Welcome to the Afibber’s Forum
Serving Afibbers worldwide since 1999
Moderated by Shannon and Carey
 |
 |
 |
 |
 |
 |
Home
>
AFIBBERS FORUM
>
Topic
LAA
Posted by Elizabeth
[a-fib.com]
Is it really a good idea to isolate the LAA?
Left Atrial Appendage (LAA)
What little is known about the LAA includes the fact that it is the source of heart stem cells needed for repair of the heart.
It was once thought that the heart cells you died with were the same ones you were born with. The latest belief is that about 40% of your heart is replaced during a full life.
This is a function I did not want to lose.
The LAA is also the source of a hormone which helps control blood pressure. The LAA also has a pumping function in parallel with the Left Atrium. And electrically isolating the LAA can often significantly reduce the contractile function of the LAA, thus making it a source of clots even when the heart is not in A-Fib.
Does using the Watchman devices outcome different than isolating the LAA, does the pumping function decrease? I understand that when isolating the LAA patients have to remain on blood thinners. What about with the Watchman device, I have read that patients are to remain on aspirin.
Liz
Is it really a good idea to isolate the LAA?
Left Atrial Appendage (LAA)
What little is known about the LAA includes the fact that it is the source of heart stem cells needed for repair of the heart.
It was once thought that the heart cells you died with were the same ones you were born with. The latest belief is that about 40% of your heart is replaced during a full life.
This is a function I did not want to lose.
The LAA is also the source of a hormone which helps control blood pressure. The LAA also has a pumping function in parallel with the Left Atrium. And electrically isolating the LAA can often significantly reduce the contractile function of the LAA, thus making it a source of clots even when the heart is not in A-Fib.
Does using the Watchman devices outcome different than isolating the LAA, does the pumping function decrease? I understand that when isolating the LAA patients have to remain on blood thinners. What about with the Watchman device, I have read that patients are to remain on aspirin.
Liz
Much of that information is dated and rather speculative. Surgeons have been routinely removing or sewing the LAA shut for decades with no negative consequences. All the functions of the LAA are duplicated by the RAA so it's not really needed. ANP, the hormone the article refers to, returns to normal levels almost immediately after the LAA is closed or removed because the RAA produces it also.
Watchman devices require aspirin only for a short period after implantation. After that all anticoagulants can be stopped.
Is it a good idea to isolate the LAA? The question almost doesn't make sense because nobody goes around isolating it willy nilly. It's only isolated when it is a source of abnormal rhythms. In my case it was producing flutter at rates between 230-250. Those occurred multiple times per week, so you're damn right isolating it was a good idea.
The article includes this gem:
Right there he demonstrates that he doesn't understand the procedure or why it's done. I've never been a fan of a-fib.com and find much of his material shallow, poorly researched, and alarmist.
Watchman devices require aspirin only for a short period after implantation. After that all anticoagulants can be stopped.
Is it a good idea to isolate the LAA? The question almost doesn't make sense because nobody goes around isolating it willy nilly. It's only isolated when it is a source of abnormal rhythms. In my case it was producing flutter at rates between 230-250. Those occurred multiple times per week, so you're damn right isolating it was a good idea.
The article includes this gem:
Quote
But cutting off incompletely understood parts of one’s heart seemed exceedingly rash. Also, if the ablation worked, there would be no advantage to having closed off the LAA. So, closing off the LAA was just preparing for a failed ablation, in my mind.
Right there he demonstrates that he doesn't understand the procedure or why it's done. I've never been a fan of a-fib.com and find much of his material shallow, poorly researched, and alarmist.
Liz,
"And electrically isolating the LAA can often significantly reduce the contractile function of the LAA, thus making it a source of clots even when the heart is not in A-Fib. "
This is true, hence the reason that ~60% of patients that have their LAA isolated need lifetime anticoagulation or to have a device like the Watchman installed.
"Does using the Watchman devices outcome different than isolating the LAA, does the pumping function decrease? "
You likely would not install the Watchman unless you had your LAA isolated.
I concur with Carry.
This would be my thought process:
1. Do I need an ablation?
if so
2. I'd go to a top notch guy like Natale. Natale would do what he could without isolating the LAA. If that did not solve the problem, then he would isolate it.
Then you wait to see what happens to LAA emptying velocity and the other parameters that Shannon has listed to see if you can get off blood thinners. This may take a year or more to evaluate (I'm making that up without referring to a reference - it does take a while).
3. If emptying velocity and other parameters are good, you may be released from taking blood thiners.
If they aren't good, then you have a choice - stay on anticoagulation for the rest of your life or get a Watchman or other device like it installed.
All of this hinges on #1, "is my afib bad enough to warrant an ablation."
LIfe is a series of trade-offs.
Also, Shannon posted several years ago about the morphology of the LAA (shape) making a difference. Different shapes have different risks.
George
"And electrically isolating the LAA can often significantly reduce the contractile function of the LAA, thus making it a source of clots even when the heart is not in A-Fib. "
This is true, hence the reason that ~60% of patients that have their LAA isolated need lifetime anticoagulation or to have a device like the Watchman installed.
"Does using the Watchman devices outcome different than isolating the LAA, does the pumping function decrease? "
You likely would not install the Watchman unless you had your LAA isolated.
I concur with Carry.
This would be my thought process:
1. Do I need an ablation?
if so
2. I'd go to a top notch guy like Natale. Natale would do what he could without isolating the LAA. If that did not solve the problem, then he would isolate it.
Then you wait to see what happens to LAA emptying velocity and the other parameters that Shannon has listed to see if you can get off blood thinners. This may take a year or more to evaluate (I'm making that up without referring to a reference - it does take a while).
3. If emptying velocity and other parameters are good, you may be released from taking blood thiners.
If they aren't good, then you have a choice - stay on anticoagulation for the rest of your life or get a Watchman or other device like it installed.
All of this hinges on #1, "is my afib bad enough to warrant an ablation."
LIfe is a series of trade-offs.
Also, Shannon posted several years ago about the morphology of the LAA (shape) making a difference. Different shapes have different risks.
George
George:
A Watchman Device can be installed without isolating the LAA. My AF episodes are not that bad or long, they are tolerable, my only concern is clots, I have had problems with Coumadin so my worry is a clot that could cause a stroke. An ablation may or may not work, also, blood thinners may still be needed, isolating the LAA does not guarantee that you will not need a blood thinner.
Carey has had his sixth and last ablation, he has had his LAA isolated and is on a blood thinner, I don't know if that is for life. A watchman may be on his horizon.
Liz
A Watchman Device can be installed without isolating the LAA. My AF episodes are not that bad or long, they are tolerable, my only concern is clots, I have had problems with Coumadin so my worry is a clot that could cause a stroke. An ablation may or may not work, also, blood thinners may still be needed, isolating the LAA does not guarantee that you will not need a blood thinner.
