Dr John Day regarding scepticism re CHADS VASc score

Interesting article regarding his reasons for not trusting the CHADS VASc for AFib

[drjohnday.com]

Don't seem to be able to find what his IMRS VASc score is about though.

Aside rrom the article, what are the members' opinion of Dr Day? I think he's done over 4000 ablations.

Thanks for posting, good article, I could never understand why doctors put people on blood thinners when they have only a couple of short AF episodes a year.

Liz

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Elizabeth
Thanks for posting, good article, I could never understand why doctors put people on blood thinners when they have only a couple of short AF episodes a year.

Because people with afib are at higher risk of stroke regardless of whether they're actively in afib. A large percentage of strokes occur with no recent afib episodes.

That said, I think the article raises some very good points. I don't think it's reasonable to say the article gives reasons for not trusting the score. That's an overstatement. It's still the only objective method available for judging stroke risk, but it does highlight some weaknesses and point out ways it needs to be improved.

It Assumes Your Atrial Fibrillation Burden Doesn’t Matter

Common sense would tell you that when it comes to your atrial fibrillation stroke risk, being out of rhythm all the time is probably much riskier than only being out of rhythm less than 1% of the time. And, as you might suspect, studies back this up. CHADS-VASc, however, doesn’t care. To the CHADS-VASc score, one brief minute of atrial fibrillation carries the same risk as one year of continuous atrial fibrillation.

I like the article, but I wish he hadn't expressed things in percentages. 1% of what amount of time? Statistics suggest that TWO HOURS of sustained AF is enough for a clot to form. That, of course, will be dependent on the individual and his or her blood viscosity and tendency to coagulate. My takeaway from the article is that it argues well for a PIP approach using DOACs for paroxysmal AF patients. I can tell you that I have Eliquis in my medicine cabinet, and if I have an episode exceeding 2 hours I will take it. I'll also stop it 24 or 48 hours after the episode terminates. The one exception being that if I ever get cardioverted, I'll take if for the entire month following.

Carey

I read his point that there are other *objective* methods. It's just that they are not the official ones. He's not even convinced CHADS VASc is better than the old one.


"Are there Any Better Scoring Systems?
Given the limitations of the CHADS-VASc scoring system, is there anything else out there? Yes, other scoring systems have been proposed. For example, there is the ABC-Stroke system which uses blood tests to help determine your stroke risk. Other scoring systems include GARFIELD-AF, ATRIA, and the Intermountain (my hospital) scoring system. "

Being new to this, I've been thinking about this a lot. The score system always seems a little weird to me in that it pretty much says everyone takes a blood thinner especially if you are a gal (though I thought thinners started at 2, not 1).

I seem to be plagued with arrythmia, but my 48 monitor only had me in AFib 0.03% of the time, longest for 4 minutes. Perhaps the 30 day monitor will tell me something different, (still waiting for the results), but I've certainly been wondering if that is worth blood thinners. I also find it odd that no one seems at all concerned about all the other arrhythmia I'm having.

It is also disconcerting that you get no points for the good stuff. My echo was normal, my heart MRI normal, my Utah score really low. I am battling BP a bit, but even that is not off the charts bad. (I also have questions about how he HBP is diagnosed!) I am still waiting for results of my stress echo.

Also, if the left atrial appendage is a big deal, how come the MRI doesn't even mention that?

If nothing else I appreciate this article being posted, as I'm by interested in reading about these other scoring systems.

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Brian_og
I read his point that there are other *objective* methods. It's just that they are not the official ones. He's not even convinced CHADS VASc is better than the old one.

Yeah, I get that, and as I said I think the article raised some very good points, but I just think saying he doesn't trust CHADS-Vasc is a bit of an overstatement. There is objective data showing that CHADS-Vasc scores do in fact correlate well with actual stroke incidence. Maybe the better assessment would be that CHADS-Vasc is too blunt of a tool.

About 12 years ago, Mayo's published a 30 year study on Lone Afibbers that lived in Olmstead County MN, which is the MN location for Mayo. The upshot was the afibbers were actually healthier than the general population - likely because they were "Lone" and many were athletes. However as time wore on, they got all the comorbidities of the general population. I decided that would not be me.

