Deciding to take Eliquis with infrequent Afib

Hello all. I used to be on this forum 15 years ago for my husband's afib, but happily, after 1 flutter and 2 Afib ablations at Duke he is in sinus rhythm! The ablations saved his life because he had a hemorrhagic stroke from an AVM that blew 6 years ago and if he had been on blood thinners, I would not be so cheery!

I have had very infrequent Afib myself for the last 8 years. Perhaps two or three times a year, rarely longer than a few hours or at most, 6. Many times because of vagal pressure (e.g., coughing too long and too hard), dehydration, and during competitive tennis matches (I am 66 but play tennis 4 plus times a week, often in the heat in Durham, which does the trick). I went into Afib three times in April, for about 2 hours each tennis related. Liquid magnesium has helped me convert quickly through the years. I doubled my daily Magnesium to four tablets and did not have another incident until August at 2:00 a.m. (in sinus at 9 a.m.) after a dehydrating beach day (1 hour of tennis and 4 hours on the beach, plus a glass of wine at dinner). Made it through a lot of tennis too (it is obvious to me when I have Afib).

My electrophysiologist (who did my husband's ablations) strongly recommended I start Eliquis back in June and doubled up after my heart monitor results. I have been resistant for a number of reasons:

1. My athletic brother was in Afib for 20 years because his doctor told him not to have an ablation (infuriating) so he was on Coumadin all that time. He is 79 and has 40 plus bleeds in his brain and mini strokes but no connection to Coumadin. Right.

2. I had a heart monitor for a month in August which indicated Atrial Tachycardia but I don't know how often or under what circumstances or if I was in sinus. I expect it was always during 2-3 hour tennis matches in the heat when I did wonder about tachycardia myself--not flutter because about 140 beats/minute

3. I have not read about an increase in stroking from tachycardia since I am in sinus rhythm?

4. I take an SSRI which negatively interacts with Eliquis

5. The side effects folks have documented on this Forum are terrible.

6. I have a sleep study Friday for sleep apnea which my doctor has insisted on (I read 50% of affibers have this?), but doubt that is another issue, so waiting to see.

7. My "Act Partial Thromboplastin Time 26.5 sec and the normal range is 26.8 - 37.1 sec Not sure if this shouldn't be performed again.

8. I think I need clarity about the atrial tachycardia, like an echo maybe? Seems flimsy to just have the heart monitor's information.

9. I am taking chips of cardizem before I play tennis, which slows my rate down nicely (and makes me sleepy if too much but I am semi retired so have flexibility to power nap). I also have cut back on even a half cup of coffee before playing, which has helped.

I am asking for folks' opinions and advice about my thinking and options for further evaluation, if needed. If I was out of rhythm for 24 hours or more, I would think about an anti-arhythmic like Tikosyn or just have the ablation.

Thanks so much,

Karin

Looks like use of AC's is substantiated if AFIB or AT lasts longer than 5 minutes, and your CHAD2DS2 or ATRIA (age and history of strokes) score is => 2.

[www.acc.org]

Thank you for that article, which is actually rather terrifying. I did know my CHAD score was at least 2. Very helpful information but so different than "rule" for needing to be converted within 24 hours.

Hello Karin and welcome back. I'm certainly glad that all turned out well for your husband but sorry to read about your situation. You've detailed well your status and protocols. Be very aware of and diligent about balancing out your electrolytes...all of them and be sure you stay well hydrated at all times as dehydration, itself, can promote arrhythmia as can alcohol which also depletes magnesium.

When you mentioned taking the SSRI, I was reminded of study findings indicating they can contribute to arrhythmia which I learned when I corresponded with an afibber who was on SSRIs and having similar difficulties.

Here's a newer reference... and then one from 14 years ago. There are undoubtedly others... but you should definitely clarify with your EP the connection between the two before adding yet another drug/chemical to your system. Be sure also about the interactions with the cardizem.



