and superiors though they respected me and my work, thought I was hyper vigilant. Especially.. after my cardiologist/ PCP said flat out it was not HCM and that it was nothing except being out of shape and the effects of high blood pressure, everyone started tilting their heads when I spoke about it.
There were a few periods of time when I shut up and put up so to speak and tried to pretend things were not as bad as they were, but overall I knew it was HCM obstructed. Honestly it was so bad at times I actually felt a voice was speaking to me and telling me to get things tidied up and that the end was near. I did tell a close friend about these visions and thoughts that would come through my mind and she said I should see a shrink. So when someone else told me, "you should go to a big hospital in Boston where they know a thing or 2," it became a challenge almost to prove one way or the other that I was not a fruit cake. Honestly at times though, I thought I was imagining the whole thing.

So the rest of the story is I was obstructed HCM at as high as 240 mm Hg gradient. I was over the top of anyone they had seen with this at the hospital I went to and they even began to get confused and did a lot of tests that had already been done at home and had been viewed as "normal." My local doc gave them a lot of conflicting info and they began to question their initial diagnosis .. had a cath and it could not be questioned any longer. It was bad, but so bad they said I could not have anything done to stop it or change it because I was very different anatomy wise and such and it had gone on too long.

In the end I added 3 more years of hopelessness and it was Lisa at the HCMA who helped me sort it out and get me to Tufts where Dr Maron was and he and Dr Rastigar proceeded to save my life.

So do check in again with Lisa and while you do order the book .. it is key to understanding this disease and answering all the questions that come to mind about HCM. Taking some BB is preferable to none when you have an obstructive gradient and HCM. So a small dose is often what some will tolerate vs a higher. Things change in HCM( the HCM heart changes) and over time you may need and tolerate more or have other meds added.
Have you considered genetic testing. I finally had it done in 2009, nine years after diagnosis and we are beginning that process for my children now who are adults and have children of their own. My middle daughter will have hers tuesday.

It is hard to say or predict if lifting will make things worse. Elevated heart rate can negatively impact. So keeping tract of BP and heart rate is important. I know initially my local doc told me to push myself harder. Of course he did not believe that what he saw was an obstructive gradient and did not think it was an issue. What we understand is pushing an obstructed heart could bring about many issues especially with possible arrythmia, increased pressures over time making heart failure and pulmonary issues and other possibilities.
HCM can be expressed at any decade of life..obstructive gradients can vary and worsen and it is hard to predict what can aggravate a gradient more. As I said some things are known much more is not.

Do touch bases with Lisa and order the book it is the best reference you will find for the long haul of HCM...AND do stay connected with this site as new things and info comes about and everyone gets helped and learns to understand this disease through knowledge and reading and sharing.

[the search for moderation]

I'm not sure about gradient. I would have to pull my paperwork from the Mayo Clinic. They were surprised that my symptoms weren't worse. I can't say that I have been completely without symptoms, over the last 10-12 years I have complained about dizziness and chest pain and have had about three "anxiety attacks".

It's funny you mentioned about "getting your affairs in order", before I was diagnosed I had this overwhelming sense of knowing that I was only good for another 3-4 years. In my mind I was going to die at age 42. This could have come from knowing my dad died in his 40's my granddad on mothers side died at 39, my sister died at 42. All sudden and all were heart related. All the men on my dad's side of the family had heart problems. HCM was never mentioned. I never even heard of it until my local cardiologist sent me to the Mayo Clinic.

It's really aggravating because I got this ICD and people ask me "how you feeling" I say fine and they say "I guess that defibrillator fixed you right up". GRRRRRRRR!!!! Nobody understands what I have and I find myself explaining, "no, this ICD does nothing for my HOCM, It's there in case my heart goes haywire" They just tilt their head and say something like "OH". Why do I even bother. Sometimes I just agree with them and say "yea, it fixed me right up". I can easily feel sorry for myself but it serves no purpose other than making me lose focus.

You mentioned genetic testing, I have a son who I adopted. My wife and I have no children together. The only other family I have is my Mother and one half sister. Since I gave my life to Christ back in early 90's our relationship went south. My mother is not really interested in what's wrong with me or genetic testing. Do you think I should quiz my half sister about this? Same mother different dads, none of us kids really know any family history. That is why it was difficult for the doc at mayo to assess risk of scd. The deaths I mentioned above, HCM was never confirmed but is now a question in my mind. That is why I agreed with the Mayo and got the ICD, not to mention it made my wife feel safer with me exercising.

You told me to check in with Lisa and order "The Book". What book are you speaking of? Also, everywhere I go on this forum everyone says "Call Lisa". What is that about? What will she help me with? I wouldn't know what questions to ask her.

I feel very fortunate that this was found at the same time though I get angry because no one knows what HCM is. They just say things like "yea, i guess you just gotta watch that cholesterol huh"? NO. MY CHOLESTEROL IF FINE!!!!

I'm sorry again for the long post but you are like a breath of fresh air in that you are clearing some things up for me.

Thanks again.

[gfox42]

Right, call Lisa and order the book. . .

Lisa has been doing this for quite a while, and has talked with thousands of patients and family members. Don't worry about knowing what to ask her -- just tell her that we recommended you call, that you have HCM, and she'll take it from there. Really: give her a call.