Back then, I looked at the CHADs2 score and asked myself, what is my stroke risk without afib and with it, and which risks can I modify - hypertension & T2 diabetes (at the time I was <54 years old)? You can use a calculator like this <[stroke.ucla.edu] to do the exercise. At that time, my stroke risk was 2.6% without afib, over 10 years, if I had afib, my risk would jump to 4.7%, Still lower than my age group risk without afib (5.9%). If I had moderate hypertension and T2 diabetes, again without afib, my risk would be 7.3% over 10 years. In Table 2 from this <[academic.oup.com] you can see that warfarin reduces the stroke risk by about 50%.

So my approach was 1) keep my blood pressure very low, without meds and 2) keep my glucose/insulin system as far away from T2 as possible (I keep my fasting blood sugar <80 mg/dL, my A1c <4.8% and my fasting insulin in the 2 range). I also created my system of electrolyte optimization to keep myself in afib remission as much as possible. Lastly, I decided I would not wait for a "natural" conversion on any afib episode I could not convert in a few minutes with exercise or positional adjustment (or more recently increasing serum CO2). I would chew the bad tasting flec to speed its delivery to my system as soon as I noticed I was in afib. I also trained myself to be able to check my pulse by just putting my attention on it to make sure it was in NSR. I could do this more than a couple of times a day without interrupting anything I was doing.

Even with minor bouts of afib, I would still have a lower risk than my age matched peers. In reality, because my burden is very low, I likely have a very reduced risk of stroke. Reducing it further with a med was, to me, unwarranted. As I've gotten older the base risks have increased, but the relative risks are about the same.

Note - stroke risk is not 0 even without afib. Also a med doesn't reduce it to zero, it reduces the risk about 50%. NOACs are deemed "non inferior " to warfarin. Hence have about the same risk reduction.

I'm not saying what I'm doing is right or that it will work for anybody else. Just going through how I analyzed it for myself.



Edited 2 time(s). Last edit at 07/26/2018 08:17AM by GeorgeN.

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Carey
Because people with afib are at higher risk of stroke regardless of whether they're actively in afib. A large percentage of strokes occur with no recent afib episodes.

Surely a lone PAFr only has a higher stroke risk during an episode and for maybe a week tops afterwards rather than in the weeks/months-long periods between episodes? In other words, I'm figuring the only way a PAFr is at higher stroke risk than the general population all of the time is owing to the co-morbidities that so often go hand in hand with/contribute to precipitating AF.

FWIW I've always been told I didn't/don't need an AC with a CHADs score of 0. That said, wolfpack's Elequis PiP approach certainly makes good sense and is a strategy I will deploy in the future myself.



Edited 1 time(s). Last edit at 07/26/2018 03:19AM by mwcf.

Interesting he had another article that recommends a PIP Anti Arrythmias drug to keep the attack under 24hrs, and thereafter a PIP blood thinner, both of which you guys are talking about

[drjohnday.com]

Brian - thanks for posting this very refreshing report. Dr. Day's website is loaded with great information.
Take note of the Editorial Board members at this link [www.innovationsincrm.com]

And this link [www.innovationsincrm.com]

George - excellent response, as usual. Thanks.

Jackie



Edited 1 time(s). Last edit at 07/26/2018 09:47AM by Jackie.

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mwcf
Surely a lone PAFr only has a higher stroke risk during an episode and for maybe a week tops afterwards rather than in the weeks/months-long periods between episodes?

It would be nice if that were true but it's not. Strokes are more common among afib patients even when they haven't had an afib episode in months or even years. And actually, there's probably no such thing as lone afib. Current thinking is that afib is a symptom of an underlying disease known as atrial myopathy. I've talked to Shannon about removing the words "lone afib" from the site and he agrees it needs to be changed.

Carey,

Thanks for the clarification.

