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Current Status Of Pots


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Found this on vanderbilt's website,though I am sure many of you have read it,it seemed like a succinct break down of pots types and current research. http://www.mc.vanderbilt.edu/root/vumc.php?site=adc&doc=4788

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Yeah its not bad.

More recently there has been a move towards theories of deconditioning (Dr.Levine), and impaired nitric oxide activation - both increased and decreased in POTS (Stewart/medow and the CHinese group). Vandy have not updated this information to include the two newer theories regarding hypovolumia - that it relates to angiotensin II and that it may relate to abnormal peripheral dopamine activity.

Also I heard somewhere that NET deficiency is making a come back as a theory.

The Clinical Trials website is a good place to look for current research directions from the various American groups at least.

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ive got a few sources and I do a bit of my own research:

Mayo - who believe most POTS is autoimmune:

http://www.mayoclini...t/82/3/308.full

Blair Grubb group on Hyper POTS:

http://www.cardiolog...1_X_Kanjwal.pdf

Vandy find that QSART is abnormal in the same ratio of 'hyper' and non hyper POTS patients:

http://www.ncbi.nlm....les/PMC3089763/

Stewart and Medow break up POTS based on peripheral blood flow and catagorise Low Flow POTS:

http://ajpheart.phys...87/3/H1319.full

http://www.clinsci.o...5/cs1100255.htm

http://www.nymc.edu/...flow%20POTS.htm

Vandy confirm the finding of elevated angiotensin II in some POTS patients and suggest that it may impaire NET function:

http://www.heartrhyt...1204-X/abstract

Stewart and Medows find that ascorbate (vitamin C) improves flow in Low Flow POTS patients:

http://www.ncbi.nlm....pubmed/21622825

Stewart/medows et al find that the largest subset of POTS patients have elevated neuronal or endothelial nitric oxide:

http://www.ncbi.nlm....pubmed/21642500

There is plenty more - on cerebral autoregulation, hydrogen sulfide and nitric oxide from China. Net Deficiency, impaired MIBG reuptake and a few other things.

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