Alchohol in the blanking period

Early recurrence in the blanking period can herald long term failure of an ablation.

I had a 'touch up' procedure 4 weeks ago on 13 Sept. The EP found the lower right PV needed one burn and the upper right needed 6 burns to isolate them. I had been enduring an episode a month since May this year one of which started during a soccer game and I had to go to hospital with a rate of 250. The cardiologist on duty that day thought it might have been SVT but after applying Adenosine and then Verapamil it unmasked to AFIB. I have had a few short isolated events since the first ablation in Jan 2009 but have been able to play sport without the need for anti-arrythmic drugs since and only took a small 12.5mg daily dose of Toprol the last 4 months or so. I have had lots of PACS though over the past three years and have written here before on that. There is no question that too much alchohol can be a trigger for me.

The second procedure was only 4 weeks ago and I tested it on Friday with celebrating my mother in laws 70th with dinner including three beers and a few glasses of red wine. The next day I was walking around a property with some friends in the morning and then played tennis in the afternoon. My chest had a pinched sensation before playing (I assumed injury from the ablation) and during the tennis game I felt AFIB coming on. That was it until the early hours of the next morning when it converted. I am hoping that the rule about early recurrence doesn't apply as I think the action of the alchohol may have been to fan the flames of inflammation and allowed the not yet scarred substrate to conduct. I played tennis the next day and was absolutely fine and I would say that I have much fewer PACS than I was having before the ablation so I am hopeful it will still be a success and that I need to be more controlled and acknowledge things are still settling down.

I don't have any pain from the procedure but can feel irritation from time to time so I guess the healing phase is still continuing. I realise the answer is stay off the alchohol but was just curious to know if anyone knows what physiological effect alchohol would have on the scarring tissue to cause it allow conduction. Red wine is supposed to in moderation reduce inflammation, my intake was not huge but then again not moderate. I think I read Tom P had a similar experience of getting too confident last week following his ablation.

Regards
MikeJ

Dr. Natale warns strongly about drinking ANY alcohol after an ablation. Especially in the blanking period and for up to a good year or more at least until you know for sure you are stable and out the woods. In reality, any afibber that has required ablation should just swear off for good if they are smart about it at all.

A glass of wine on a special event might be okay after some time. But anyone drinking at all in those first 3 to 6 months and really first year after an extensive ablation are truly playing russian roulette with their ablation.

Dr.Natale told me in August after my LAA isolation ablation when we were discussing post-ablation triggers that about the onlky one he is really strong everyone avoiding is Alcohol.

Having seen first hand the effects of more ablation outcomes that he has performed than any other person on earth, I'd think he is a man worth listening too on the subject!

If you need to get loose and relaxed learn some breathing exercises/ some meditation or take a few Theanine or a small dose of Xanax or Ativan if need be for the time being.. just stay away from wine, beer and especially hard liquor. Some people seemingly get away with it ... for a while .. but it usually will catch up to most people who ignore this common-sense advice.

Shannon

Thanks Shannon, I appreciate now I shouldn't drink any red wine atleast during the blanking period no matter how good I feel. I was asking why red wine / alchohol affects the scar tissue allowing conduction and lead to AFIB even though in theory the PVs are now isolated. I assume that when lesions are fully formed then AFIB should not be possible even with a few glasses of red ( in reasonable moderation).

MikeJ

Hmm---I guess we are all different. I have consumed wine with my evening meals all during the 20 plus years of having Afib as it never seemed to be a trigger. When I had my Afib with Dr. Natale in May of 2011 he never said anything to me about avoiding alcohol during the Blanking Period or any time there after so I continued as usual. I have had no Afib since the ablation.

Lon, sounds like you are doing well after the ablation and whilst you say you have continued to drink wine I expect you did take it easy in the weeks after ablation. There is lots written about red wine / alchohol and palpitations. Where I live we have fantastic red wine which I do enjoy, that said I am active and try to moderate but come the weekend I am guilty of over indulging in good company. I am seeing my EP for a follow up in two weeks and I'll fess up to having a couple of glasses more than I should have last weekend, like your experience he didn't make a big fuss about not drinking wine (he enjoys the stuff too) but I am sure he would not condone having too many especially in the healing phase. I'll avoid it for the next while and see what happens.
MikeJ

I've been erratic all week so I threw caution to the wind yesterday and had two 16oz Pilsners. Now in sweet NSR again go figure!