Antidepressants categories and their cardiovascular side effects

Cardiovascular Considerations in Antidepressant Therapy: An Evidence-Based Review (2013)
Although antidepressants are commonly used in clinical setting, numerous negative effects of antidepressants on the cardiovascular system have been reported to date, including bradycardia, tachycardia, hypertension, hypotension, orthostatic hypotension, electrocardiogram (ECG) changes, electrolyte abnormalities, reduced cardiac conduction and output, arrhythmias, and sudden cardiac death.


Cardiovascular Side Effects of New Antidepressants and Antipsychotics: New Drugs, old Concerns (2004)
.....an increasing number of case reports have demonstrated that the use of SSRIs and new antipsychotics (e.g. clozapine, olanzapine, risperidone, sertindole, aripiprazole, ziprasidone, quetiapine) is associated with cases of arrhythmias, prolonged QTc interval on electrocardiogram (ECG) and orthostatic hypotension in patients lacking cardiovascular disorders, raising new concerns about the putative cardiovascular safety of these compounds
[www.ncbi.nlm.nih.gov]

Hope you can get this sorted out so you can continue your active live.

Jackie

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karin
2. I had a heart monitor for a month in August which indicated Atrial Tachycardia but I don't know how often or under what circumstances or if I was in sinus. I expect it was always during 2-3 hour tennis matches in the heat when I did wonder about tachycardia myself--not flutter because about 140 beats/minute

A rate of 140 doesn't rule out flutter at all. In fact, that's a very likely flutter rate. Anything near 150 with a regular rhythm is quite possibly 2:1 flutter, and flutter carries the same stroke risk as afib. Also, an echo can't diagnose arrhythmias. To get a definitive diagnosis of what that tachycardia is you'll need a 12-lead ECG during an episode.

All in all, I don't agree with your logic for avoiding ACs and I think you're taking unnecessary risks. Your brother's experiences aren't particularly relevant since modern NOACs have lower bleed risks than warfarin. And to keep it in perspective, there's a very good chance your brother would be dead or severely disabled today had it not been for the warfarin.

Thanks Jackie. I am so amazed you are still giving your excellent advice so many years later. You were so helpful to me in the past, even though you didn't know it! I am on a tiny dose of the SSRI but another questions for my EP.

Obviously the CHADS VASc score is the scoring system that is used by most people to figure out stroke risk, and far be it from me to argue with it. However there are at least two other scoring systems out there that would look different. One is the ATRIA scoring system

[academic.oup.com]

I'm assuming here that you're a 2 on the CHADS VASc because you're over 65 and female. If you look at the above paper you would score a 4 on the ATRIA scale. See table 1. Now looking at table 4, that gives you a 1.7% risk of stroke, which we see is somewhere between a CHADS VASc score of 0 and 1. Same table , next few columns.

Also John Day also argues against the CHADS VASc here in this article and he has a different scoring system that he claims is better. He specifically states that being female might be irrelevant.

[drjohnday.com]


Personally I have no clue which is correct. But it does make it difficult for corner cases like many of us to really weigh the noac decision.

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Brian_og
that gives you a 1.7% risk of stroke

To be clear, that gives her a 1.7% annual risk of stroke, which doesn't sound so bad, but people need to understand that annual risks are cumulative. A 1.7% annual risk translates to a 15.7% risk of stroke over 10 years, or 29% over 20 years. It's a non-trivial level of risk.

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Carey

that gives you a 1.7% risk of stroke

To be clear, that gives her a 1.7% annual risk of stroke, which doesn't sound so bad, but people need to understand that annual risks are cumulative. A 1.7% annual risk translates to a 15.7% risk of stroke over 10 years, or 29% over 20 years. It's a non-trivial level of risk.

Thanks. Crap. I didn't know that either.

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Brian_og


that gives you a 1.7% risk of stroke

To be clear, that gives her a 1.7% annual risk of stroke, which doesn't sound so bad, but people need to understand that annual risks are cumulative. A 1.7% annual risk translates to a 15.7% risk of stroke over 10 years, or 29% over 20 years. It's a non-trivial level of risk.