Carey has had his sixth and last ablation, he has had his LAA isolated and is on a blood thinner, I don't know if that is for life. A watchman may be on his horizon.
Liz
Quote
Elizabeth
Carey has had his sixth and last ablation, he has had his LAA isolated and is on a blood thinner, I don't know if that is for life. A watchman may be on his horizon.
Correct on all points and a Watchman (or other device) very likely is on my horizon. Around next Oct/Nov I'll make the decision whether to do it or wait longer, and which device to use if I go for it.
Your desire for a Watchman makes sense, but I suspect you're going to have a fight with your insurance company. Many of them are still refusing Watchman procedures for people who truly need them claiming it's an experimental procedure. That's nonsense but that's the way insurance companies are. It will change, but it's going to be slow.
Carey is totally right here, the uninformed comments by the afib patient who wrote a testimonial on A-fib.com is full of errors that are simply misunderstood speculation by those who have never worked with LAA isolation, ligation or closure first hand and resort to pure supposition and ‘educated’ guess work starting from the initial assumed mistaken premise that LAA isolation, ligation and closure all must be ‘bad’ inherently.
The Kansas University AFIB Research Center has done a wealth of neurohormonal research the last 5 years on LAA ligation specifically, that has completely undermined and debunked most all of such old school hearsay ‘science’ regarding all things LAA. It’s a real shame this kind of thing still gets published even on some AFIB blogs, as it only fosters further misunderstanding and can lead to poor decision making by patients as a result.
For example, completely contrary to the comments from the no doubt well-meaning, but misinformed author whose thought piece on LAA issues was published at the link above, both the hormones ANP and BNP rebound entirely within 24 to 48 hours post LAA ligation or amputation to regain the exact same statistical equivalence as these same two key hormone levels were maintained prior to the LAA ligation procedure. Over 5 to 6 times the amount of ANP is produced by the right atrial appendage (RAA) alone which is never ligated in most modern mini-maze and certainly not during closure of the LAA after an LAA isolation. Keep in mind the RAA is not involved in increased stroke or TE risk since the RAA is not directly connected to the left-sided vascular system, as is the LAA which allows possible embolic cerebral vascular events to occur.
Plus, in terms of added ANP and BNP hormonal reservoir, much of the endothelial tissue cells lining both the left and right atriums are fully capable of revving up and producing both of these important hormones on demand. And that is in addition to the huge reservoir for these hormones in the RAA. No wonder there is essentially an nearly instant and stable compensation that occurs shortly after LAA ligation. You would not have a clue about those facts from reading this article!
Also, positive net level changes of certain adrenal hormones whose over-expression often contribute to AFIB and other atrial arrhythmias such as excess adrenaline, noradrenaline and aldosterone are all handily down-regulated typically from 40% to 60% persistently in post-LAA ligation in a group of patients that typically can benefit significantly from turning down the volume some on these important adrenal hormones.
Blood pressures often drop 8 to 11 points in those with mild to severe hypertension after LAA Ligation as well, long term, often resulting in cutting one’s dose of BP meds. Adiponectin hormone is increased to healthy levels in many Post LAA ligation patients which helps curb appetite too in those who tend to eat too much.
In other words, the well-vetted science regarding impact of LAA ligation shows quite the opposite and far more positive potential benefit with little to no residual harm noted to-date.
Dr James Cox the world renowned cardiovascular surgeon and creator of the Cox-Maze procedure told me that the often poorly researched nay-sayer comments regarding LAA ligation was ‘pure hogwash’, by those clearly not working in the field of LAA treatment and management and who simply don’t have a clue what they are talking about from real world experience.
More later, it’s midnight here and lights out time and tomorrow (Sunday) I must finish my taxes first.
Be well,
Shannon
Edited 2 time(s). Last edit at 04/08/2018 09:25AM by Shannon.
The Kansas University AFIB Research Center has done a wealth of neurohormonal research the last 5 years on LAA ligation specifically, that has completely undermined and debunked most all of such old school hearsay ‘science’ regarding all things LAA. It’s a real shame this kind of thing still gets published even on some AFIB blogs, as it only fosters further misunderstanding and can lead to poor decision making by patients as a result.
For example, completely contrary to the comments from the no doubt well-meaning, but misinformed author whose thought piece on LAA issues was published at the link above, both the hormones ANP and BNP rebound entirely within 24 to 48 hours post LAA ligation or amputation to regain the exact same statistical equivalence as these same two key hormone levels were maintained prior to the LAA ligation procedure. Over 5 to 6 times the amount of ANP is produced by the right atrial appendage (RAA) alone which is never ligated in most modern mini-maze and certainly not during closure of the LAA after an LAA isolation. Keep in mind the RAA is not involved in increased stroke or TE risk since the RAA is not directly connected to the left-sided vascular system, as is the LAA which allows possible embolic cerebral vascular events to occur.
Plus, in terms of added ANP and BNP hormonal reservoir, much of the endothelial tissue cells lining both the left and right atriums are fully capable of revving up and producing both of these important hormones on demand. And that is in addition to the huge reservoir for these hormones in the RAA. No wonder there is essentially an nearly instant and stable compensation that occurs shortly after LAA ligation. You would not have a clue about those facts from reading this article!
Also, positive net level changes of certain adrenal hormones whose over-expression often contribute to AFIB and other atrial arrhythmias such as excess adrenaline, noradrenaline and aldosterone are all handily down-regulated typically from 40% to 60% persistently in post-LAA ligation in a group of patients that typically can benefit significantly from turning down the volume some on these important adrenal hormones.
Blood pressures often drop 8 to 11 points in those with mild to severe hypertension after LAA Ligation as well, long term, often resulting in cutting one’s dose of BP meds. Adiponectin hormone is increased to healthy levels in many Post LAA ligation patients which helps curb appetite too in those who tend to eat too much.
In other words, the well-vetted science regarding impact of LAA ligation shows quite the opposite and far more positive potential benefit with little to no residual harm noted to-date.
Dr James Cox the world renowned cardiovascular surgeon and creator of the Cox-Maze procedure told me that the often poorly researched nay-sayer comments regarding LAA ligation was ‘pure hogwash’, by those clearly not working in the field of LAA treatment and management and who simply don’t have a clue what they are talking about from real world experience.
More later, it’s midnight here and lights out time and tomorrow (Sunday) I must finish my taxes first.
Be well,
Shannon
Edited 2 time(s). Last edit at 04/08/2018 09:25AM by Shannon.
Long answer short:
Natale does currently recommend continuing aspirin therapy indefinitely but only because that's the accepted protocol in the US. Everywhere else in the world six months post procedure is considered adequate and that's what the science supports.
Even shorter answer:
No, lifelong aspirin is not required.
Natale does currently recommend continuing aspirin therapy indefinitely but only because that's the accepted protocol in the US. Everywhere else in the world six months post procedure is considered adequate and that's what the science supports.
