Dr John: LAA Closure should stop

Medscape article by Dr. John M.: LAA Closure should stop now

The problem I have with this article is Dr. John says nothing about the Atri-Clip alternative to the Watchman for LAA closure. After carefully studying it I prefer the Atri-Clip, even if I have to travel to Austin Texas to have it done. But is Dr. John suggesting no advantage for any method of LAA closure? I'm presently leading a healthy lifestyle in NSR but taking Eliquis twice daily. No discernible side effects but I would like to get off of it eventually. I won't be working and have health insurance benefits forever.

Yes, this just added to the confusion for me.
Plus the LAA low blood flow after ablation is not black and white either.
Low LAA flow with a chadsvasc of 0 is the same as a 2 or higher score.
Logic makes it seem as though being in afib with a chadvasc of 0 would at least be the same as being in NSR with a low a LAA velocity with a chadsvasc of 0.
Anti coagulation medication is not near a 0 risk.

It is all very frustrating.

" Active LAA flow is commonly observed in patients with AF, with alternating positive and negative sawtooth-appearing flow signals of variable amplitude and regularity (Fig. 3A). Mean LAA flow velocities have greater physiologic significance than peak velocities. These should be averaged for each cardiac cycle and then averaged for several cycles. Characteristically, flow signals have lower velocities during ventricular systole (LAA contraction in the presence of a closed mitral valve) than during diastole (34). In addition to flow resulting from active appendage contraction, a discrete early diastolic outflow signal, similar to that in sinus rhythm, is observed occasionally (22), although commonly it is difficult to identify this signal clearly and to differentiate it from fibrillatory flow signals."

"Generally, flow velocities during AF are lower than those during sinus rhythm (12,32,35). However, flow velocities in patients with AF are highly variable, with high velocity flows on one end of the spectrum (velocities similar to, or even exceeding, those observed in sinus rhythm), and minimal to absent flow on the other end (12). This represents the wide continuum of LAA contractile dysfunction in patients with AF, from relatively preserved contraction to complete paralysis of the appendage."

From: <[content.onlinejacc.org]

George,
So what does this mean after an LAA isolation?
Flow velocity is worse than when in afib without an LAA isolation?
And affer an LAA isolation if afib again occurs, then LAA velocity is also lower which translates into a higher stroke risk.

"So what does this mean after an LAA isolation? "

From what I understand, there is a wide variability by individual.

Also, I recall you've posted on LAA morphology before. As has Shannon <[www.afibbers.org]

So LAA morphology would likely have an impact either in afib or post LAA isolation.

George

This article is total bunk and once again Dr. Mandrola is playing the role of the contrarian. I've talked to Shannon on the phone at length about this article. He's going to be working on a "rebuttal" of sorts to this article. He'll be posting it soon I hope. Stay tuned.

In the mean time, if you're considering an LAA occlusion, don't let Mandrola's article change your mind. Do your own homework and seek an experienced EP to do your LAA occlusion.

Travis

In the short time I've been watching AF forums my opinion of Dr. Mandrola is he's a professional contrarian. That said, I believe Medscape threw gasoline on the fire with the title of the article. The article I read talked about the Watchman device being inferior to warfarin. It didn't address the other LAA closure devices in any significant depth. Let the developers of the Watchman perfect it, if possible, and move on. In the interim, if one's EP recommends a Watchman I'd probably pass if were the recommendee.

The main issue I have with the article, as not uncommon with the author, is he is looking mostly in the rear view mirror at early data and not accounting for the progress made in the last two years, nor does the article factor in that the for Watchman periprocedural risk associated with Watchman implant and following couple of months has lessened considerably with improved installation methods.

Also, for our group especially, as Dr Natale has suggested his patients who are good candidates for LAA occlusion and who need to be anticoagulated to stay on a NOAC like Eliquis or Warfarin for now (if they can tolerate any of the OAC drugs at all for the next 4 to 6 months when the new generation 'Watchman Flex' should be fully sorted out and FDA approved before signing up for an LAA occlusion ( which is not exactly the same thing as an LAA ligation (i.e. LARIAT or Atriclip as JayBros noted). I'll share more on this important story in a couple days, but its almost midnight and time to hit the hay.

I had another surprise notable floater appear in my right eye again yesterday late afternoon and had to get my eyes fully dilated again this morning so was not able to do much with reading or typing to speak of today and until right now before bed when checking the forum.

Check back by the weekend and will try to have more nuance and facts to this story, I seems once again this particular cardio blogger demands a lot of my time periodically having to address well-meaning stories with some good points but also some opinions he shares that are only partially relevant or on target, in my view and experience. One thing of note, it seems the issues I take biggest issue with in his columns are areas he has never done any, or very little, actual frontline work with himself. And those cheering him on are largely in the same boat it seems.

For example, last year the author of the article in question took issue with LAA isolation simply based on his 'gut feel' and almost zero first hand experience with same, and now his well known bias against all things LAA treatment-wise shows up in a sweeping condemnations of LAA closure while painting the issue with far too wide a brush in my view and from a narrow focus based mostly on rear view mirror data. And the position he arrives at is not at all shared by the majority of experts who actually perform these procedures successfully every day in top centers across the world, and who have largely moved on from the perspective he speaks of, and have incorporated many new lessons learned from those early two studies PROTECTS-AF and PREVAIL to the benefit of the patients of such experienced high volume Watchman installers addressing good candidates for the procedure.

