Mechanisms of Vagal Atrial Fibrillation

Please please all you high level physiologists, chemists, biochemists read this article and give me feedback. Best research I've found on vagal atrial fibrillation mechanisms at the link below

[www.tsoc.org.tw]

Just for curiosity. Elizabeth, which Elizabeth are you? Perez or H?Are you the relative newbie Elizabeth Perez or the regular longtime poster Elizabeth H?
PeggyM

p4: "Sharifov et al. showed that catecholamine can induce AF (about 20% of the time) in open chest dogs, and
atropine completely prevents catecholamine-mediated AF, indicating an important role of cholinergic tone in
these AF episodes. "

p6: "The patient was treated successfully with disopyramide, which has anticholinergic properties."

The paper is shot through with references to cholinergic influences on vagal tone and therefore vagal afib. However, little reference is given to the use of anticholinergic meds such as propantheline bromide, which have been successfully used to control afib.

Search on propantheline in this forum:

Peggy, note that this Elizabeth posted from Hawaii (look at the IP/Host in the upper right hand corner).

George

Peggy
Aloha I am the newbie paroxysmal a. fibber with RVR in Hawaii. I started a baby dose I mean baby dose 7.5 mg last night of propantheline and stopped my benadryl which also has anticholinergic action. I take nothing else. Third trip to hospital last week with rate of 206 sustained but have ok in the last 5 days on only benadryl. Someone told me I must use Flec to stop the cluster and shelter the AERPatrial effective refractory period. What do you think>

Elizabeth,

I sent you an email with more info.

George

I have no science on this - can only state experientially. But once I start an afib cluster, where I am in and out with self-conversion, it seems that only flecainide shocks me into NSR for a sustained period.

Acta Cardiol Sin 2007;23:112 [www.tsoc.org.tw]
Vagal Atrial Fibrillation
Yung-Hsin Yeh, Kristina Lemola, and Stanley Nattel.

Hi Elizabeth, and all -

The essence of the above article is the action of vagal neurotransmitter acetylcholine in decreasing atrial muscle cells’ “action potential duration” (APD) and “effective refractory period” (ERP), thus encouraging AF.

Quotes:

-- Cholinergic stimulation abbreviates APD and ERP, mainly through the activation of IKACh*. Experimental studies also show that vagal stimulation increases the spatial dispersion in atrial refractoriness, as well as in APD. Both absolute APD/ERP shortening and increased APD/ERP heterogeneity facilitate reentry and tachyarrhythmia.

-- …either increased susceptibility of the heart to vagal influences or increased vagal tone could potentially play important roles in vagal AF.

-- The electrophysiological mechanisms of vagal AF mainly comprises atrial APD/ ERP shortening and increased dispersion of atrial refractoriness via activation of IKACh. Cholinergic stimulation may also enhance focal firing from PVs.

Notably absent from the article is any mention of cellular energy and its relationship with atrial cell ERP, often the principal determinant of NSR or AF. A while back there was a comment saying lone atrial fibrillation involves a dysfunction of the autonomic nervous system. This is definitely not true in all cases, and is probably not true in the vast majority of LAF. More typically, LAF involves dysfunction of the cells’ energy production / utilization, making the cells’ membrane potential (voltage) too low for optimal AP and ERP duration. The neurotransmitter acetylcholine inhibits Na/K pump activity, thereby additionally lowering cells’ voltage, reducing the ARP duration further, thus increasing AF probability.

======================

Biokhimiia. 1975 Sep-Oct;40(5):1032-8. [www.ncbi.nlm.nih.gov]
Mechanism of the inhibitory effect of acetylcholine and its analogs on sarcolemma Na, K-ATPase.
[Article in Russian]
Takachuk VA, Lopina OD, Boldyrev AA.

Abstract
Effect of acetylcholine on Na, K-ATPase from cardiac and skeletal rabbit muscles is studied. The inhibition of the enzyme by acetylcholine was shown to depend on the Na+/K+ ratio and Mg2+ concentration in the incubation medium. The sensitivity of Na, K-ATPase to acetylcholine and its analogues decreased as follows: acetylcholine, propionylcholine butyrylcholine, arecoline, carbacholine, choline. Muscle denervation resulted in 20-fold increase of the enzyme sensitivity to acetylcholine. Preparations of Na,K-ATPase from different muscles have the increasing sensitivity to acetylcholine in the following order: white, mixed, cardiac, denervated muscles.

======================

Cell voltage (membrane potential) increase / decrease in response to nutritional and other factors and consequent NSR or AF is the basis of CR Session 72: The Potassium/Sodium Ratio in Atrial Fibrillation [www.afibbers.org] Its essential facts are presently being expanded to include current understandings from the sciences of ‘epigenetics’ and ‘quantum biology’. “The Good Lord willing and the creek don’t rise”, a book about this will be published within a year. AF cure by natural means is the substance of the book. Not sure if “Cure” will be in the title, but “Naturally” will naturally be included.

A few relevant CR 72 quotes/ excerpts:

p. 1: Our bodies are 'The Body Electric'..[referring to the brilliant 1985 The Body Electric. Electromagnetism and the Foundation of Life by biophysicist/ orthopedic surgeon Robert O. Becker.] Heart performance being electrical is the essential fact pointing to AF cure.

p. 2: From Cardiac action potential [en.wikipedia.org] "...if the resting membrane potential becomes too positive [lower voltage], the cell may not be excitable, and conduction through the heart may be delayed, increasing the risk for arrhythmias."

p. 15: Quotes from biophysicist Richard Moore on the reason low cell voltage (from inhibition of Na/K pump activity) increases excitatory calcium within the cells.

p. 29: Characterisation of the Na, K pump current in atrial cells from patients with and without chronic atrial fibrillation: [eprints.gla.ac.uk]

p. 33: [en.wikipedia.org]: "The ion pump most relevant to the action potential is the sodium–potassium pump...."

p. 42: The following AHA article supports the theory that inhibition of the Na/K pumps is arrhythmogenic via slowing of the Na+/Ca++ exchanger pumps in the cardiomyocyte membranes. (see p. 64, Richard D. Moore, MD, PhD, The High Blood Pressure Solution 2001)
.
Circulation Research, 2008 [circres.ahajournals.org] [www.ncbi.nlm.nih.gov]
Burst Emergence of Intracellular Calcium Waves Evokes Arrhythmogenic Oscillatory Depolarization via the Na+ -Ca2++ Exchanger: Simultaneous Confocal Recording of Membrane Potential and Intracellular Ca++ in the Heart

“Our findings provide a cellular perspective on abnormal [Ca++] ion handling in the genesis of triggered arrhythmias in the heart.”

Best wishes! Erling.

* The Journal of Physiology 2011 [jp.physoc.org]
IKACh at the whim of a capricious M2R
Riccardo Olcese



Edited 4 time(s). Last edit at 06/04/2012 01:56PM by Erling.

Hi George -

From CR 72, p. 40: [www.afibbers.org]

"George, you provided some excellent information at [www.afibbers.org]. Your logical conclusion re: anticholinergics in vagal AF: "So, if you keep the Mg and K up, you don't need to take the PB or another anticholinergic med". With further understanding, this should probably read, "... if you keep the Mg and K up, and the Na down"?

Erling



Edited 1 time(s). Last edit at 06/03/2012 02:13AM by Erling.

Hi Erling - . Sign me up for the first autographed copy!
I look forward to owning your book when published. Sure to be a critically important handbook for afibbers.

Jackie