Even shorter answer:
No, lifelong aspirin is not required.
Shannon,
I am confused and concerned by your post. You seem to argue for homeostasis of hormonal function and then say that
This raises several questions which I hope you can clarify
1. What evidence is there that over-expression of certain adrenal hormones (e.g. adrenaline) often contribute to AFIB? How is this over expression quantified and evaluated?
2. The down regulation of hormones and drop in blood pressure seems significant, especially 40% - 60% in the hormones. How does this compare with a beta blocker which seems to have a very similar effect if not mechanism, and what about beta blocker type side effects? Are you asserting and is there evidence that LAA ligation only produces these results in adrenergic and/or hypertensive patients? That would seem to be a very unusual mechanism indeed.
You will have to forgive me for not taking the word of an esteemed cardiac surgeon at face-value, since as you know I was given a hard sell by another esteemed cardiac surgeon to have an 8 hour FIRM ablation. Is there conclusive evidence here? Thank you
Peter
I am confused and concerned by your post. You seem to argue for homeostasis of hormonal function and then say that
Quote
Shannon
Also, positive net level changes of certain adrenal hormones whose over-expression often contribute to AFIB and other atrial arrhythmias such as excess adrenaline, noradrenaline and aldosterone are all handily down-regulated typically from 40% to 60% persistently in post-LAA ligation in a group of patients that typically can benefit significantly from turning down the volume some on these important adrenal hormones.
Blood pressures often drop 8 to 11 points in those with mild to severe hypertension after LAA Ligation as well, long term, often resulting in cutting one’s dose of BP meds. Adiponectin hormone is increased to healthy levels in many Post LAA ligation patients which helps curb appetite too in those who tend to eat too much.
In other words, the well-vetted science regarding impact of LAA ligation shows quite the opposite and far more positive potential benefit with little to no residual harm noted to-date.
This raises several questions which I hope you can clarify
1. What evidence is there that over-expression of certain adrenal hormones (e.g. adrenaline) often contribute to AFIB? How is this over expression quantified and evaluated?
2. The down regulation of hormones and drop in blood pressure seems significant, especially 40% - 60% in the hormones. How does this compare with a beta blocker which seems to have a very similar effect if not mechanism, and what about beta blocker type side effects? Are you asserting and is there evidence that LAA ligation only produces these results in adrenergic and/or hypertensive patients? That would seem to be a very unusual mechanism indeed.
You will have to forgive me for not taking the word of an esteemed cardiac surgeon at face-value, since as you know I was given a hard sell by another esteemed cardiac surgeon to have an 8 hour FIRM ablation. Is there conclusive evidence here? Thank you
Peter
SAFIB The evidence is strong for many people in our general age group (Mid-50s and above) who ALSO have a variety of Cardiovascular issues including AFIB/ other Atrial Arrhythmias such as Aflutter or ATachy which can be worsened and/or Triggered by a revved up RAAS system.
Such folks, (and I'm obviously not talking about otherwise fully healthy folks with no CVD or Arrhythmia), in fact most people who require LAA Isolation/ligation, who by definition tend o have more advanced atrial substrate disease .. i.e. often (but not always) marked by an enlarged LA and LAA ... such folks often also suffer from an 'over-expression of the RAAS system' ... Renin, Angiotensin, Aldosterone System ... hence the plethora of ARBs (or Angiotensin Blockers) and ACE-Inhibitors doled out to such patients all over the world.
These drugs which are known for their ability to tone down an overactive RAAS ... and RAAS hormones are close relatives of adrenal hormones .. in fact, they included some of the classic adrenal hormones such as Adrenaline, Nor-Adrenaline, Aldosterone and the classic Cortisol .. all of which at excessive levels can indeed trigger arrhythmia!
There is a lot of very solid evidence for this impact on Ligated/Amputated LAA. I certainly didn’t just pull these figures out of thin air here, and this research has continually been expanded and shared over the last several years at the ISLAA Conferences as we as at HRS Scientific sessions and AF Symposium each year now for the last 5 to 6 years and of which Ive attended 4 of the 6 years at ISLAA, the main conference dedicated to research on all things LAA related.
But Instead of me wrestling to type all this out for you it will be easier and more descriptive to get hold of some of the slides on this topic from Univ. of Kansas AFIB research center , rather than bang away with my bum peripheral neuropathy-challenged thumbs and hands these days, where, among several other centers, such in-depth discoveries have been made over the last 6 to 7 or so years l, it will be better to post them here so you can see them first hand, and we hope to be able to more easily post graphics and images on the forum in general as well.
I just must check first with the authors to get permission to post these slides or at least the ones that have been published so far and thus are public domain info. I think you will be pleasantly surprised SAFIB.
The BP Lowering impact of LAA ligation really is a powerful factor, and there really does seem to be even a modest 'adaptogenic' effect in that the rate of BP change is ... to some degree ... apparently mediated by the degree of over expression of the RAAS hormone to begin with. And whose partial inhibition by both LAA Ligation as well as to a lesser (though still important degree) also by the right patient with a revved up RAAS taking ARBs and/or ACE-Inhibitors, that is, depending on which of these RAAS control drugs the patient best responds too.
There are exceptions of course, but, by and large, the vast bulk of the patients studied so far who are both good candidates for LAA isolation and LAA Ligation tend to benefit from the overall RAAS lowering effect of either/or LAA ligation/Isolation and in some cases also from use of this class of drugs assuming the patient can benefit from even greater overall inhibition of RAAS.
One of the possible factors on this RAAS inhibiting connection could derive, in part, from a suddenly smaller overall LA surface area after ligation or amputation of the LAA, which typically will not be called for unless there is frank AFIB/AFL/ATachy triggered from the LAA to begin with, and which in turn, is not infrequently found in folks with enlarged and often scared, fibrotic left atriums with enlarged LAAs as well.
The sudden removal of the LAA ... an appendage Dr Cox and many other highly esteemed Cardiac Surgeons. EPs and ICs, label as "the most lethal appendage in the Human anatomy past 50 years old", ... does indeed tend to tighten up the overall LA volume and thus reduces what has become an overly-stretched and flabby LAA from the often years of persistent arrhythmia, prior to terminating said persistent AFIB often via successful LAA Isolation and often followed by LAA Ligation.
And keep in mind too, that while Dr Cox's international credentials far exceeds that of the other very kind and very good EP educator we both know that you mention in reference to FIRM (and whose name will not be used here), Dr Cox is far from the only top level cardiac surgeon, EP or IC that holds these views from their own extensive years of direct experience in working with LAA removal and management. The other gentleman you mention, to my knowledge, does not have much direct LAA isolation or ligation experience, if any. Though your point as an analogy of not taking any one doctors’ word alone as gospel is well taken, and yet is not at all the case meant here in my reference to Dr Cox’s comments with many other highly respected physicians who work directly in this field of LAA science and research also sharing the same perspective and research findings.