[www.ncbi.nlm.nih.gov]

Wouldn't it be something if FIRM pans out and no amount of former triggers could induce AFIB because the elusive rotors were never properly ablated?

Hopefully statements like this no longer be valid:
Even if the pathological, electrical and physiological phenomena leading to AF have been described in ever more detail, the mechanisms underlying these changes remain largely unknown. The relative occurrences of paroxysmal atrial fibrillation (PAF) and other forms of this arrhythmia in the population are also not well known.



Edited 1 time(s). Last edit at 10/16/2012 11:54AM by McHale.

McHale,

Top-notch, experienced EPs like Natale, Haissaguerre and Jais routinely find and ablate rotors and have been doing so for years. There is nothing new in doing this. The novelty is in how you locate the rotors.

Hans

I avoided alcohol for 3 months after my ablation in Bordeaux. I just wanted to make sure that I didn't screw it up. But when I asked Dr. Haisseguerre in the hospital about drinking, he replied "I think you should try it. Life would be very dull without alcohol!" Of course he's French, and living in one of the wine capitals of the world, so not drinking wine would be unimaginable.

Personally, though, I think it's a trigger for me. One or two seems OK, after that, could be trouble.

I hope my Shiraz induced rotor was found and zapped or I may have to look at changing to Chardonay in keeping with the link provided by George or abstain altogether.

I note that Narayans team appear to claim a poor correlation between CFAEs and rotors not sure what that means. In redos I think the standard procedure is to check PV isolation first and then if AFIB can still be induced then go after other CFAE hot spots. I haven't seen reference in my research to looking for rotors. In my redo procedure isolation of the PVs was advised to me to be enough. I am hopeful that will prove to be correct and that my red wine binge last weekend which was followed the next day by AFIB does not indicate procedure failure.
MikeJ

My take on PVI is you fence off the triggers at the 4 pulmonary veins to keep the beast inside the atria from triggering. What FIRM does it slays the beast so they no longer exist which are actually the rotors/pulses. A poor correlation between CFAEs and rotors means human AF may be sustained by localized sources in the form of either electrical rotors or focal impulses not CFAEs. Complex fractionated atrial electrograms (CFAEs) are commonly recorded during atrial fibrillation (AF), but their role in the pathogenesis of AF has not been clearly defined. Studies have suggested that CFAEs may represent sites necessary for maintenance and perpetuation of AF. However, CFAEs recorded during paroxysmal AF and those recorded during persistent AF may represent a different underlying phenomenon. Dr Narayan has identified the beast inside and triggers should no longer matter because there is nothing left at these patient-specific sites that were terminated by Brief ablation (FIRM). This is why this may be a game changer. Let's hope!



Edited 2 time(s). Last edit at 10/17/2012 02:52AM by McHale.

Yes let's hope it proves to be the beast slayer and key to the wine cellar door. Will be interesting to see how long it takes to be considered proven and then the software and wizardry deployed around the EP labs world over. I hope I dont have need for it but the realist in me thinks that I'll be in the lab on the slab at some point in the future.
MikeJ

Oh it will be trust me.........

Hi MIkej,

Top EPs on a redo will first confirm if any PVIs have reconnected. The more skilled the EP, the less percentage of his cases will have reconnected PVs to begin with. Then they check other anatomical structures and all other potential 'hot spots' either at ganglionated plexi, CAFEs or at the LAA as does Natale's group and Bordeaux.

Keep in mind that one of the main reasons it pays to hold out for the top centers and EPs, as these two represent, is that from their vast experience they wind up addressing most all active 'focal points and rotor areas' by design as part of their ablations.

The main claim from Narayan and FIRM is that their proprietary system and software makes if much easier for most EPs to find and zero on on these 'focal points and rotors' and there is supposedly the first software to provide more visual cues of where the rotors begin. They can certainly make a compelling point by restricting their direct comparison to just those cases who had an anatomical PVI alone where there was never any attempt either to map and find nor to address any focal triggers or rotors as part of those control group ablations!