Thanks. Crap. I didn't know that either.

Hmm..that doesn't sound right. If your risk increases 1.7% this year, next year it's still 1.7%. It's like gambling..your chances of winning don't increase because you play more.

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jpeters
Hmm..that doesn't sound right. If your risk increases 1.7% this year, next year it's still 1.7%. It's like gambling..your chances of winning don't increase because you play more.

It is correct. That's how cumulative risks work. The 1.7% figure is the risk of having a stroke during a single year, and you're right that the chance next year will still be 1.7% for that one year, but if you change the question and ask what is the risk of having at least one stroke during the next 10 years, the calculation goes like this:

Probability of having at least one stroke = 1 − probability of never having a stroke

Probability of not having a stroke in a given year = 1 - .017 = 0.983

Probability of not having a stroke in 10 years = 0.983 ^ 10 = 0.842

Therefore, the probability of having at least one stroke in 10 years = 1 − .842 = 0.158 or 15.8%.

And, BTW, your chances of winning do increase if you play more. The odds don't change on each roll of the dice, but rolling the dice 10 times definitely increases your chances of winning at least once. It also increases your chances of losing, but that's a different (but similar) calculation.

Feel free to call your high school math teacher and check my work. ;-)



Edited 1 time(s). Last edit at 09/24/2018 04:52PM by Carey.

So according to the article posted by jpeters above even 5 mins AF or fast AT greatly increases stroke risk. Like by 5 or 10 times. So where does that leave all the traditional stuff I’ve read everywhere for the last 20 years saying no increased stroke risk unless an AF episode lasts over 24 or 48 hours?!

I recall - I think - Wolfpack saying he takes AC for a few days after every PAF episode - like an AC PiP if you like. Sounds sensible to me, but for just how long after an AF episode would one need to continue the AC for?

As for me, even with an ATRIA score (and CHADs) of 0 I still have a 0.4% annual risk of stroke. I wonder how much Apixaban reduces this by..... maybe down to 0.1% or 0.2%? Is that pretty much the same as non-AFrs?

Did the study where the 1.7% increased risk was quoted say for every year?

Could you please tell me what the abbreviations stand for? I know pip is pill in pocket. 'Is an aspirin? Thanks.

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jpeters
Did the study where the 1.7% increased risk was quoted say for every year?

Stroke risk is normally quoted as an annual risk and that number jives with other sources I've seen for a CHADS 1.

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Erin
Could you please tell me what the abbreviations stand for? I know pip is pill in pocket. 'Is an aspirin? Thanks.

Aspirin is abbreviated as ASA, and you do correctly understand PIP. Are there other abbreviations you don't understand?

Thanks so much everyone's contribution.

Wonder what the general population risk for a stroke is?

I think I actually understand Carey's explanation of cumulative risk! I will not tolerate the atrial tachycardia or flutter, or Afib outbreaks for 10 years because I will have an ablation if I increase above my 2 times a year Afib. I need to understand this tachycardia better as that is new but I can feel it now (like in a too long tennis match in the heat and getting dehydrated). I am backing off competitive tennis in hot weather and decreasing caffeine. I do see my EP on 10/29 so you all have helped me feel like if I play it safe, I could wait until a face to face with him. He is very bright, studied with Natale when Natale was at Duke I believe, has done the 1000 plus ablations, and his success rate is quite good (I don't have the exact number at hand). And he did great with my husband so we are asking for a group rate!

mwcf--I am glad you are asking about this 5 to 10 minute risk result and what I have also heard for 15 plus years about getting cardioverted within 24-48 hours. I asked my EP who thought I should go before 24 hours to be safe. I typically have afib for 2-7 hours and rarely have been able to get to doctor, urgent care or the ER (I converted in the waiting room) to get a 12 Lead ECG. Tachycardia so far lasts minutes or at most an hour, but only when I have pushed it in tennis in the heat.


Brian--thanks for the scoring systems! You are so kind to check into my score too! Will look at your links.