In any event, hang loose for a bit while I get these slides and figure out how to post them on this open-source forum platform we use. These slides are from the latest conference in LA this past February I attended. Im sure you will find them interesting and enlightening, especially in their unmasking of the past erroneous concepts about LAA ligation fostered by certain segments of the Cardio community who, for the most part, based their negative speculation regarding LAA ligation/isolation on 'educated guess' assumptions with little to no actual in the field in-depth long-term research on the real world impact of LAA ligation.
Let’s return to this thread later in the week after I get the permission to post a few of these slides from the authors that previously were pre-publication when presented at the conference but whose publication dates may by now have already occurred. If so, I should be able to get a handful of impressive slides to share with you and the rest of our group.
Until then, please hold this conversation here rather than everyone running off after more 'what if's', at least until I show some of the research behind these numbers and findings.
Cheers!
Shannon
Edited 5 time(s). Last edit at 04/10/2018 10:30AM by Shannon.
Such folks, (and I'm obviously not talking about otherwise fully healthy folks with no CVD or Arrhythmia), in fact most people who require LAA Isolation/ligation, who by definition tend o have more advanced atrial substrate disease .. i.e. often (but not always) marked by an enlarged LA and LAA ... such folks often also suffer from an 'over-expression of the RAAS system' ... Renin, Angiotensin, Aldosterone System ... hence the plethora of ARBs (or Angiotensin Blockers) and ACE-Inhibitors doled out to such patients all over the world.
These drugs which are known for their ability to tone down an overactive RAAS ... and RAAS hormones are close relatives of adrenal hormones .. in fact, they included some of the classic adrenal hormones such as Adrenaline, Nor-Adrenaline, Aldosterone and the classic Cortisol .. all of which at excessive levels can indeed trigger arrhythmia!
There is a lot of very solid evidence for this impact on Ligated/Amputated LAA. I certainly didn’t just pull these figures out of thin air here, and this research has continually been expanded and shared over the last several years at the ISLAA Conferences as we as at HRS Scientific sessions and AF Symposium each year now for the last 5 to 6 years and of which Ive attended 4 of the 6 years at ISLAA, the main conference dedicated to research on all things LAA related.
But Instead of me wrestling to type all this out for you it will be easier and more descriptive to get hold of some of the slides on this topic from Univ. of Kansas AFIB research center , rather than bang away with my bum peripheral neuropathy-challenged thumbs and hands these days, where, among several other centers, such in-depth discoveries have been made over the last 6 to 7 or so years l, it will be better to post them here so you can see them first hand, and we hope to be able to more easily post graphics and images on the forum in general as well.
I just must check first with the authors to get permission to post these slides or at least the ones that have been published so far and thus are public domain info. I think you will be pleasantly surprised SAFIB.
The BP Lowering impact of LAA ligation really is a powerful factor, and there really does seem to be even a modest 'adaptogenic' effect in that the rate of BP change is ... to some degree ... apparently mediated by the degree of over expression of the RAAS hormone to begin with. And whose partial inhibition by both LAA Ligation as well as to a lesser (though still important degree) also by the right patient with a revved up RAAS taking ARBs and/or ACE-Inhibitors, that is, depending on which of these RAAS control drugs the patient best responds too.
There are exceptions of course, but, by and large, the vast bulk of the patients studied so far who are both good candidates for LAA isolation and LAA Ligation tend to benefit from the overall RAAS lowering effect of either/or LAA ligation/Isolation and in some cases also from use of this class of drugs assuming the patient can benefit from even greater overall inhibition of RAAS.
One of the possible factors on this RAAS inhibiting connection could derive, in part, from a suddenly smaller overall LA surface area after ligation or amputation of the LAA, which typically will not be called for unless there is frank AFIB/AFL/ATachy triggered from the LAA to begin with, and which in turn, is not infrequently found in folks with enlarged and often scared, fibrotic left atriums with enlarged LAAs as well.
The sudden removal of the LAA ... an appendage Dr Cox and many other highly esteemed Cardiac Surgeons. EPs and ICs, label as "the most lethal appendage in the Human anatomy past 50 years old", ... does indeed tend to tighten up the overall LA volume and thus reduces what has become an overly-stretched and flabby LAA from the often years of persistent arrhythmia, prior to terminating said persistent AFIB often via successful LAA Isolation and often followed by LAA Ligation.
And keep in mind too, that while Dr Cox's international credentials far exceeds that of the other very kind and very good EP educator we both know that you mention in reference to FIRM (and whose name will not be used here), Dr Cox is far from the only top level cardiac surgeon, EP or IC that holds these views from their own extensive years of direct experience in working with LAA removal and management. The other gentleman you mention, to my knowledge, does not have much direct LAA isolation or ligation experience, if any. Though your point as an analogy of not taking any one doctors’ word alone as gospel is well taken, and yet is not at all the case meant here in my reference to Dr Cox’s comments with many other highly respected physicians who work directly in this field of LAA science and research also sharing the same perspective and research findings.
In any event, hang loose for a bit while I get these slides and figure out how to post them on this open-source forum platform we use. These slides are from the latest conference in LA this past February I attended. Im sure you will find them interesting and enlightening, especially in their unmasking of the past erroneous concepts about LAA ligation fostered by certain segments of the Cardio community who, for the most part, based their negative speculation regarding LAA ligation/isolation on 'educated guess' assumptions with little to no actual in the field in-depth long-term research on the real world impact of LAA ligation.
Let’s return to this thread later in the week after I get the permission to post a few of these slides from the authors that previously were pre-publication when presented at the conference but whose publication dates may by now have already occurred. If so, I should be able to get a handful of impressive slides to share with you and the rest of our group.
Until then, please hold this conversation here rather than everyone running off after more 'what if's', at least until I show some of the research behind these numbers and findings.
Cheers!
Shannon
Edited 5 time(s). Last edit at 04/10/2018 10:30AM by Shannon.
Quote
Elizabeth
[a-fib.com]
The latest belief is that about 40% of your heart is replaced during a full life.
... What about with the Watchman device, I have read that patients are to remain on aspirin.
Liz
Liz, as far as I know, every cell in our body is replaced every few years...and I expect that replacement does not depend on stems cells. So, the amount of your heart replaced during a full life is likely to be closer to 1000% than 40%...so IMHO loss of LAA would not concern me.
From my reading, Aspirin is something of a miracle drug, and a low dose worth taking regardless of its blood thinning benefit. Studies I have found quoted have reported reduced incidence of certain cancers, including bowel cancer and prostrate cancer. There is also some suggestion aspirin offers protection against alzeimers disease. All this beside a 28% reduced risk of heart disease amongst persons who have never had a heart attack or stroke, but are considered high risk...of course, it carries a risk of increased bleeding, which is particularly dangerous where stomach ulcers are present.
I believe they were talking about stem cells in the LAA.
