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roxie

A Good Vandy Paper

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I found this last night and thought it was super!

http://hopealways.wordpress.com/2010/06/12/must-read-for-all-p-o-t-s-patients-and-their-doctors/

It says a few things I hadn't realized. One of them touches in what I think Issie posted that mayo is now saying, there's two types of hyperPOTS. The true hyperPOTS and a secondary form to hypovolemia and some other things. Primary hyperPOTS is the rarest subtype at about 10%. The secondary form is 30%. And the partial dysautonomia type is about 60% of patients.

Do you think that's why some of us seem hyperPOTS sometimes or have hyperPOTS symptoms with out being fully hyperPOTS at every moment?

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Thanks for sharing, this is perfect! I'm going to be printing this out for my cardiologist for my next appointment. Also read a few things I didn't realize as well.

I don't mean to intrude on your share but the formatting on that blog was hard on the eyes (with the unnecessary line breaks, etc) Here's the original source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1501099/

Thanks for posting this!

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I've noticed that too Rama & monstrosity and researchers say its pretty rare. It's something I wonder about ?

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I think most POTS patients believe they have hyper POTS.

I agree

I think many patient have hyperadrenergic component like adrenaline surges, jitters, etc., but not Hyper POTS with high blood pressure. That's at least what my doctor thinks is going on with me.

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My BP runs over 150/90 and if anything goes up a bit when I go to a standing position. Does that by definition mean I have Hyper POTS?

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Potluck- I think you also would have to test high for Norepinephrine levels on standing catecholamines, plus some other symptoms usually go along with it. As Rama said, the whole "hyper" POTS classification is somewhat controversial amongst the researchers as they try to define sub-types.

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Exactly - all patients have a common finding of increased sympathetic drive to the heart and perhaps beta receptors creating feelings of anxiety potentially.

the current theoretical breakup is something along these lines:

10% have genetic or acquired NET deficiency supposedly creating sympathetic excess but reduced central outflow - more work is pending

A larger subset that JS said are mainly female have low blood volume, some of these have excessive ang II levels, some just have weird aldosterone reactions, all have low blood volume, some also have impaired vasoconstriction from impaired angiotensin II receptor vasoconstriction. Again research is unclear but indicative.

Biggest subset have neuropathic or autoimmune regional neuropathies at various locations that impair adrenergic vasoconstriction. This means that the body requires more NE to vasoconstrict these areas, but the areas that arent neuropathic feel the full force of that large NE level. So far the levels of titers of pathological autoantibodies have been low and equivocal. Cytokine driven neuropathy and even autoantibodies to various cardiac and nerve proteins have been postulated.

But remember there are currently around 24 different suggested pathyphysiological/etiological mechanisms being now suggested in published medical research with more unpublished. Either the disorder is that heterogenious or some are wrong and time will tell...

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