QUESTION? Have you all noticed if there are a lot of people complaining of serious side effects of Eliquis (e.g., nausea, joint pain, fatigue) as I have read on this forum?

Than you Carey. Wolfpack takes AC after an episode. Not sure about AC. Thanks again. Is that also aspirin or is it another drug?

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Erin
Than you Carey. Wolfpack takes AC after an episode. Not sure about AC. Thanks again. Is that also aspirin or is it another drug?

Around here AC usually means anticoagulant (but that's not a standard medical abbreviation like ASA for aspirin is). The anticoagulants are warfarin and all the NOACs such as Eliquis, Pradaxa, Xarelto, etc. Aspirin is not an anticoagulant; it's an anti-platelet. Big difference, actually, and the major reason aspirin can be more dangerous than the anticoagulants. The NOACs all have fairly short half-lives, like on the order of 12 hours or so for most. So that means if you have a major bleeding incident that can't be controlled, the doctors only have to support you for a day or so before the anticoagulant wears off. But aspirin disables platelets, and it takes your body 7 days to replace all your platelets, so a single dose of aspirin will make you clot slower for a week. Add that to the fact that anticoagulants do not cause bleeding. They will prolong bleeding caused by something else, but they do not cause it. Aspirin, however, can actually cause bleeding (in the GI tract) and it will prolong that bleeding just as well or better than anticoagulants will.

Taking aspirin instead of anticoagulants because you think it's safer is like driving cross-country because you think it's safer than flying.

Okay, end of aspirin rant. ;-)

Oh, and for full disclosure, I'm taking aspirin and will be for at least the next 4.5 months. It has its uses; it's just that afib isn't one of them.

Carey said: Add that to the fact that anticoagulants do not cause bleeding. They will prolong bleeding caused by something else, but they do not cause it" I took Coumadin for a few weeks and got bloodshot eyes never had anything like that before taking Coumadin, had to stop the Coumadin, my mother was on Coumadin for a few years, she had internal bleeding, she had black, tarry stools, doc stopped the AC, I would like to see some stats on strokes caused by AF of those taking some natural means or aspirin and stats of strokes of people that are on ACs. There are a lot of stories about the problems caused by ACs, strokes and even death.

Liz

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Carey

Did the study where the 1.7% increased risk was quoted say for every year?

Stroke risk is normally quoted as an annual risk and that number jives with other sources I've seen for a CHADS 1.

Risk assessment is determined by studies that are typically long term that compare large groups. Example: "AFIB patients are 5X more likely to have stroke." I don't think you'll find a study in which stroke risk increased 29% because it was followed for 20 years, high school mathematics aside. (People in the control group have more strokes over time as well).



Edited 1 time(s). Last edit at 09/25/2018 01:04AM by jpeters.

Interesting discussion! I have been in nsr for 15 years since ablation and touch up in Bordeaux, but since I am female and over 80 years old I should be taking anticoagulants.

I choose not to for various reasons. I avoid medication of any kind unless it will be lifesaving - seems to me that all medications have side effects which then require another medication, which has side effects and so on...

I do take fish oil and nattokinase, I take magnesium, potassium, taurine and d-Ribose. I exercise three times a week, I lost 80 pounds post ablation and have maintained a normal weight since then. Until last year I did 3 scuba diving trips a year in remote parts of the world. I eat healthy, except when I’m on holiday when I eat and drink all my favourite things with gay abandon.

Seems to me that in the end it’s all a gamble, our days are numbered. We can look at the statistics but they won’t tell us how long we have left. I am glad I have the right to make my own choices, even if they might turn out to be foolish ones. But of course I won’t be around to worry about that!

Gjill (pronounced Jill, and female)

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jpeters
(People in the control group have more strokes over time as well).

I'm currently in the land of very little and very spotty wifi bandwidth, so looking up studies is difficult Point is that the control group will have a non-zero stroke risk that increases with age. Also, as I recall, warfarin will reduce whatever your statistical stroke risk is in half, the studies of the new AC's compare them to warfarin and they are acceptable if they are "non inferior."

