6 months no afib

I don't post here very often, but I have been a "student" of this forum for a couple of years, trying to learn all I can. I greatly appreciate having access to all the knowledge and experience here.
I have experienced afib since 2006, at first only one episode a year, then in 2010, 4 episodes about 3 months apart. I've been through 2 cardiologists and 2 EPs and numerous drugs. I have been converted with drugs a couple of times, and then electrocardioversion was necessary. Last fall I researched Propantheline Bromide as a possible choice, and decided to start on a low dose after finally getting my EPs blessing and prescription. I had an episode soon after and upped the Propantheline dose. I take it only at bedtime as all my episodes come on at night in my sleep. Propantheline has anticholinergic properties that my be beneficial to vagal afibbers.
I also have been taking magnesiun, potassium and taurine for almost 2 years now. My EP said "we won't really know if the Propantheline is working unless you go a period of time with no episodes". Well- I am very hopeful, as I just hit 6 months of NSR. I realize this doesn't prove that the Propantheline is working but it sure feels good! I thought I would report my experience so far in case it could help someone else like me where nothing else has worked. I know I haven't provided much detail here but figure if anyone is curious, they will ask. Praying for continued NSR, Jill

Jill:
That is great, I remember reading about Propantheline, 6 months is very good, I am vagal as well. Keep us informed, I will have to re-read those articles.

Liz

Hi Jill,

Great news! My PB correspondent recently told me it also continues working without issue.

To me, the concept of vagolytic drugs makes sense for vagal afibbers. Here is one list: [www.provet.co.uk] Propantheline Bromide makes sense as, from my reading, it is the only one that does not pass the blood brain barrier. The late Dr. Coumel speaks to the concept here: [eurheartj.oxfordjournals.org]

"These theoretical notions have practical consequences; for instance beta-blockade is indicated much more in the latter case compared to the former. The adrenergic paradox explains why rhythmologists have overlooked the therapeutic aspects of betablockade: a large body of evidence now indicates that adrenergic-dependent tachyarrhythmias must be more common in heart failure than in the absence of myocardial impairment. The former actually benefit more than the latter from the beta-blocking treatment although the adrenergic mechanisms of their arrhythmias are not easy to see[2]. Logically, the same sort of paradox should apply to the vagal side of the autonomic nervous system. The trouble is that vagolytic drugs cannot be used as easily as beta-blockers. Not only are we missing vagolytic drugs that could be active by the oral route, but their pharmacological action is often ambivalent: at low dosages, atropine or scopolamine are clearly vagotonic rather than vagolytic. Finally it should be recalled how complex is the interaction between the two facets of the autonomic nervous system and how cautious should be
our hypotheses, which a ppear simple compared to reality[3]. The notion of accentuated vagal antagonism proposed by Levy[4] is probably as important in our understanding of vagally-mediated arrhythmias as the
adrenergic paradox is in the management of adrenergically-mediated tachyarrhythmias."

A thread on Propantheline Bromide is here: <[www.afibbers.org];

I have copies of Dr. Reiffel's papers (he is retired, but was the primary exponent of this approach) if somebody wants to read them.

George

Thank you, George! I was hoping you would come on to explain it better. I will add that I have experienced almost no side effects. A little dry mouth until I fall asleep, and sometimes a little light sensitivity the next morning if I take the dose later than usual the night before. Thats it! Also after the first few weeks, no PACs or PVCs! I'm keeping my fingers crossed. I am also careful with electolyte balance and supplements as well as a mostly Paleo diet. If I eat something stupid, I can feel it.

Jill, George -

We could look more deeply into the fact that raising the cellular K:Na ratio has the same effect on lengthening atrial ERP as the anti-cholinergic PB has by reducing the Na,K-pump inhibiting effect of acetylcholine, i.e. raising cellular K:Na increases Na,K-pump performance which increases cells' membrane potential, affecting a lengthening of the refractory period. We touched on this previously but didn't quite complete the analogy.

Erling

Erling,

I would agree this is an avenue that should be pursued. Additionally I would suggest that afibbers try the 12 Step Plan [www.afibbers.org] prior to initiating Propantheline Bromide (P. I would modify step 2 to include a 4:1 K:Na ratio. I would suggest a PB approach after step 9 for vagal afibbers.

From what I can see, most problems with PB come from too large a dose. However, even a little may have negative effects for some. So starting with a small dose and increasing it to the minimum necessary to control afib is the preferred method.

Here are excerpts from some papers by Dr. Reiffel:

Selecting an Antiarrhythmic Agent for Atrial Fibrillation Should Be a Patient-Specific, Data-Driven Decision James A. Reiffel, MD Am J Cardiol 1998; 82:72N–81N

"In patients who appear to have a parasympathetic contribution to the development of AF (as with nocturnal, postprandial, or bending-associated onset), a regimen that possesses anticholinergic properties may be particularly useful (e.g., disopyramide), whereas vagomimetic drugs (e.g., digitalis) may be profibrillatory. Although the literature does not contain prospective series contrasting drugs with different autonomic profiles in such patients, my own experience suggests that nocturnal paroxysmal AF can be totally or substantially limited by the pre-bedtime administration of either propantheline bromide (without an associated AAD) or controlled-release disopyramide without a repeat dose in the morning."