Here's an interesting article about atrial myopathy:

[www.ncbi.nlm.nih.gov]

Atrial myopathy to me looks like a catch-all phrase for all sorts of precipitating factors such as atrial fibrosis and ANS/electrolyte imbalance/s. Each person with AF is likely to have their own unique mix of these factors. I've had PAF for almost 20 years and am still paroxysmal whereas many AFrs become persistent and then permanent quite quickly as in a few years.

From the above article:

"The parasympathetic nervous system may have a more dominant contribution to AF substrate – primarily by leading to shortening and heterogeneity of refractoriness in the atria – with the sympathetic nervous system playing a more modulatory role. The pulmonary veins, often involved in the pathogenesis of AF, are much more densely innervated - with both parasympathetic and sympathetic nerves – than the rest of the LA"

FWIW and IMO only, I put myself more in the 'ANS/electrolyte issues' category and I'd broadly put those who progress to persistent/permanent AF quite quickly in the atrial fibrosis category.

Great discussion guys!

Mike F



Edited 1 time(s). Last edit at 07/26/2018 04:32PM by mwcf.

Carey said It would be nice if that were true but it's not. Strokes are more common among afib patients even when they haven't had an afib episode in months or even years". How about some stats to prove your statement.

L

Carey, you have to ask what causes a stroke to form in the first place. Right.
Fibrin causes the platlets to stick together and build up, Natto and nattokinase dissolves fibrin, problem solved..

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Jackie

Take note of the Editorial Board members at this link [www.innovationsincrm.com]

That's a who's who of the heavy hitters in electrophysiology. Very impressive.

Colindo - Yes... very important point... and then you also have to ask and evaluate, what sets the stage in each individual that makes clot formation conducive or more likely? The #1 influencing factor is Silent Inflammation. Others are mentioned in the previous posts on Silent Inflammation, Clot Risk, etc. Lifestyle risk factors are included and risk from oxidative stress damage.

As people age, they lack various natural, intrinsic systems that help keep those risk factors controlled. One factor is the production of natural enzymes since some of those start to diminish as people approach age 30. So, while the 'senior' population is obviously, a logical target for risk factors, people not yet considered 'seniors' are also at risk and that's why those specialized tests for the markers of inflammation are so important to monitor for overall healthy blood flow and less tendency for adverse clotting. And, of course, just as you mention, the use of natural enzymes that manage fibrin.

I will forever be grateful and also very impressed with the efficacy of the nattokinase I took during the years prior to my ablation that kept me safe during many long bouts of AF that often lasted 24 hours and more. A day off, and then, it would start again. And, I was in my 60's so obviously considered a prime clot risk patient. However, I did keep close track of those critical markers as well and continue to do that to this day. If I were to get off Eliquis, I'd be right back on nattokinase - in a heartbeat.

Jackie

From another board: <[www.apoe4.info] and ~25-30% of the population have at least 1 ApoE4 allele...

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Stacey

1. ApoE4 (genotype) doubles your risk of ICH (Intra Cranial Hemorrhage)
2. Warfarin doubles anyone's risk of ICH
3. The combination of e4 and warfarin risk of ICH is much greater than additive
4. People who have E4 have much poorer outcomes and more frequent death from ICH than from stroke
5. ICH is much more dangerous and damaging than stroke
6. Afib increases the onset of Alzheimer's

So I am a bit in a panic mode. What is very disheartening is that, here in Minnesota, cardiologists and electrophysiologists seem to know nothing about apoe4. My Chad Score stroke risk is 2.2%. My ICH risk, with anticoagulation, is somewhere between 10% and 36%. Yet my doctors think one must charge ahead with anticoagulation.

From the Olmstead County MN paper, "Equally important is the finding that thromboembolic complications occurred only after the development of risk factors (including advanced age), highlighting their important interaction with atrial fibrillation."