I'm guessing that at some low level of stroke risk the bleeding risk will counter the stroke risk reduction, hence AC's are not prescribed below a certain risk.

As to aspirin, my doc had me on 83 mg/day to enhance the anti inflammatory properties of fish oil. My forearms started looking like someone on warfarin who was above the therapeutic range. Hence I quit the aspirin. I rock climb all the time, so my limbs are normally bruised, scratched and scabby from paying "tithes to the rock god," but this was a lot worse.

Just a comment on the overall risk of stroke... which has to do with blood's hypercoagulability property... a topic that has been discussed in various previous posts explaining the science of Hemorheology and the sheer-stress factor that influences clotting tendencies. This equates to thick, sticky blood which then has the tendency to form clots more easily... whether or not you experience AF events. There are natural remedies that help keep blood 'thin and slippery' and there are lab tests that can be done routinely to monitor that so you stay in the safe ranges.

I used these for many years during my afib onset and then eventually, after my initial ablation because warfarin/Coumadin was the only available anticoagulant at the time... and since I have low platelets, it was extremely difficult to maintain the requisite INR.

(Obviously, aspirin is out for me.) From the onset of the initial AF (age 59) to the first ablation, it was 8 years and as is typical, I started with relatively low event recurrence and escalated to many, close together and for long durations...typically 20+ hours. Then I had the Exatest and learned I was low in magnesium and potassium. I had a date for an ablation in 6 months and I decided to do all I could to reverse the event recurrence. After 3 months of intense repletion of electrolytes, I went to zero AF and was on the fence about cancelling the ablation date but as I’ve commented, a change in my insurance was upcoming so I went ahead and kept the date with Dr. Natale.

Once I was free to stop warfarin post-ablation, I went back on the natural protocols including Nattokinase (fibrinolytic enzyme) that kept all my lab ranges in the low risk for hyperviscosity and continued faithfully until 11 years later when I began having flutter episodes which I knew would need to be ablated. I was prescribed Eliquis and remain on half dose.

The side effects of Eliquis are real and undoubtedly affect some individuals, more than others, but since I am typically sensitive to chemicals and drugs, the side effects for me are worsening with time. Since it’s the only medication I take, it’s fairly obvious that’s the culprit.

I agree with Gill’s summary statement. Thanks Gill. I’m so glad you are enjoying life.

Jackie

In one of the studies mentioned in the John Day article above it states the following:

"Atrial fibrillation (AF) is a commonly encountered arrhythmia, which is not yet fully understood. Catheter ablation has shown to be an effective strategy for rhythm management and several small or retrospective studies have shown that stroke rates are decreased in ablated AF patients compared to those medically managed. Several studies even show that ablation returns stroke risk to that of non-AF patients. Large scale, prospective trials will further illuminate this connection and provide mechanistic understanding of the role of the procedure versus the process of selection for the procedure and peri- and post-procedural therapy and management. Furthermore, modification of risk factors associated with AF show a significant increase in the sustained success of AF ablation and can also moderate the progression of AF."

Does anyone know anyone that recommends just stopping AC after a successful Ablation? Depending on how we define successful also I guess.

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Brian_og


Does anyone know anyone that recommends just stopping AC after a successful Ablation? Depending on how we define successful also I guess.

That's the point, but only after the blanking period and only if all arrhythmia is gone.

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karin
QUESTION? Have you all noticed if there are a lot of people complaining of serious side effects of Eliquis (e.g., nausea, joint pain, fatigue) as I have read on this forum?

It seems that Eliquis is the most prescribed NOAC for people on this forum, so you'll read more about it.
Here in Belgium, it seems Xarelto and Pradaxa are more often prescribed than Eliquis.
Having taken successively Pradaxa, Xarelto, Lixiana (= Savaysa) and Pradaxa again, I've noticed I'm doing better with the latter than with Xarelto and Lixiana. I've not tried Eliquis.
I've asked the question to my pharmacist, and she replied it's just a personal thing. She's got good and bad reports for each of those NOACs.

