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Re: Dr. Olgin presentation Boston A-Fib Symposium 2004

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In a message dated 3/17/04 12:49:39 PM Eastern Standard Time,

a-fibfriend@... writes:

> Dr. Olgin, University of California at San Francisco

>

Thanks Steve.

Rich O

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<<Dr. Olgin concluded from canine studies of Congestive Heart

Failure and Mitral Valve Regurgitation (A-Fib is often seen with CHF

and MVR), that the Pulmonary Veins " do not appear to drive the A-

Fib. " >>

If this theory holds true in humans then what is the point of

isolating the pulmonary veins in the PVI procedure? Or does it just

apply to people with CHF and MVR?

<<He also suggested that this increase in Connexin 40 (through

the Angiotestin receptor, a hormone that causes dilation of the

blood vessels and contraction of smooth muscles), may have important

implications in treating patients with A-Fib.>>

Does this mean increasing the Connexin 40 might stop Afib?

Steve, thanks for keeping us informed.

P <MI>

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>

>

> <<Dr. Olgin concluded from canine studies of Congestive Heart

> Failure and Mitral Valve Regurgitation (A-Fib is often seen with CHF

> and MVR), that the Pulmonary Veins " do not appear to drive the A-

> Fib. " >>

>

> If this theory holds true in humans then what is the point of

> isolating the pulmonary veins in the PVI procedure? Or does it just

> apply to people with CHF and MVR?

Hi ,

it sounded to me like although the area wasn't 'driving the AFib'

it still 'helps propagate A-Fib signals'.

do a google search for

" dispersion of refractoriness in atrial fibrillation "

I'm guessing the PVs will be related to this problem.

> <<He also suggested that this increase in Connexin 40 (through

> the Angiotestin receptor, a hormone that causes dilation of the

> blood vessels and contraction of smooth muscles), may have important

> implications in treating patients with A-Fib.>>

>

> Does this mean increasing the Connexin 40 might stop Afib?

> Steve, thanks for keeping us informed.

Interesting question, Cx40 comes up quite a lot in research

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?db=PubMed & cmd=search & term=Conne\

xin+40+atrial+fibrillation

(http://tinyurl.com/yrvsf)

we may have to reduce the number though..

http://circ.ahajournals.org/cgi/content/full/103/6/842

or just redistribute what we've got :)

My view is that fixing the channels/ion pumps will be the best approach

to fixing AF. (and some fibrosis might need fixing which I'm guessing

will be an even trickier job!)

--

D

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Guest guest

>

>

> <<Dr. Olgin concluded from canine studies of Congestive Heart

> Failure and Mitral Valve Regurgitation (A-Fib is often seen with CHF

> and MVR), that the Pulmonary Veins " do not appear to drive the A-

> Fib. " >>

>

> If this theory holds true in humans then what is the point of

> isolating the pulmonary veins in the PVI procedure? Or does it just

> apply to people with CHF and MVR?

Hi ,

it sounded to me like although the area wasn't 'driving the AFib'

it still 'helps propagate A-Fib signals'.

do a google search for

" dispersion of refractoriness in atrial fibrillation "

I'm guessing the PVs will be related to this problem.

> <<He also suggested that this increase in Connexin 40 (through

> the Angiotestin receptor, a hormone that causes dilation of the

> blood vessels and contraction of smooth muscles), may have important

> implications in treating patients with A-Fib.>>

>

> Does this mean increasing the Connexin 40 might stop Afib?

> Steve, thanks for keeping us informed.

Interesting question, Cx40 comes up quite a lot in research

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?db=PubMed & cmd=search & term=Conne\

xin+40+atrial+fibrillation

(http://tinyurl.com/yrvsf)

we may have to reduce the number though..

http://circ.ahajournals.org/cgi/content/full/103/6/842

or just redistribute what we've got :)

My view is that fixing the channels/ion pumps will be the best approach

to fixing AF. (and some fibrosis might need fixing which I'm guessing

will be an even trickier job!)

--

D

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