And for those who may be candidates for LAA Occlusion or Ligation, we are fast approaching greater clarity and options in both areas. In the meantime, by following the latest guidelines for even the current generation Watchman, which includes ONLY allowing an experienced operator to install the device within a registry study at a center that does lots of these procedures as well and fir those patients who truly don't tolerate an OAC drug long term has greatly reduced the early periprocedural risk that is largely the total risk associated with Watchman, while the risk for bleeding from Warfarin (and no doubt from NOACs too to a degree, though the degree long term we don't have great stats on yet ... but we can be sure that as time goes on the efficacy in both embolic stroke prevention 'from LAA-sourced clots' or from avoiding 'hemorrhagic events or bleeds' will continue to increase with time, long after any real world periprocedural risks during the procedure and in the first couple months after Watchman install by an expert operator , which fall off very quickly in a short time. Failure to account for the ongoing long term risks of OAC therapy can make the still quite small overall risks from Watchman installation seem much larger in the big picture than they are when looking at long term outcomes.

Anyway, a good deal more to consider on this subject and some rules of thumb, if and when, any of our forum members may become a good candidate for LAA Closure (and keep in mind only a small percentage of overall afibbers are likely to ever benefit from LAA closure to begin with so we will
review that reality as well .. check back by the weekend when I hope to have fleshed this story out a bit more for you all.

Shannon

PS We are starting to get a good deal more folks who are discovering our Forum and a larger number per day and week who are registering for posting on the forum ... although not all have started to post yet ... but it shows already the impact of our opening up the forum to the internet that happened two weeks ago with the upgrade to our Phorum Platform, plus the addition of new spam blocking features that eliminated the unhandy initial universal login credentials that wound up blocking our forum activity from the view of any internet search engines the last 17 years!



Edited 1 time(s). Last edit at 11/16/2016 01:12PM by Shannon.

George and gmperf,

The issue about LAA emptying velocity when in AFIB versus after an LAA isolation, is comparable. Of course, there are individual variations in flow velocities both when in AFIB and after an LAA isolation as seen in the roughly 35% to 40% of LAA isolation patients from our group, all of which are from Natale's LAA-isolation patients list, who maintain robust enough LAA mechanical function and emptying velocities AFTER confirmed LAA Isolation to allow them to stop taking OAC drugs, or at least reduce to half dose size.

While roughly 60% to 65% will have too weak or inconsistent an LAA mechanical function after isolation an LAA emptying velocity of at least 0.4m/sec must be consistent among with a consistently robust Doppler A-Wave as measures into the Mitral valve inflow, and finally the absence of ANY visible 'smoke' or SEC (spontaneous echo contrast) is required... one must pass all 3 measures before consideration of stopping OAC therapy is on the table.

If any one of these three thresholds for confirming a safe level of LAA mechanical function is NOT achieved, they the patient will either need to stay on OAC for life or at some point go for an LAA Closure system (either an LAA Occluder such as Watchman Flex, Amplatzer Amulet LAA Occluder, or the up-coming Wavecrest Occulder ... OR as an alternatuve an LAA Ligation procedure for those who may still have some AFIB/Flutter/ATachy triggers from a not yet fully isolated LAA. Ligation procedures such as the new generation LARIAT PLUS, improved Atriclip or good ole fashion surgical amputation or stapling the LAA closed are the options for ligation which kills two birds with one stone providing both electrical isolation of the LAA and structural closure of the LAA thus eliminating any possible stroke risk arising from LAA-based emboli clots ... since the LAA no longer exists.

Keep in mind, that the degree of mechanical function of the LAA maintained after LAA isolation will depend on a number of variables including the fact that having a full LAA isolation in which LAA flow velocity is below a safe level will require constant protection and thus presents a 24/7 ongoing stroke risk without said protection ... just as will persistent or LSPAF equal a permanent stroke/TIA risk. Indeed, the vast majority of persistent and LSPAF cases will require constant OAC therapy or structural LAA closure protection.

Those in paroxysmal AFIB often have reduced mechanical function too during prolonged episodes, and even possibly for sometime after NSR is restored due to the possible stunning effect from a long episode of self-terminating AFIB. In practice, those paroxysmal afibbers whose CHADS-VASc risk scores are 2 and above will also typically require long term OAC, and some with a more aggressive LAA morphology might even benefit from both LAA closure and possibly ongoing OAC in some cases (perhaps at reduced dose) if they have both a high risk open LAA as well as a high AFIB burden plus significant non-LAA based systemic stroke risk too, and whether this added risk is AFIB-related or truly systemic from other causes (i.e. carotid artery plaque, arteriosclerosis etc ... clearly a case for careful vetting and decision making by the patient and an experienced EP.

Shannon



Edited 1 time(s). Last edit at 11/16/2016 09:53PM by Shannon.