The question is, WHY does the stroke risk increase each year? What is the cause?
It doesn't make any sense that your risk factor can be 1.7 and the nest year it's approx double.
WHY? What is the cause?

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colindo
The question is, WHY does the stroke risk increase each year? What is the cause?
It doesn't make any sense that your risk factor can be 1.7 and the nest year it's approx double.
WHY? What is the cause?

It does not increase each year. Your risk of having a stroke in 2018 is exactly the same as your risk of having a stroke in 2019, 2020, and so on (until your CHADS-Vasc score changes).

What I was trying to explain is that risk is cumulative. It's exactly like rolling dice. Your odds of rolling a particular number is exactly 1-in-6 every time you roll a single die. No matter how many times you roll, your odds of rolling that number are the same each time. However, the more times you roll, the more likely it is that you'll eventually roll that number. Makes sense, right? The more tries you make, the more likely it is you'll eventually roll the number you're looking for. The same thing happens with stroke risk. Think of living for a year as being like rolling the dice one time. If you roll the dice once a year, every year for 10 years, the odds that a stroke will happen at least once will go up by the formula I explained earlier.

Similar analogies abound. The odds of you being in a car crash is the same for every mile you drive, but driving 100 miles obviously puts you at greater risk of an accident than driving one mile. That's exactly the same math at work.

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Brian_og
Does anyone know anyone that recommends just stopping AC after a successful Ablation? Depending on how we define successful also I guess.

Sure, Natale will for some patients. So will my local EP. A lot of EPs will advise patients to stop anticoagulants following a successful ablation, but it depends on their CHADS-Vasc score and the EP's assessment of their stroke risk from other aspects. But there is no standard formula for who can stop and who can't. It's very patient specific.

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Carey

Does anyone know anyone that recommends just stopping AC after a successful Ablation? Depending on how we define successful also I guess.

Sure, Natale will for some patients. So will my local EP. A lot of EPs will advise patients to stop anticoagulants following a successful ablation, but it depends on their CHADS-Vasc score and the EP's assessment of their stroke risk from other aspects. But there is no standard formula for who can stop and who can't. It's very patient specific.

Noted Carey and thanks as always for your input, but at Bordeaux the protocol is AC for 3 months after ablation for all patients including paroxysmal AFrs and regardless of CHADS-Vasc score. Likely in case of possible blanking period arrhythmia episodes plus I’m sure I’ve read before that ablation-related embolisms can occur as much as 90 days after an ablation. And see for example.....

[www.medscape.com]



Edited 1 time(s). Last edit at 09/25/2018 05:44PM by mwcf.

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mwcf
Noted Carey and thanks as always for your input, but at Bordeaux the protocol is AC for 3 months after ablation for all patients including paroxysmal AFrs and regardless of CHADS-Vasc score.

Yes, sorry for not being clear. I wasn't counting the blanking period. All EPs will insist on ACs for at least 90 days following an ablation. And that's way to soon to declare success anyway. Six months would be the minimum, and true success is defined as no atrial tachycardias after the blanking period for one year without the need for antiarrhythmic drugs.

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colindo
The question is, WHY does the stroke risk increase each year? What is the cause?
It doesn't make any sense that your risk factor can be 1.7 and the nest year it's approx double.
WHY? What is the cause?

Not per Carey's example, but stroke risk in general increases as we age, afibber or not. Just like blood pressure and heart disease risk. However, this is not true for all, and is likely lifestyle related. For example at 63, I strive to keep my BP at 105/65 without meds. I also strive to keep my blood sugar low with fasting around 4.1 mmol/L in your units (75 mg/dL for the US), and so on for all the metabolic markers. From my reading there is a correlation of blood viscosity with these other metrics.