Functions of the Left Atrial Appendage
1.The Left Atrial Appendage functions like a reservoir or decompression chamber or a surge tank on a hot water heater to prevent surges of blood in the left atrium when the mitral valve is closed.Without it, there is increased pressure on the pulmonary veins and left atrium which might possibly lead to heart problems later.
2.Cutting out, stapling shut or closing off the LAA reduces the amount of blood pumped by the heart and may result in exercise intolerance for people with an active life style. (In dogs the LAA provides 17.2% volume of blood pumped by the Left Atrium.)
3.The LAA also has a high concentration of Atrial Natriuretic Factor (ANF) granules which help to reduce blood pressure. The LAA functions as a storage device for ANF. But recent preliminary research indicates that the Right Atrial Appendage compensates for the loss of the LAA by producing more ANF.
4.The Left Atrial Appendage may also function as a reservoir of different types of stem cells which can stimulate the heart to repair itself (thanks to the research of the above Israeli scientists).
I take aspirin but the thinking of the Medical establishment is that aspirin is not as highly thought of as it once was for blood thinning, of course that could be because of all these new blood thinners that they want all of us to take.
Liz
Functions of the Left Atrial Appendage
1.The Left Atrial Appendage functions like a reservoir or decompression chamber or a surge tank on a hot water heater to prevent surges of blood in the left atrium when the mitral valve is closed.Without it, there is increased pressure on the pulmonary veins and left atrium which might possibly lead to heart problems later.
2.Cutting out, stapling shut or closing off the LAA reduces the amount of blood pumped by the heart and may result in exercise intolerance for people with an active life style. (In dogs the LAA provides 17.2% volume of blood pumped by the Left Atrium.)
3.The LAA also has a high concentration of Atrial Natriuretic Factor (ANF) granules which help to reduce blood pressure. The LAA functions as a storage device for ANF. But recent preliminary research indicates that the Right Atrial Appendage compensates for the loss of the LAA by producing more ANF.
4.The Left Atrial Appendage may also function as a reservoir of different types of stem cells which can stimulate the heart to repair itself (thanks to the research of the above Israeli scientists).
I take aspirin but the thinking of the Medical establishment is that aspirin is not as highly thought of as it once was for blood thinning, of course that could be because of all these new blood thinners that they want all of us to take.
Liz
Quote
Elizabeth
1.The Left Atrial Appendage functions like a reservoir or decompression chamber or a surge tank on a hot water heater to prevent surges of blood in the left atrium when the mitral valve is closed.Without it, there is increased pressure on the pulmonary veins and left atrium which might possibly lead to heart problems later.
Surgeons have been routinely removing/closing the LAA for decades. No negative effects have been observed.
Quote
2.Cutting out, stapling shut or closing off the LAA reduces the amount of blood pumped by the heart and may result in exercise intolerance for people with an active life style. (In dogs the LAA provides 17.2% volume of blood pumped by the Left Atrium.)
People are not dogs. Closing the LAA has no significant effect on heart function.
Quote
3.The LAA also has a high concentration of Atrial Natriuretic Factor (ANF) granules which help to reduce blood pressure. The LAA functions as a storage device for ANF. But recent preliminary research indicates that the Right Atrial Appendage compensates for the loss of the LAA by producing more ANF.
It's not preliminary research. The RAA has no problem supplying all the ANP needed by the body.
Quote
4.The Left Atrial Appendage may also function as a reservoir of different types of stem cells which can stimulate the heart to repair itself (thanks to the research of the above Israeli scientists).
So? See #1.
Quote
I take aspirin but the thinking of the Medical establishment is that aspirin is not as highly thought of as it once was for blood thinning, of course that could be because of all these new blood thinners that they want all of us to take.
Aspirin is 20% less effective at preventing atrial clots and has a higher bleed risk. It offers no benefits whatsoever. That's why they want us to take anticoagulants. If you don't like the NOACs or can't afford them, warfarin is still an option.
Quote Carey:
Aspirin is 20% less effective at preventing atrial clots and has a higher bleed risk. It offers no benefits whatsoever. That's why they want us to take anticoagulants. If you don't like the NOACs or can't afford them, warfarin is still an option.
Man---If I can't take NOACs, why would I then take warfarin, as for affording them that isn't why I don't take them. If aspirin is so bad why does dr. Natale advise patients to be on it for life after LAA? Also, if aspirin is 20% less affective than it is 80% effective, so by you saying that it offers no benefits whatsoever is not correct.
I understand you are very knowledgeable, doesn't mean I always agree with you, or that you are always right.
L
Edited 1 time(s). Last edit at 04/14/2018 07:14PM by Elizabeth.
Aspirin is 20% less effective at preventing atrial clots and has a higher bleed risk. It offers no benefits whatsoever. That's why they want us to take anticoagulants. If you don't like the NOACs or can't afford them, warfarin is still an option.
Man---If I can't take NOACs, why would I then take warfarin, as for affording them that isn't why I don't take them. If aspirin is so bad why does dr. Natale advise patients to be on it for life after LAA? Also, if aspirin is 20% less affective than it is 80% effective, so by you saying that it offers no benefits whatsoever is not correct.
I understand you are very knowledgeable, doesn't mean I always agree with you, or that you are always right.
L
Edited 1 time(s). Last edit at 04/14/2018 07:14PM by Elizabeth.
Liz,
Of course I'm not always right. Look, I'm not trying to disagree with you or criticize you or be unfriendly, but I'm not going to remain silent when anyone posts incorrect or misleading things. People are here for help, and they often don't know who or what to believe, so it's important that we provide them with correct information. It also helps to be positive. People are scared and they don't need to be told their doctors are corrupt and can't be trusted.
Natale does not advise patients to be on aspirin following LAA isolation. We've been through this before just days ago.
Aspirin being 20% less effective doesn't mean it's 80% effective. That's not how that works. Aspirin has no benefits whatsoever when compared to anticoagulants in patients with (non-valvular) afib. That's simply a fact, not an opinion. Are some people unable to take anticoagulants but able to take aspirin and so take it because it's the best they can do? Yeah, sure, and if that's your situation so be it. You're not alone. But it's no reason to cast doubt on anticoagulants in general and the motives of doctors prescribing them. They're the right solution for the majority of patients.
Of course I'm not always right. Look, I'm not trying to disagree with you or criticize you or be unfriendly, but I'm not going to remain silent when anyone posts incorrect or misleading things. People are here for help, and they often don't know who or what to believe, so it's important that we provide them with correct information. It also helps to be positive. People are scared and they don't need to be told their doctors are corrupt and can't be trusted.
Natale does not advise patients to be on aspirin following LAA isolation. We've been through this before just days ago.