Thanks Shannon for your coments.
For me, being afib free and having a 0 score, and also being 52, with no other health problems, being on a anti coagulation med for life is very frustrating.
I just know it is a matter of time before thier is a bleeding problem.
When I blow my nose and see some dried red, I worry about when a big bleed will come.
I also worry about if a big nose bleed occurs when I am piloting an aircraft.
It is a very un-ideal situation.

You are welcome gmperf, more on the topic in next few days. Also send me your cell number again, and I'll try to call in next couple of days to discuss your specific situation as things stand as of now and for the foreseeable near future. I agree, with your pilots license issue having a solid mechanical solution on board may well be preferable longer term in your case.

Shannon

Glad to see intelligent and informed rebuttal to the medical-journalism.

I, for one, have stopped paying any attention at all to this physician's website as I believe it is in violation of the Hippocratic Oath.

Dr Mandrola argues that implant of the Watchman should stop until further research can be done to determine if stroke risk is really reduced with its use. He points to current research that indicates a lack of superior results using the device when compared to blood thinners. He says more research is needed. I don't think this argument should concern most of us. Dr Natale seems to agree as he has stopped using the Watchman and is advising patients to wait for the next generation. Madrola is being pushed by colleagues to start implanting the device, because competitors are doing so, and he is pushing back. It's economics that is the real motivator of his article. Hats off to Dr John, patient care should come before physician compensation.

The article is limited to a review of the Watchman results because that is the only device commonly being implanted by EPs. The atriclip is not mentioned because EPs do not implant them, they are done by heart surgeons. If you are interested in LAA closure devices you need to broaden your area of research beyond the EP community.

None of the closure devices are supported by a lot of independent research free of conflicts of interest. There is a lot of money being spent in this area and it is only a matter of time before some solid research will give us some reliable answers. This is a good time to be patient, it is going to take a few years.

If you need to go to a closure device now I would look hard at the Atriclip as over 50,000 have been implanted, far far more than any other device. But even here little real follow-up research has been published. I had the Atriclip installed 18 months ago and I am quite happy with it and off all meds and blood thinners other than an 81 mg aspirin. But, no one, Natale included, can tell me my new stroke risk. Common sense tells me that if one eliminates the LAA, the source of 90+% of emboli affecting AF patients, that my risk profile is improved, but there is no proof - no one has done the research.

I'll be at Montifiore,Bronx NY w Dr Di Biase and Dr Garcia who will perform my TEE this Wednesday after my LAA isolation at St David's with Dr N March 1.
Just had my two year stress test Friday which I was told looked excellent, waiting on the
Stress-Echo Test results to see the parameters and actually results.

McHale

Sounds good McHale, I'm expecting a call when you wake up

Shannon

BillK,

I think your statement "it is a good time to be patient" is spot on.

Risk of bleeding on Eliquis has been shown to be similar to aspirin. Being that aspirin has also been shown to not do much to prevent afib stroke. It would seem that you being on aspirin with the clip is not much better than being on Eliquis (unless the aspirin is for other risk prevent).
For me, when I was on aspirin, bleeding from minor cuts was much worse than when on Eliquis. Not scientific, but interesting.

The use of low dose aspirin has been called into question by the FDA in recent years. This report offers a good overview and a well-referenced collection of various reasons why.
[articles.mercola.com]

On its website, the FDA now says:^{1, 2}

"FDA has concluded that the data do not support the use of aspirin as a preventive medication by people who have not had a heart attack, stroke or cardiovascular problems, a use that is called 'primary prevention.' In such people, the benefit has not been established but risks — such as dangerous bleeding into the brain or stomach — are still present."

I'm also on low dose Eliquis and I would not want to also be using aspirin as well... mainly because I don't want the stomach or GI issues. Instead, I've gone back to low dosing of the natural blood thinners that I used safely and successfully all the years prior, during and after ablations 1, 2 and 3.

Jackie

The last time that i was at my EP, he wanted me to take Aminodorne (spelling), I can't take blood thinners, I said I take an aspirin he said that doesn't do any good. That shocked me as that is what he has told me to take, so I guess he must be informed as to what you just said Jackie.

Liz

Yes Elizabeth,

Aspirin in no longer recommended for AFIB-related or any stroke prevention outside of having had an MI heart attack to help prevent a second MI (to a modest degree), but the risk of bleeding, especially GI Bleeds on aspirin long term are not worth the risk based on a collection of far better, larger and longer term studies over the last 5 to 7 years that have confirmed taking an aspirin each day is more risky and with essentially no AFIB-related stroke reduction benefit.

If you have a metal stent or other hardware placed inside the venous or arterial blood flow ... like a Watchman in the LAA or my Amplatzer Duct Occluder II vascular plug used to plug the leak in my LARIAT-ligated LAA, then a baby aspirin is often recommended temporarily just for its anti-platelet effect to prevent a small embolism from forming on any part of the metal exposed to the blood flow until the metal has been covered over with your own endothelial tissue growth ... at which time you can usually stop the aspirin.

Be well Elizabeth
Shannon



Edited 1 time(s). Last edit at 11/24/2016 12:49PM by Shannon.