I'm not sure at all though, that their system will prove superior in real world long term results compared the current best who are already doing a step wise sequential ablation addressing the PVs, CS, SVC and as needed the mitral isthmus, back wall of the LA and LAA in addition to as many real time focal point triggers as they can find and feel from their long experience are worth also ablating.

Keep in mind too, that the left atrium is more or less the size of the inside of a tennis ball, there aren't that many places to address, once you do a thorough job of ferreting out the likely triggers anatomical as well as real-time focal triggers.

Shannon

McHale,

You may be interested in my review of the CONFIRM trial as published in the October/November 2012 issue of The AFIB Report:

Focal ablation for atrial fibrillation (CONFIRM trial)
SAN DIEGO, CALIFORNIA. Since 1998 when Prof. Haissaguerre and colleagues in Bordeaux discovered that 94% of AF episodes are triggered by impulses originating in the pulmonary veins, the mainstay of catheter ablation for atrial fibrillation (AF) has been pulmonary vein isolation (PVI) in which the pulmonary veins are electrically isolated from the left atrium by rings of lesions created by cauterizing the heart tissue with catheters powered by radiofrequency energy or liquid nitrogen (cryoablation). There are two mapping approaches used to guide the ablation catheter.

• Segmental PVI (Haissaguerre/Natale protocol) in which electrophysiological mapping (using a multipolar Lasso catheter) is used to locate the pathways taken by aberrant impulses from the pulmonary veins. Once found, the pathways are eliminated by ablation around the veins approximately 5 to 10 mm from the ostium of the veins.

• Circumferential anatomical PVI (Pappone protocol) in which the anatomy, rather than the electrophysiological properties of the junction between the pulmonary veins and the left atrium are mapped, usually using a CARTO or Nav-X system. The anatomical structure shown on a computer screen is used to guide the creation of two lesions rings in the left atrium – one completely encircling the left pulmonary veins and another completely encircling the right pulmonary veins; the two rings are usually joined by a linear lesion.

The two protocols are about equally effective when it comes to paroxysmal AF; however, in the case of persistent and permanent AF, the Haissaguerre/Natale protocol is superior because the “trouble spots” or focal points involved in persistent/permanent AF, as well as in paroxysmal AF with long episodes (24 hours or greater) are located, not within the lesion rings encircling the pulmonary veins, but rather on the walls of the left and right atria, or in specific structures of the heart such as the left atrial appendage or the crista terminalis or superior vena cava in the right atrium. An electrophysiologist (EP) skilled in interpreting the information received during an electrophysiological study is far more likely to find and successfully ablate these trouble spots than an EP who relies solely on anatomical mapping.

The existence of focal points (reentrant circuits) in the atria liable to initiate AF has probably been known for a hundred years and ablation based on eliminating them was the norm prior to 1998, but with rather limited success. We now appear to have come full circle with the rediscovery of the importance of targeting these focal points or rather areas (local electrical rotors and focal impulse sources) in ablations, especially in the case of persistent AF.

Dr. Sanjiv Narayan and colleagues at the University of California at San Diego now report the results of the CONFIRM trial involving the mapping and elimination of focal impulse and rotor modulation (FIRM) with the aid of a 64-pole basket catheter and a sophisticated computer program known as the Topera system. The clinical trial involved 92 patients who underwent a total of 107 procedures (31 for paroxysmal AF and 76 for persistent AF). Thirty-six (34%) of the procedures were performed using FIRM-guided ablation followed by an anatomically-guided PVI. The FIRM-guided procedures included mapping and appropriate ablation in the right atrium as well.

The remaining 71 procedures were conventional anatomically-guided PVIs with an added left atrial roof line, again based on anatomic guidance. It would appear that no electrophysiological mapping was used during these procedures, nor was the right atrium mapped, or any effort made to locate and eliminate focal sources which can only be found using electrophysiological mapping. This would seem to be an unfortunate omission for the patients with persistent AF (66% of procedures were for persistent AF).

Not surprisingly, the outcome of the FIRM-guided procedures was far superior to the outcome of the conventional procedures. Patients were evaluated at 3, 6, 9, 12, 18 and 24 months and the incidence of AF episodes (recorded on implanted ECG monitors/ICDs, or with 7-day patient activated event recorders) was noted. An average (median) 273 days after their procedure, 82.4% of the participants of the FIRM-guided ablation group were AF-free as compared to only 44.9% in the conventional ablation group. The UCLA researchers conclude that the results of the FIRM-guided approach offer “a novel mechanistic framework and treatment paradigm for AF.”