Aspirin being 20% less effective doesn't mean it's 80% effective. That's not how that works. Aspirin has no benefits whatsoever when compared to anticoagulants in patients with (non-valvular) afib. That's simply a fact, not an opinion. Are some people unable to take anticoagulants but able to take aspirin and so take it because it's the best they can do? Yeah, sure, and if that's your situation so be it. You're not alone. But it's no reason to cast doubt on anticoagulants in general and the motives of doctors prescribing them. They're the right solution for the majority of patients.
Hi Liz, keep in mind too that semantics and definitions are important here as well when defining ‘LAA’.
For example, when describing ‘LAA Isolation’, aspirin has no role to speak of in LAA-based and/or AFIB-Related stroke/TIA reduction. There your two choices are full time OAC/NOAC drugs with NOT missing any doses ... and/or LAA Closure via LAA Occlusion or Ligation.
And going for either the life-long OAC/NOAC option or for LAA Mechanical Closure are only relevant if the post LAA isolation 6 month TEE shows too low an LAA Emptying Velocity and reduced LAA Mechanical function from that 6 month TEE scan. About 58% of LAA Iso patients will have to chose between a life long OAC drug, or LAA Closure, leaving roughly 42% of LAA Iso patients being great candidates for stopping OAC drugs and foregoing LAA Closure ... which is the best odds anyone will ever get for stoping OAC drugs who have defined active LAA triggers to begin with!
In fact, no one with active LAA triggering will ever be taken off an OAC drug so long as they still suffer from bouts of AFIB/AFlutter (unless they undergo successful LAA Closure, and only then if their CHADSVASc score remains at least <2.0. So the whole debate is a bit of a Red Herring.
Aspirin can come into play, as used by Dr Natale at times, for folks who have had an LAA Occlusion with WATCHMAN or Amulet devices in which at this point long term aspirin is still included in the indefinite follow up routine for these devices in the US Guidelines ... aspirin is not required definitely in other parts of the World post LAA Occlusion. But the final verdict on how long an aspirin or baby aspirin might still be recommended after the 6 week course of an OAC drug plus aspirin/Plavix, post LAA Occlusion device is finished
and the patient is then just recommended to take one baby aspirin a day indefinitely at this time.
Also, a daily baby aspirin is still recommended for folks who have had a prior MI for the minor statistical reduction in second MI recurrence. And, of course, there is the common prescription for aspirin/Plavix for those with CVD and blocked coronary arteries who undergo PCI stent placement to open blocked coronary arteries. This use of aspirin is often applied by many Cardios for existing CVD in general, even in the absence of stents or blocked arteries... though this may be more a function of certain docs feeling better (themselves) just to be giving something rather than nothing to such patients.
As the full data from long term ongoing trials on Watchman/Amulet come in over the next year or two, it is quite possible the post LAA Occlusion aspirin regime may well be greatly shortened. Time will tell, but based on current data it looks promising that daily aspirin may not be a life-long requirement afterall once a comforatable level of confirmation from studies in which no OAC drugs and no anti-platelet drugs at all have been used during and after the LAA Occlusion procedure ... and so far with a very solid safety experience.
Shannon
Edited 1 time(s). Last edit at 04/16/2018 12:33PM by Shannon.
For example, when describing ‘LAA Isolation’, aspirin has no role to speak of in LAA-based and/or AFIB-Related stroke/TIA reduction. There your two choices are full time OAC/NOAC drugs with NOT missing any doses ... and/or LAA Closure via LAA Occlusion or Ligation.
And going for either the life-long OAC/NOAC option or for LAA Mechanical Closure are only relevant if the post LAA isolation 6 month TEE shows too low an LAA Emptying Velocity and reduced LAA Mechanical function from that 6 month TEE scan. About 58% of LAA Iso patients will have to chose between a life long OAC drug, or LAA Closure, leaving roughly 42% of LAA Iso patients being great candidates for stopping OAC drugs and foregoing LAA Closure ... which is the best odds anyone will ever get for stoping OAC drugs who have defined active LAA triggers to begin with!
In fact, no one with active LAA triggering will ever be taken off an OAC drug so long as they still suffer from bouts of AFIB/AFlutter (unless they undergo successful LAA Closure, and only then if their CHADSVASc score remains at least <2.0. So the whole debate is a bit of a Red Herring.
Aspirin can come into play, as used by Dr Natale at times, for folks who have had an LAA Occlusion with WATCHMAN or Amulet devices in which at this point long term aspirin is still included in the indefinite follow up routine for these devices in the US Guidelines ... aspirin is not required definitely in other parts of the World post LAA Occlusion. But the final verdict on how long an aspirin or baby aspirin might still be recommended after the 6 week course of an OAC drug plus aspirin/Plavix, post LAA Occlusion device is finished
and the patient is then just recommended to take one baby aspirin a day indefinitely at this time.
Also, a daily baby aspirin is still recommended for folks who have had a prior MI for the minor statistical reduction in second MI recurrence. And, of course, there is the common prescription for aspirin/Plavix for those with CVD and blocked coronary arteries who undergo PCI stent placement to open blocked coronary arteries. This use of aspirin is often applied by many Cardios for existing CVD in general, even in the absence of stents or blocked arteries... though this may be more a function of certain docs feeling better (themselves) just to be giving something rather than nothing to such patients.
As the full data from long term ongoing trials on Watchman/Amulet come in over the next year or two, it is quite possible the post LAA Occlusion aspirin regime may well be greatly shortened. Time will tell, but based on current data it looks promising that daily aspirin may not be a life-long requirement afterall once a comforatable level of confirmation from studies in which no OAC drugs and no anti-platelet drugs at all have been used during and after the LAA Occlusion procedure ... and so far with a very solid safety experience.
Shannon
Edited 1 time(s). Last edit at 04/16/2018 12:33PM by Shannon.
Shannon:
You said "In fact, no one with active LAA triggering will ever be taken off an OAC drug so long as they still suffer from bouts of AFIB/AFlutter (unless they undergo successful LAA Closure, and only then if their CHADSVASc score remains at least <2.0. So the whole debate is a bit of a Red Herring.
Shannon also said:, keep in mind too that semantics and definitions are important here as well when defining ‘LAA’., I agree and I will try to remember that.
So,it doesn't matter if undergoing a successful LAA closure if CHAD score is 2.0 or more, blood thinners are indicated---so of course for me it would be, over 75 and a woman, two right off the bat, I give up----I will try to use whatever I can to try and keep my blood thin.
I also have been under the understanding since originally coming to this site that we all were looking for knowledge, good or bad, different methods that posters have employed that has benefitted them in their quest for taming AF. There have been many posters that have related their stories about their doctors and their failed ablations, should they keep quiet because it may frighten new posters? For me, coming to this site made me feel a lot better about my AF knowing that others had episodes and it didn't kill them, it calmed me.
Liz
You said "In fact, no one with active LAA triggering will ever be taken off an OAC drug so long as they still suffer from bouts of AFIB/AFlutter (unless they undergo successful LAA Closure, and only then if their CHADSVASc score remains at least <2.0. So the whole debate is a bit of a Red Herring.