George

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GeorgeN
Not per Carey's example, but stroke risk in general increases as we age, afibber or not. Just like blood pressure and heart disease risk. However, this is not true for all, and is likely lifestyle related. For example at 63, I strive to keep my BP at 105/65 without meds. I also strive to keep my blood sugar low with fasting around 4.1 mmol/L in your units (75 mg/dL for the US), and so on for all the metabolic markers. From my reading there is a correlation of blood viscosity with these other metrics.

Good point about risk rising as we age, but I didn't want to muddy the waters with that since the change from one year to the next is barely measurable. You get one more CHADS point at 65, but I'm pretty sure that on the morning of your 65th birthday nothing significant happens to your stroke risk.

Oh, and your dedication to managing your afib with near-superhuman efforts is impressive, but I don't think you've defeated the aging thing. So saying it's not true for all isn't quite right. You've delayed it or slowed it, probably significantly, but nobody can eliminate it.

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Brian_og
In one of the studies mentioned in the John Day article above it states the following:

"Atrial fibrillation (AF) is a commonly encountered arrhythmia, which is not yet fully understood. Catheter ablation has shown to be an effective strategy for rhythm management and several small or retrospective studies have shown that stroke rates are decreased in ablated AF patients compared to those medically managed. Several studies even show that ablation returns stroke risk to that of non-AF patients. Large scale, prospective trials will further illuminate this connection and provide mechanistic understanding of the role of the procedure versus the process of selection for the procedure and peri- and post-procedural therapy and management. Furthermore, modification of risk factors associated with AF show a significant increase in the sustained success of AF ablation and can also moderate the progression of AF."

Does anyone know anyone that recommends just stopping AC after a successful Ablation? Depending on how we define successful also I guess.

I suspect John Day is onto something (or my wishful thinking?)
My Cardiologist recommended against my stopping AC a year ago but i did anyway as i was not in afib for about one year.
Last week i got the AF back (HR90 - 130) and began taking Eliqus and Sotalol after 2/3 hours or so again.
Still taking it after 9 days even though my HR is in the 50s/60s and sometimes up to 90s/110s for short instances but predominately in the lower ranges.

Chads etc scores are valuable but i think George is onto something with diet and life style.
Can't see any reason for stroke risk to increase in non AF people with risk factors as low as George mentions. Perhaps LAA appendage shape and ejection fraction of it and generally come into it as well? Ah, and a coronary calcium score of zero would help? Mine is 36 so i don't know what to think re AC for me

BTW, love your attitude Gill! (post 373) Hope i get there some day

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Carey


Good point about risk rising as we age.



That is the question, what causes the risk to rise as we age?
Is it the junk that flows around in our blood caused by the increase in fibrinogen etc.?
If so then natto can clean most that up, and lower fibrinogen levels.

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Carey



Similar analogies abound. The odds of you being in a car crash is the same for every mile you drive, but driving 100 miles obviously puts you at greater risk of an accident than driving one mile. That's exactly the same math at work.

Good drivers acquire experience, so can actually lower their risk. When experience won't help, say playing a slot machine, a lot of data points eventually approaches the true odds against you. In the beginning, however, it's pure chance, so winning or losing streaks are not uncommon.

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Carey

Does anyone know anyone that recommends just stopping AC after a successful Ablation? Depending on how we define successful also I guess.

Sure, Natale will for some patients. So will my local EP. A lot of EPs will advise patients to stop anticoagulants following a successful ablation, but it depends on their CHADS-Vasc score and the EP's assessment of their stroke risk from other aspects. But there is no standard formula for who can stop and who can't. It's very patient specific.

But that confuses me too. If the ablation is successful then why bother looking at the CHADS VASc score at all. They don't give AC to non afibbers with scores above 1 or 2 or even more as far as I know. The only way this makes sense to me is if they are never sure that an ablation has been really "successful". Is that the case?

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Carey

that gives you a 1.7% risk of stroke

To be clear, that gives her a 1.7% annual risk of stroke, which doesn't sound so bad, but people need to understand that annual risks are cumulative. A 1.7% annual risk translates to a 15.7% risk of stroke over 10 years, or 29% over 20 years. It's a non-trivial level of risk.