"The book" is Hypertrophic Cardiomyopathy: For Patients, Their Families and Interested Physicians by Barry Maron and Lisa Salberg. Dr. Maron is one of the leading HCM docs; Lisa is the person you should call. The book will give you a lot of information on what HCM is, what it means for patients, and how it's treated.

You won't regret doing either of these things.

As for genetics and genetic testing of your relatives, a couple of comments. First, genes don't cause disease in quite the sense most people think: it's not like a black mark that means that you immediately have a disease. A mutation that contributes to the disease acts by causing particular proteins to be of a different form than normal, or to be less available to your body. The changed form or changed availability can lead to disease. Sometimes this is immediate -- for some genetic disorders, people are born with acute symptoms. For other kinds of disorders, the problems may crop up at any point in life. That's the case with HCM: most of the genes contributing to HCM act to reduce the efficiency of some of our heart muscle cells and in turn that can lead to actual disease at some point in life. It's quite common for people with these mutations to have no problems for many years. So "I've never had a problem before" isn't an argument against a genetic contribution to the disease.

Now, should you start on the road to testing? Only you can decide that, but let me give you some information that may be helpful. The way it would work is that you'd be tested, and they would either find a mutation that is a probably contributor to HCM, or they wouldn't. These mutations are currently found in about 2/3 of HCM patients. If you fell into the other 1/3, it wouldn't mean that there's no genetic cause, because they can only look for mutations known to cause HCM. There is much about genetics that still isn't known!

OK, if they identified a mutation in you that's known to cause HCM, it could be used to look for the same mutation in family members. What's the chance of it occurring in them? Well, let's see: half your genes came from your mother and half from your father, so any gene in you has a 1/2 chance of also occurring in your mother. A full sibling also has a 1/2 chance of sharing a gene with you, but your half-sister has a 1/4 chance. I'll add that if your mother was found to be carrying such a gene, then the chance your half-sister also carries it would be 1/2.


Gordon

[the search for moderation]

I am going to throw some stuff out there that I don't understand. It's my results from my visit to the Mayo Clinic.

HCM with sam and a gradient of 85 mm hg at rest (what is normal)

The Doctor said "Mr. x has obstructive HCM that is severe but, he is completely asymptomatic" (Should I still take med if I am sob with and not without it since I am asymptomatic)

The doctor also said "I prefer him to be on Metoprolol for HTN and the obstruction" (what is HTN?)

"The maximum instantaneous gradient increased from 31 mmHg at rest to 85 mmHg with valsalva and 100 mmHg with amyl nitrite inhalation." (I have no idea if all that is bad or how bad or normal or what)

My septum is 18 mm at the anteroseptal base and 20 mm at the inferoseptal base.

I am not sure what alot of this means and was looking for some deciphering.

Thanks

[Pam Alexson]

I am going to throw some stuff out there that I don't understand. It's my results from my visit to the Mayo Clinic.

HCM with sam and a gradient of 85 mm hg at rest (what is normal)
SAM =systolc anterior motion of the mitral valve...the leaflets= 3 of them get sucked into the outflow tract as the blood tries to exit the heart. Gradient should be close to "0" to be normal.

The Doctor said "Mr. x has obstructive HCM that is severe but, he is completely asymptomatic" (Should I still take med if I am sob with and not without it since I am asymptomatic)
I would take it.

The doctor also said "I prefer him to be on Metoprolol for HTN and the obstruction" (what is HTN?)
Hypertension or high blood pressure

"The maximum instantaneous gradient increased from 31 mmHg at rest to 85 mmHg with valsalva and 100 mmHg with amyl nitrite inhalation." (I have no idea if all that is bad or how bad or normal or what)
At 50 mmHG is when an expert starts to look at septal reduction as necessary.

My septum is 18 mm at the anteroseptal base and 20 mm at the inferoseptal base.
Normal is 10-12 mm, one does not have to be very thick when they have HCM to still have some serious issues. Your thickness is what a good many of us share, the variation from 18-20 just speaks to the assymetric nature of your HCM --- which is most common in HCM.

I am not sure what alot of this means and was looking for some deciphering.

Thanks

Some reading for you.....

http://jama.ama-assn.org/cgi/content/full/287/10/1308

http://www.lifeclinic.com/fullpage.aspx?prid=511384&type=1

http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/hypertrophic-cardiomyopathy/

[Deedee]

...The doctor also said "I prefer him to be on Metoprolol for HTN and the obstruction" (what is HTN?) ...

Hypertension (high blood pressure)

[Cynaburst]

You do have a pretty significant gradient. Normal is somewhere under 15 usually. Surgery is considered for those who have a gradient of 50 or higher, though they usually only do surgery to relieve severe symptoms. Amyl nitrate will tend to make the gradient worse, and will show your "provocable" gradient. That is the most that your gradient will increase under stressed conditions. If they give amyl to a person without obstruction, nothing will happen.

There is some evidence that taking beta blockers will slow the progression of HCM, and prevent wear and tear of the heart as well as reducing symptoms. Since you do have a signficant gradient, that is another consideration. Untreated gradients can have bad long term implications.