Shannon also said:, keep in mind too that semantics and definitions are important here as well when defining ‘LAA’., I agree and I will try to remember that.
So,it doesn't matter if undergoing a successful LAA closure if CHAD score is 2.0 or more, blood thinners are indicated---so of course for me it would be, over 75 and a woman, two right off the bat, I give up----I will try to use whatever I can to try and keep my blood thin.
I also have been under the understanding since originally coming to this site that we all were looking for knowledge, good or bad, different methods that posters have employed that has benefitted them in their quest for taming AF. There have been many posters that have related their stories about their doctors and their failed ablations, should they keep quiet because it may frighten new posters? For me, coming to this site made me feel a lot better about my AF knowing that others had episodes and it didn't kill them, it calmed me.
Liz
Hi Liz,
Your assumption that (in paraphrase) "undergoing a successful LAA closure, if stroke risk scores were 2.0 or greater, would offer no benefit" is not the conclusion at all I would draw.
First of all, most experienced EPs and even Cardio's will tend to determine your stroke risks not just on the cookie cutter CHA2DS2-VASc numbers alone .. these scores form the basis for making a more nuanced decision based on also including the individual patient. After the basic scores are calculated, smart docs will then consider individual variables for each patient in determining their actual overall stroke risk assignment. As such, most smart docs will often underuse 'Female sex' as an added point, especially if there are little to no other real CVD risk factors adding to a higher stroke score..
Once over 75yrs old there will be less 'discounting' of such stroke scores, but even then, when the person is in otherwise good cardiovascular health and doesn't have type two diabetes, is not significantly overweight or obese, has no sleep apnea and no longer has any AFIB ...even though having OSA and AFIB, oddly enough, do not add official points on these admittedly imperfect stroke score metrics ... Then, also using the all-important professional judgment and assessment of each individual person's overall health and CVD signs and symptoms along with adding in the stroke risk and bleeding risk scores, makes good common sense.
Dr Natale is known to discount a women's age in some cases, especially when she has taken very good care of her own health and has limited 'real world' risk factors like Hypertension, prior Strokes, TIAs or other CVAs (often the most significant risk factors) Vascular disease, T2Diabetes, etc. assuming that revised assessment of her stroke scores and overall CVD health results in an overall stroke score under 2 ... not counting her sex.
In any event, did you appreciate the rest of what I was saying about aspirin use? There are legitimate reasons for including aspirin in one's drug protocol, as I noted in my reply to your previous post above and as we discussed on the phone a couple of weeks ago Liz. But using Aspirin in lieu of a true blood- thinner such as a NOAC or Warfarin when AFIB/LAA-based stroke risk is one's primary concern, is little more than a waste of time,.and for some people is clearly counter-productive if they are prone to more bleeding risk with a daily aspirin.
Again, the exceptions in which a smart Doc like Dr Natale might cotinue recommending at least a baby aspirin include those patients of his that may also have had a previous MI and thus the risk/reward in possibly helping to prevent a second heart attack grants a very minor edge to continuing an 81mg baby a day. By extension though, some docs also stretch that recommendation rational to those patients who have had, or still have, AFIB and who also have clear cardiovascular disease with arteriosclerosis, plaque build up etc more as a preventative measure in those for whom they make a professional assumption that the risk reward of the baby aspirin 'probably' falls narrowly on the side of continuing the baby aspirin. However, there is remaining controversy about even this class of patients taking aspirin.
This is not at all true for those patients without prior history of CVD, or prior MI, and with no stents or other metallic devices implanted in the vascular system, few of whom will typically get an aspirin at all in place of a blood thinner by knowledgeable up-to-date EPs.
And the other group of patients who will get a daily aspirin are often those who have had a prior stent or other metallic device inserted into the vascular system where said device will be in contact with systemic blood flow, at least until complete endothelial-ization encases any metal exposed to blood flow.
In a case like yours Liz, with ongoing AFIB since you are ruling out an ablation process at your more advanced age, a strong case could be made too for an even more robust stroke-risk reduction protocol that might include both a Watchman and an oral anti-coagulant (OAC). Though in a case such as yours it might be possible to rely on a half dose of Eliquis along with a Watchman device in patients with little to no CVD risk factors making up your stroke scores. But clearly that would have to be discussed with Dr Natale or whatever doctor you choose, if you were to decide to install a Watchman.
One BIG advantage of having one's LAA closed off, especially with on-going AFIB, is not solely depending on a blood thinner for protection since even the best blood thinners are NOT guaranteed stroke/TIA preventatives and they certainly are not going to eliminate bleeding risks, just the opposite!
The very real possibility of being able to reduce the NOAC dose in half for some afibbers, assuming the overall individual's scenario makes that a good bet in combination with total closure of one's LAA, makes good sense and could be the safest course of action for many folks such as yourself who are otherwise quite healthy for your age and with minimal CVD risk factors.
Consider, too, the vagaries of not uncommon advancing memory decline in which doses of NOAC are often forgotten, and/or simple drug supply interruptions too can and do occur. The possible impact of such missed doses might not have such a risky consequence with a sealed up LAA! Especially for those living alone.
In any event, its not nearly as black and white as your assumption that, " ... If my stroke score is 2.0 or greater there it no benefit at all for considering an LAA closure since I will likely require life-long Oral anti-coagulant to some degree in any event,". This decision needs to be sorted through carefully with a very well-informed EP, in your case one who can help you assess all angles of your real world scenario.
Finally, in your last paragraph in your post above, you seem to be questioning whether or not Afibbers.org still encourages people to share their experiences with AFIB, as well as various therapeutic approaches and their outcomes? I''m not sure I understand where this is coming from Liz? Nothing at all has changed in our format or the foundation of this website and forum that promotes controlling or stifling dialogue about AFIB and not sharing the full range of experiences people have had during often years of trial and adjustments in learning how best to manage or eliminate this lousy condition from their lives.
This wonderful resource has always been a gathering place for folks of all walks of life who want to better understand all the best options available to them during the ever evolving course of their live's history in dealing with the challenges that living with AFIB certainly brings.
However, with that open investigation also comes the responsibility to do our best in vetting those options presented here, such that less well thought-out and less well validated concepts are giving a hearing, but are not automatically embraced as clear recommendations for our readers.
One of the things that make our forum somewhat unique is our focus of including the very best of cardiology and electrophysiology combined with the best of integrative/functional medicine that has also been well-vetted too, often by peer-reviewed research. And that many of us have found can confer at least strong anecdotal support offering some degree of help in managing AFIB and/or reducing life-style risks that we know contribute to a worsening of arrhythmia and cardiovascular health in general.