"The risk for stroke/transient ischemic attack was similar to that of the expected population risk during the initial 25 years of follow-up but increased thereafter (Figure 3C). The probability of survival free of stroke/transient ischemic attack was 94% at 15 years and 88% at 25 years (similar to expected rates of 96% and 89%, respectively) but was significantly worse at 30 years (72% versus 85% in expected; P
0.004, log-rank test). Of the 17 cerebrovascular events (5 strokes, 12 transient ischemic attacks) observed over the 30-year followup,10 occurred in those with permanent atrial fibrillation and 7 in those with paroxysmal or persistent atrial fibrillation.Four of these neurological events were characterized as embolic, 3 as probably embolic in patients who had underlying atherosclerotic vascular disease, and 6 as nonembolic; in 4, the cause of transient ischemic attack could not be ascertained. In patients with nonembolic cerebrovascular event, 3 had severe atherosclerotic cerebrovascular disease and 2 had intracranial hemorrhage (1 with brain tumor, 1 with subdural hematoma). Symptoms and signs of stroke in 1 patient were subsequently found to be due to hemangioblastoma of the cervical spinal cord. The mean age of patients who had stroke/transient ischemic attack was 73.610.7 (range, 54.2 to 94.0 years), and the mean interval from diagnosis of atrial fibrillation to the cerebrovascular event was 21.810.2 years (range, 0 to 34 years). All patients who had a cerebrovascular event had developed
1 risk factors for thromboembolism (hypertension in 12, heart failure in 4, diabetes mellitus in 3). Of the 17 patients who had neurological events, 11 were not taking antiplatelet agents or anticoagulants at the time of the event. None of the patients who had a cerebrovascular event were receiving warfarin therapy. After initiation of warfarin therapy, no patient had recurrence of stroke/transient ischemic attack." The full paper is worth reading, here is the abstract <[europepmc.org]

In simple terms, the risk didn't come in the first 25 years of having afib, but in the last 5 of the 30 when they started to get all the comorbidities.



Edited 1 time(s). Last edit at 07/26/2018 04:41PM by GeorgeN.

Quote
colindo
Carey, you have to ask what causes a stroke to form in the first place. Right.
Fibrin causes the platlets to stick together and build up, Natto and nattokinase dissolves fibrin, problem solved..[/quote

Even though Japan is the world's largest consumer of nattokinase, ischemic stroke is the most prevalent cardiovascular disease in Japan.

I wish it were so simple as "problem solved."

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Carey
Even though Japan is the world's largest consumer of nattokinase, ischemic stroke is the most prevalent cardiovascular disease in Japan.

"The prevalence of intracerebral hemorrhage (ICH) and intracranial arterial sclerosis is another unique feature of Asian patients."

"The autopsy results in the consecutive residents proved that the prevalence of ICH was not so high as was believed by Japanese physicians but also showed that ICH was still more common than ischemic stroke as a cause of death in Japan."

March 29, 2017 - Intracranial Bleed Risk Compared for Apixaban, Warfarin in A-fib Patients

[www.empr.com]

"Patients taking apixaban showed significantly less intracranial hemorrhage (0.33% per year) vs. patients taking warfarin (0.80% per year) no matter the type and location. Factors associated with higher intracranial hemorrhage risk included: enrollment in Asia or Latin America, older age, prior stroke/transient ischemic attack, and aspirin use at baseline.

"This highlights the clinical relevance of reducing ICH [intracranial hemorrhage] by using apixaban rather than warfarin and avoiding concomitant aspirin, especially in patients with older age," the authors concluded."

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mwcf
March 29, 2017 - Intracranial Bleed Risk Compared for Apixaban, Warfarin in A-fib Patients



"Patients taking apixaban showed significantly less intracranial hemorrhage (0.33% per year) vs. patients taking warfarin (0.80% per year) no matter the type and location. Factors associated with higher intracranial hemorrhage risk included: enrollment in Asia or Latin America, older age, prior stroke/transient ischemic attack, and aspirin use at baseline.

"This highlights the clinical relevance of reducing ICH by using apixaban rather than warfarin and avoiding concomitant aspirin, especially in patients with older age," the authors concluded."

There are a number of correlations that increase risk of bleeding (drinking, stress level, etc.). Statistics are great, but you need to look at effect sizes (.8 vs .33 per hundred) and balance with downsides of any particular drug.