I didn't want my original point/question to get lost here but according to the ATRIA scoring system Karin's 1.7% chance of stroke would place her between 0 and 1 on the CHADS VASc scoring system, rather than the 2 she's now getting. That's the difference between don't worry about AC and definitely use AC.

Another article re ATRIA

[www.the-hospitalist.org]


"Bottom line: The ATRIA risk score better identifies Afib patients who are at low risk for stroke compared to CHADS2 and CHA2DS2-VASc scores."

Here is a paper Prediction of stroke or TIA in patients without atrial fibrillation using CHADS2 and CHA2DS2-VASc scores
<[pdfs.semanticscholar.org]

Stroke, TIA & death risk do increase materially in non-afibbers.

I think there is a calculator where you can predict stroke risk by age with or without afib, including CHADs or whatever risks. There are also papers showing the impact of OAC (risk reduction). Doing this for yourself would give you an idea of your risk and risk reduction by taking OAC's. That is the way to make an informed decision.


Separately:

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Carey
Oh, and your dedication to managing your afib with near-superhuman efforts is impressive, but I don't think you've defeated the aging thing. So saying it's not true for all isn't quite right. You've delayed it or slowed it, probably significantly, but nobody can eliminate it.

I'm well aware that I'm aging. My objective is to have my health span and life span coincide as closely as possible. Also to be able to continue to follow my active passions. I look at not having metabolic issues as foundational. While detraining from endurance exercise is part of my "system," maintaining a very high level of fitness using other modalities is also very important.

In the article that George has given a link to has this about anticoagulants:

The trials involving dabigatran and apixaban were stopped early
because of increased bleeding rates.

Carey says anticoagulants don't cause bleeding?

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colindo
That is the question, what causes the risk to rise as we age?
Is it the junk that flows around in our blood caused by the increase in fibrinogen etc.?
If so then natto can clean most that up, and lower fibrinogen levels.

Blood clots when the flow gets turbulent. Smooth endothelia (inside walls of ateries) promote smooth, laminar flow. As we age, those inner walls get "stuff" stuck on them (plaque), and they also get less "stretchy" so the pressure goes up and the flow becomes more turbulent. This is why your cardiologist likes to listen to your carotids when he or she examines you. He's listening for something called bruit (brew-wee) and it is the sound of turbulent blood flow, and its easiest to hear in that location given the arteries' close proximity to the surface of the skin.

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Elizabeth
Carey says anticoagulants don't cause bleeding?

They don't. The only prolong bleeding caused by other things.

So why does stopping an anticoagulant causes bleeding to cease? Oh well, believe what you want and so will I.

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Elizabeth
So why does stopping an anticoagulant causes bleeding to cease?

Because the anticoagulant effects wear off and your blood coagulates again.

Warfarin will cause bleeding, it eats away at the arteries, that's how it kills rats.

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colindo
Warfarin will cause bleeding, it eats away at the arteries, that's how it kills rats.

Never heard that one. Got something to back that up?

Warfarin-induced gastric bleeding


[www.ncbi.nlm.nih.gov]

also

[abcnews.go.com]



Edited 1 time(s). Last edit at 09/27/2018 06:37PM by colindo.

The first paragraph of the abcnews story pretty much sums it up. As I said, anticoagulants prolong bleeding caused by other things. They don't cause bleeding. Warfarin eating away at the arteries is particularly the thing I wanted to hear about. I don't believe that's true.

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Carey
. Warfarin eating away at the arteries is particularly the thing I wanted to hear about. I don't believe that's true.

"How much warfarin will kill a rat?
Mice and rats like the taste of the bait, while the warfarin prevents their blood from clotting which will kill the rodents within a few days because of bleeding into their brain. The safety of warfarin was not determined in humans until a farm worker attempted to commit suicide by eating the rat poison"


[www.setma.com]



Edited 1 time(s). Last edit at 09/28/2018 02:47AM by jpeters.