Narayan, SM, et al. Treatment of atrial fibrillation by the ablation of localized sources. Journal of the American College of Cardiology, Vol. 60, August 14, 2012, pp. 628-36
Kuck, K-H and Wissner, E. A FIRM grip on atrial fibrillation. Journal of the American College of Cardiology, Vol. 60, August 14, 2012, pp. 637-38

Editor’s comment: Despite the clearly biased design of this trial, it certainly is encouraging to see a 2-year success rate of 82% for persistent afibbers. However, it should be kept in mind that the FIRM-guided approach was only used in 36 procedures. Independent confirmation of the efficacy of the approach obviously needs to be obtained before it can be declared “the future of ablation”. Nevertheless, if efficacy is indeed confirmed, the approach will be of significant benefit, especially for EPs who are now relying on anatomical rather than electrophysiological mapping to guide their ablation procedures. NOTE: I find it difficult to reconcile the statements “single-procedure success rate” and “repeat ablation was not permitted” with the fact that the trial involved 92 patients who underwent a total of 107 procedures.

Hans

Shannon,
What Narayan claims is there are ONLY 2 or 3 critical rotors that sustain any Human AFIB that are being found thru his Topera mapping system and ablated stopping afib in its track so it doesn't matter all where all these other spots the top EP's are ablating. All this is done well before any PVI takes place and his new evidence is pointing toward FIRM with no PVI being just as successful. See this is the beauty of the system is it pans out. Just like you talked about 27% of triggers really being found in the LAA that were resonating into the atruim that Natale claims. Dr Reddy doesn't really accept this and is rare. What if all along its been what Narayan work is finding 2 or 3 rotors or impluses? Up till now nobody knew the dynamics of what is causing afib from all I've read; we just knew how to cage it off so to speak.
The old thinking of AF perpetuation had multiple wavelets propagating through structurally diseased atria. AF persisted as long as enough wavelets continued. For persistent AF this theory led to treatments that aimed to debulk the atria into smaller sections of tissue, which would then prohibit propagation of wavelets. This would mean using a shotgun approach invasive in nature and the potential for disrupting long-term atrial transport function. This is not what Dr Narayan's is doing.
I know it sounds simple and too good to be true but lets see what more news comes out and its coming.......



Edited 3 time(s). Last edit at 10/20/2012 02:00PM by McHale.

Hi Shannon,
I am seeing my EP for the 6 week follow up this week. Things seem to be settling down and I have much less ectopics and a sense that the 'injury' site is healing though I get twinges. I recall my EP saying after the first ablation that he was very careful with the right PV burns because my oesophagus lay directly behind. Sure enough the gaps were found there with the other PVs still fully isolated. He went looking for other hot spots but didnt find anything. I am hopeful despite the AFIB episode two weeks ago that the new scarring will now complete the block. I elected to have a PVI very soon after first being diagnosed with the condition ie within a few months in an effort to fix it early. In cases like mine which are paroxysmal PVI seems to be a good chance of cure without the need for burns of CFAEs and Rotors. Apparently double lung transplant patients who had AFIB before generally find they don't have it afterwards which is probably small consolation for those patients but a good indicator for the efficacy of PVI. When PVI doesn't work then that may be where FIRM may provide a lot of hope, I will be following it with interest as will the Professor who did my PVI, he is very sceptical though.
MikeJ

When I was first diagnosed with AFib and saw my first EP who confirmed it was AFib, he told me the first line treatment was a beta blocker, and then the second-line treatment was anti-arrhythmic drugs, and then ablation. From what it sounded like, he wasn't going to do the ablation on me right then. Although, 6 months later, when the beta blocker stopped working, he seemed willing to do the ablation then, rather than me having to go on an anti-arrhythmic.

But, based on your post above, that might be an argument to have an ablation sooner rather than later, rather than staying on Flecainide and waiting for it to fail.