[www.ncbi.nlm.nih.gov]

"Data from a trial in a UK community showed 39.8 minor, 0.4 major, and no fatal haemorrhagic events per 100 patient years for the total study population, with 3.9 serious thromboembolic events per 100 patient years, of which 0.79 were fatal.

Warfarin is therefore a relatively safe drug, particularly if therapeutic monitoring is performed well."



Edited 1 time(s). Last edit at 07/27/2018 11:20AM by jpeters.

According to this study <[www.bloodjournal.org] Apixaban had a 41% lower incidence of ICH than warfarin, hence a better choice. Especially for those with one or more ApoE4 alleles.

{Edit - didn't see the posts above when I posted}



Edited 1 time(s). Last edit at 07/27/2018 12:19PM by GeorgeN.

I was wondering about reducing my Eliquis dose to 2.5 bid from 5bid as I haven't had AF for over 6mths and was thinking perhaps doing the reduced dose (I am constantly fearful of brain bleed) along with fish oil etc and then taking full dose when in AF. anneh

Quote
wolfpack
I like the article, but I wish he hadn't expressed things in percentages. 1% of what amount of time? Statistics suggest that TWO HOURS of sustained AF is enough for a clot to form. That, of course, will be dependent on the individual and his or her blood viscosity and tendency to coagulate. My takeaway from the article is that it argues well for a PIP approach using DOACs for paroxysmal AF patients. I can tell you that I have Eliquis in my medicine cabinet, and if I have an episode exceeding 2 hours I will take it. I'll also stop it 24 or 48 hours after the episode terminates. The one exception being that if I ever get cardioverted, I'll take if for the entire month following.

Anneh, GP and Cardiologist tell me that it isn't enough for me (2.5g 2x/day Eliquis). Perhaps because i weigh 70kg?

I took the risk of natto and raw garlic as well as a high plant diet instead of Eliquis after about one year of not having AF (well, not that i have noticed) but still have occasional 'miss beats'.
Have had a few short episodes of AF this year. Also my heart beat was irregular during a recent virus infection. GP thought i was in AF but EKG showed that i wasn't.
I'm reasonably comfortable with the changes i made but they may not suit others for maximum safety or peace of mind.

As others say, no bullet proof studies that alternatives work as well as drugs.

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anneh
I was wondering about reducing my Eliquis dose to 2.5 bid from 5bid as I haven't had AF for over 6mths and was thinking perhaps doing the reduced dose (I am constantly fearful of brain bleed) along with fish oil etc and then taking full dose when in AF. anneh
I like the article, but I wish he hadn't expressed things in percentages. 1% of what amount of time? Statistics suggest that TWO HOURS of sustained AF is enough for a clot to form. That, of course, will be dependent on the individual and his or her blood viscosity and tendency to coagulate. My takeaway from the article is that it argues well for a PIP approach using DOACs for paroxysmal AF patients. I can tell you that I have Eliquis in my medicine cabinet, and if I have an episode exceeding 2 hours I will take it. I'll also stop it 24 or 48 hours after the episode terminates. The one exception being that if I ever get cardioverted, I'll take if for the entire month following.

That risk is VERY low. Far more likely, if at all, would be GI bleed which is eminently treatable. Eliquis doesn’t make you bleed uncontrollably. My own mother is on it and recently fell, hit her head, and caused a one-inch gash which needed stitches. The ER did a CT due to the Eliquis, but it showed nothing. The cut was stitched and that was the end of it. No more blood than usual, and it was stopped with pressure.

Eliquis is not a death sentence. It would never have been approved if it did more harm than good.

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anneh
(I am constantly fearful of brain bleed)

That's an instinctive fear for many people, but the reality is your chances of a stroke due to a clot are probably higher than your chances of a bleed. Reducing your dosage would probably increase your risk of stroke, not decrease it. But that depends on your particulars. If you're a CHADS-Vasc 0 or 1, then going to a half dose probably makes sense. If you're over 2, it's the wrong thing to do.

how about adding nattokinase to my 2.5mgs bid Eliquis?