With this truly 'holistic' approach of combining the best of both ends of medical and nutritional/life style risk-reduction research, this forum and website can hopefully continue to contribute toward educating and fostering the most informed group of afibbers we possibly can, going forward. But in order to do so, we have to base our recommendations on careful discrimination and evidence-based analysis as well, and thus lend our support only to those protocols that are seen to work reliably and repeatedly over our almost two decades now as the oldest patient education and advocacy resource on the web.
Be well,
Shannon
Edited 1 time(s). Last edit at 04/23/2018 01:57AM by Shannon.
Your assumption that (in paraphrase) "undergoing a successful LAA closure, if stroke risk scores were 2.0 or greater, would offer no benefit" is not the conclusion at all I would draw.
First of all, most experienced EPs and even Cardio's will tend to determine your stroke risks not just on the cookie cutter CHA2DS2-VASc numbers alone .. these scores form the basis for making a more nuanced decision based on also including the individual patient. After the basic scores are calculated, smart docs will then consider individual variables for each patient in determining their actual overall stroke risk assignment. As such, most smart docs will often underuse 'Female sex' as an added point, especially if there are little to no other real CVD risk factors adding to a higher stroke score..
Once over 75yrs old there will be less 'discounting' of such stroke scores, but even then, when the person is in otherwise good cardiovascular health and doesn't have type two diabetes, is not significantly overweight or obese, has no sleep apnea and no longer has any AFIB ...even though having OSA and AFIB, oddly enough, do not add official points on these admittedly imperfect stroke score metrics ... Then, also using the all-important professional judgment and assessment of each individual person's overall health and CVD signs and symptoms along with adding in the stroke risk and bleeding risk scores, makes good common sense.
Dr Natale is known to discount a women's age in some cases, especially when she has taken very good care of her own health and has limited 'real world' risk factors like Hypertension, prior Strokes, TIAs or other CVAs (often the most significant risk factors) Vascular disease, T2Diabetes, etc. assuming that revised assessment of her stroke scores and overall CVD health results in an overall stroke score under 2 ... not counting her sex.
In any event, did you appreciate the rest of what I was saying about aspirin use? There are legitimate reasons for including aspirin in one's drug protocol, as I noted in my reply to your previous post above and as we discussed on the phone a couple of weeks ago Liz. But using Aspirin in lieu of a true blood- thinner such as a NOAC or Warfarin when AFIB/LAA-based stroke risk is one's primary concern, is little more than a waste of time,.and for some people is clearly counter-productive if they are prone to more bleeding risk with a daily aspirin.
Again, the exceptions in which a smart Doc like Dr Natale might cotinue recommending at least a baby aspirin include those patients of his that may also have had a previous MI and thus the risk/reward in possibly helping to prevent a second heart attack grants a very minor edge to continuing an 81mg baby a day. By extension though, some docs also stretch that recommendation rational to those patients who have had, or still have, AFIB and who also have clear cardiovascular disease with arteriosclerosis, plaque build up etc more as a preventative measure in those for whom they make a professional assumption that the risk reward of the baby aspirin 'probably' falls narrowly on the side of continuing the baby aspirin. However, there is remaining controversy about even this class of patients taking aspirin.
This is not at all true for those patients without prior history of CVD, or prior MI, and with no stents or other metallic devices implanted in the vascular system, few of whom will typically get an aspirin at all in place of a blood thinner by knowledgeable up-to-date EPs.
And the other group of patients who will get a daily aspirin are often those who have had a prior stent or other metallic device inserted into the vascular system where said device will be in contact with systemic blood flow, at least until complete endothelial-ization encases any metal exposed to blood flow.
In a case like yours Liz, with ongoing AFIB since you are ruling out an ablation process at your more advanced age, a strong case could be made too for an even more robust stroke-risk reduction protocol that might include both a Watchman and an oral anti-coagulant (OAC). Though in a case such as yours it might be possible to rely on a half dose of Eliquis along with a Watchman device in patients with little to no CVD risk factors making up your stroke scores. But clearly that would have to be discussed with Dr Natale or whatever doctor you choose, if you were to decide to install a Watchman.
One BIG advantage of having one's LAA closed off, especially with on-going AFIB, is not solely depending on a blood thinner for protection since even the best blood thinners are NOT guaranteed stroke/TIA preventatives and they certainly are not going to eliminate bleeding risks, just the opposite!
The very real possibility of being able to reduce the NOAC dose in half for some afibbers, assuming the overall individual's scenario makes that a good bet in combination with total closure of one's LAA, makes good sense and could be the safest course of action for many folks such as yourself who are otherwise quite healthy for your age and with minimal CVD risk factors.
Consider, too, the vagaries of not uncommon advancing memory decline in which doses of NOAC are often forgotten, and/or simple drug supply interruptions too can and do occur. The possible impact of such missed doses might not have such a risky consequence with a sealed up LAA! Especially for those living alone.
In any event, its not nearly as black and white as your assumption that, " ... If my stroke score is 2.0 or greater there it no benefit at all for considering an LAA closure since I will likely require life-long Oral anti-coagulant to some degree in any event,". This decision needs to be sorted through carefully with a very well-informed EP, in your case one who can help you assess all angles of your real world scenario.
Finally, in your last paragraph in your post above, you seem to be questioning whether or not Afibbers.org still encourages people to share their experiences with AFIB, as well as various therapeutic approaches and their outcomes? I''m not sure I understand where this is coming from Liz? Nothing at all has changed in our format or the foundation of this website and forum that promotes controlling or stifling dialogue about AFIB and not sharing the full range of experiences people have had during often years of trial and adjustments in learning how best to manage or eliminate this lousy condition from their lives.
This wonderful resource has always been a gathering place for folks of all walks of life who want to better understand all the best options available to them during the ever evolving course of their live's history in dealing with the challenges that living with AFIB certainly brings.
However, with that open investigation also comes the responsibility to do our best in vetting those options presented here, such that less well thought-out and less well validated concepts are giving a hearing, but are not automatically embraced as clear recommendations for our readers.
One of the things that make our forum somewhat unique is our focus of including the very best of cardiology and electrophysiology combined with the best of integrative/functional medicine that has also been well-vetted too, often by peer-reviewed research. And that many of us have found can confer at least strong anecdotal support offering some degree of help in managing AFIB and/or reducing life-style risks that we know contribute to a worsening of arrhythmia and cardiovascular health in general.
With this truly 'holistic' approach of combining the best of both ends of medical and nutritional/life style risk-reduction research, this forum and website can hopefully continue to contribute toward educating and fostering the most informed group of afibbers we possibly can, going forward. But in order to do so, we have to base our recommendations on careful discrimination and evidence-based analysis as well, and thus lend our support only to those protocols that are seen to work reliably and repeatedly over our almost two decades now as the oldest patient education and advocacy resource on the web.
Be well,
Shannon
Edited 1 time(s). Last edit at 04/23/2018 01:57AM by Shannon.
Does anyone have the links to the studies that discuss the LAA and BP? alxndr01@hotmail.com
Sorry, only registered users may post in this forum.