Have Sanctioned Algorithms Replaced Empiric Judgment in the Selection
Process of Antiarrhythmic Drugs for the Therapy for Atrial Fibrillation?
James A. Reiffel, MD, Current Cardiology Reports 2004, 6:365–370

"Furthermore, there are some forms of paroxysmal AF that do not fit into the major published algorithm categories. These include autonomically mediated AF (vagal, sympathetic), usually in patients without SHD, where, for sympathetically-induced AF, β-blockade may be sufficient as the AAD of choice whereas for parasympathetically mediated AF I have found that vagolytic agents (eg, propantheline bromide, urecholine, tincture of belladonna) may be sufficient as a preventative therapy (or may be added to another AAD) and disopyramide may have uniquely advantageous efficacy. The selection among these agents is empiric."

George

George,

I agree. While not discounting the value of anti-cholinergic PB in appropriate cases and doses, a 4:1 potassium-to-sodium dietary intake (along with magnesium and other essentials*) should be the recommendation for anyone struggling with AF, and not only for the required voltage of atrial myocytes, but for that of all body cells (50 trillion?), as they are all charged electrically for their tasks by millions of Na,K pumps that require a proper ratio between K and Na for their activity.

It's often emphasized that AF can be an early warning sign for what perhaps is silently lurking throughout the body - and rightly so - therefor the concern about masking even greater problems by "fixing" just the AF via chemicals or surgery without permanently employing well-understood, efficacious, simple, inexpensive, non-toxic, evolutionarily dictated natural means.

AF is a disease of civilization via its dietary ways, and is now considered epidemic (see Hans's April Afib Report).

Erling

*see [www.afibbers.org]

Some references discovered by a PB correspondent:

Erling, this first paper goes into the Cholinergic stimulation and ERP relationship in depth.

Vagal Atrial Fibrillation
Yung-Hsin Yeh,1,2,4 Kristina Lemola1,2 and Stanley Nattel1,2,3
Acta Cardiol Sin 2007;23:1-12
[www.tsoc.org.tw]

"The autonomic nerve system plays an important role in atrial fibrillation (AF). Vagal AF refers AF (generally paroxysmal) arising in contexts of enhanced parasympathetic tone. Heterogeneity of refractoriness and action potential abbreviation resulting from spatially variable parasympathetic enhancement of the acetylcholinedependent K+-current (IKACh) underlie vagal AF. Adrenergic influences may also contribute to the occurrence of vagal AF. Cholinergic stimulation may enhance ectopic firing from pulmonary vein cardiomyocytes, which potentially contribute to the occurrence of vagal AF. On the other hand, underlying heart disease modulates cholinergic regulation of atrial myocytes."

"Tissue effects of cholinergic stimulation 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,25-28 as well as in APD. Both absolute APD/ERP shortening and increased APD/ERP heterogeneity facilitate reentry and tachyarrhythmia. Liu et al.27 showed that vagal stimulation increases the variability in atrial refractoriness, as indicated by the standard deviation of ERP at different atrial sites and of activation frequency during AF. Although sympathetic stimulation also decreases atrial ERP, it has no significant effect on these indexes of ERP heterogeneity.27 Perhaps because of its lack of effect on spatial ERP dispersion, sympathetic stimulation was much less effective than vagal stimulation in promoting AF. In another animal study in which AF was induced by vagal stimulation,29 flecainide doses that terminated AF significantly reduced refractoriness heterogeneity during nerve stimulation, to the same range under control conditions without nerve stimulation. These observations suggest that increased heterogeneity may be a very important atrial proarrhythmic vagal mechanism"


Cardiology for the Primary Care Physician By Joseph S. Alpert. Page 495

"For vagally mediated atrial fibrillation disopyramide or propantheline can be effective".

You can find this quote by searching in the book on Amazon:
[tinyurl.com]
Search on
vagally mediated atrial fibrillation
and choose page 495

Clinical Cardiac Electrophysiology: Techniques and Interpretations. By Mark E. Josephson Page 326

"Those patients who most likely have vagally mediated atrial fibrillation include those who develop the arrhythmia when fatigued, following large meals, during sleep or upon rising in the morning, and during episodes of upper airway obstruction. An additional subgroup of such patients is those with deglutition-induced (swallowing) atrial fibrillation. These arrhythmias are difficult to treat, but their recognition allows the potential to use drugs with anticholinergic properties and to avoid drugs (e.g., digitalis) or situations (e.g., eating large meals) that precipitate the arrhythmia".

You can find this quote by searching in the book on Amazon:
[tinyurl.com]
Search on
anticholinergic properties
and choose page 326

George