Due to plans I have, I think I'll wait until March to make a final decision. I've already picked out the EP I want to do it, and I'm going to switch to him to be my examining cardiologist (the one I go to every 3 months to be looked at), even though he's an hour farther from my home than my current EP. He is much more knowledgeable about AFib in younger athletes and is a bike rider himself (although he says he doesn't have time to do really long bike rides). Although when I saw him for a consultation, he did tell me if it were him, he'd wait a couple of years to see if any breakthroughs in treatment happened. Next time I see him, I'll have the discussion with him (that'll actually fall in March, as I have an appointment with my current cardiologist in November, and I'll probably just keep it).

Hi Diane, never an easy decision. I found it the only solution to my highly symptomatic AFIB and playing sport. Flecainide just wasn't controlling it and my cardiologist had no qualms referring me to the EP. Good luck with your decision, get the best EP you can who has done 100's of procedures. Lots of info here on questions to ask the EP.
MikeJ

Hi McHale,

Yes that is the theory Topera/Narayan is promoting, and it sounds very similar to the theory of CAFE only ablations from soem years ago taht also had a very compelling story and some selected case studies to back it up. Lets see how is works in the bigger world of independent testing.

The main point I have is not that there might not be some worthwhile contribution in helping to easier locate rotor areas to ablate, but that his results so far seem to exaggerate his claims compared to what the top EPs at Bordeaux and Natale are getting and theres in not a "Shotgun" approach at all.

After addressing the PVs and in most but not all c ases the CS and SVC each case is very individual based on their own developed skill from many years of recognizing and knowing how best to address those remaining real time aberrant focal triggers/rotor areas to acheive their excellent results that in particular when looking at recent years that reflect use of the more modern mapping and irrigated catheters as well as their increased experience is very good indeed even with persistent AFIB and definitely on par at least with what Dr. Narayan has reported in far more limited and/or preliminary reports.

My sense is that when the dust settles on what Topera really offers, it may well offer a useful new view and tool that could make everyone's job easier, especially those EPs who hardly do any electrophysiology and rarely if ever venture beyond the PVs as it is now. That would be a very good thing!

But it very much remains to be seen if his theories pan out any where near representing a genuine breakthrough in concept and efficacy compared to the current state of the art. That is why I caution against jumping the gun yet based on what we have heard mostly from Narayan/Topera to date.

One thing Dr. Natale once told me, not about Topera per se, but in general in this high tech and innovative field, is that many less experienced operators often a bit naively get overly excited by every new system and method that comes down the pike and thus are too easily swayed by great sounding stories and want to try every single thing that has an interesting story up front. However, more experience brings greater discrimination as well, and thus less likelihood of getting swept away by marketing hype that doesn't pan out in the long run.

As always, the knowledge and systems that have the best , well-vetted track record have a tendency to rise to the top, and the best operators in the world who get first crack at all these new systems will wind up adopting whichever tools gives them the best chance for improving their own success rates and make their jobs easier for themselves and for their patients. That is our best clue of which way to go which again underscores the wisdom of picking the best and most experienced operator one can arrange and let them worry about the technology they feel most comfortable using.

Shannon

Hi Shannon,
There is more news coming from Dr Narayan..........all good

I have another consultation with another top Elite EP in New York next month highly rated doing FIRM after a brief pause to assess the patients he's already done. He's moving forward again after seeing excellent results..........It's not just Dr Narayan promoting it any more.



Edited 1 time(s). Last edit at 10/24/2012 01:51AM by McHale.

MikeJ, I have the same question. If the PVI cut off the electricity why would alcohol be a trigger unless there is some other point generating the stimulus? I've read that it can be anything from a week to 3 months for the scars to heal or thicken enough (in the case of 3 mths). So, in my case, the EP said he'd be very surprised if AF returned based on some outcome testing I'll find more about when I have a follow-up visit. Meanwhile, I was back to red wine for a couple weeks and finally, after being blissfully in NSR as I reported yesterday, I got a bout of my pre-ablation ectopics followed by 60 bpm AF. Got rid of it with Flec and Diltiazem. So I guess I should've followed this thread earlier, but while I hear what Natale said, and realize he's the best in the business (my EP trained with him at Cleveland when he was there and has done a ton of ablations since) I don't get the underlying logic. However after last night I'm going to follow it. My own EP saif nothing about it, but then I haven't spoken to him for more than a minute or so since the procedure.



Edited 1 time(s). Last edit at 11/17/2012 02:28PM by afhound99.