Cerebral Small Vessel Disease after catheter ablation

Posted by thisnthat @thisnthat, Nov 3 8:58am

Does anyone have any insight into Cerebral Small Vessel Disease following successful catheter ablation for AF/AFl? While CSVD is common in those over 60, one would think that a successful ablation mught slow the progression of CSVD as NSR stabilizes hemodynamics. Despite maintaining sinus rhythm, what other factors are at work that would continue to disrupt the integrity of the brain’s vasculature? How can you assess if damage was sustained from a one-time insult (such as an overly long CA procedure) or is occurrng on a continuing basis? Even if a CHA2DS2-VASc is low, should one still be mantained on an anticoagulant, or would microbleeds be a greater issue with CSVD?

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It's only the discharge of clots from the left atrial appendage that is the great risk in AF. The DOAC is meant to forestall it, maybe not entirely 'prevent' it. That is to say, the DOACs only retard clotting, they don't actually prevent it. Really bad bleeds, yes, there'd be a problem, but what we're only attempting to do here is to delay the issue of substantial clots from the LAA...IF they form at all, and that's what Eliquis and Xarelto are meant to reduce to a very low probability.

The problem with clots escaping the left atrial appendage goes on for weeks after returning successfully to NSR. This is established firmly in the literature, and that is why you should continue to take DOACs for several weeks after an apparently successful ablation or the insertion of a watchman device.

Vasculitis, vascular disease, peripheral artery disease....these are all different problems not associated at all with atrial fibrillation the way I understand it. Little bleeds from small cerebral veins and arteries is indeed a risk...for some more than others. It might not be good to have a anti-coagulant in one's system if this happens, but then you run the risk of an outright stroke caused by a clot traveling from the heart to the brain, or a thrombosis in the lungs or heart itself. A clot doesn't care which blood vessel, or whose, that it blocks. It just blocks it willy nilly.

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I listened to this several times - it's GOOD data!


Then I used Garfield to get percentage risk per year
https://af.garfieldregistry.org/garfield-af-risk-calculator

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@gloaming

It's only the discharge of clots from the left atrial appendage that is the great risk in AF. The DOAC is meant to forestall it, maybe not entirely 'prevent' it. That is to say, the DOACs only retard clotting, they don't actually prevent it. Really bad bleeds, yes, there'd be a problem, but what we're only attempting to do here is to delay the issue of substantial clots from the LAA...IF they form at all, and that's what Eliquis and Xarelto are meant to reduce to a very low probability.

The problem with clots escaping the left atrial appendage goes on for weeks after returning successfully to NSR. This is established firmly in the literature, and that is why you should continue to take DOACs for several weeks after an apparently successful ablation or the insertion of a watchman device.

Vasculitis, vascular disease, peripheral artery disease....these are all different problems not associated at all with atrial fibrillation the way I understand it. Little bleeds from small cerebral veins and arteries is indeed a risk...for some more than others. It might not be good to have a anti-coagulant in one's system if this happens, but then you run the risk of an outright stroke caused by a clot traveling from the heart to the brain, or a thrombosis in the lungs or heart itself. A clot doesn't care which blood vessel, or whose, that it blocks. It just blocks it willy nilly.

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More research, more rabbit holes!!!! 🐇🐇🐇

Apparently, there may be different manifestations of CSVD arising from different causes. Microbleeds tend to occur in amyloid-related CSVD (e.g., Alzheimer’s), while WMH and lacunae predominate in arteriosclerosis (as in diabetes and hypertension). Genetic mutations may also have their own characteristics, such as the lacunas in CADASIL. AF itself has many possible causes. So many confounders, it is hard to know where AF begins and CSVD ends, or how the sequelae of a catheter ablation may contribute to brain function.

It’s nice to know that those who have had a successful CA tend to do better cognitively than those just treated with medications, but we really don’t have a handle on some of the after effects—or how someone with CSVD may respond longterm to such a procedure.

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This is a great article on what CSVD is and how it is diagnosed and treated. Nowhere in this article is Afib for NSR even mentioned. This is the story of a 54 year old woman without heart problems but has CSVD.
Cerebral Small Vessel Disease: Learn About One Person’s Story of Early Dementia, Misdiagnosis, and Living With CSVD
https://www.americanbrainfoundation.org/julies-story/

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Thank you, harveywj, that really was a great article. Sad that there are not more effective treatments.

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@thisnthat

More research, more rabbit holes!!!! 🐇🐇🐇

Apparently, there may be different manifestations of CSVD arising from different causes. Microbleeds tend to occur in amyloid-related CSVD (e.g., Alzheimer’s), while WMH and lacunae predominate in arteriosclerosis (as in diabetes and hypertension). Genetic mutations may also have their own characteristics, such as the lacunas in CADASIL. AF itself has many possible causes. So many confounders, it is hard to know where AF begins and CSVD ends, or how the sequelae of a catheter ablation may contribute to brain function.

It’s nice to know that those who have had a successful CA tend to do better cognitively than those just treated with medications, but we really don’t have a handle on some of the after effects—or how someone with CSVD may respond longterm to such a procedure.

Jump to this post

"So many confounders, it is hard to know where AF begins and CSVD ends, or how the sequelae of a catheter ablation may contribute to brain function.'

Searching the literature on PUB MED reveals a paucity of articles combining the search of CSVD and Afb. CSVD which occurs independently of Afib shows that Afib is a multiplier of morbidities and not a primary driver of the brain disease. When searching "CSVD Burden" that appears in many articles Afib is not mentioned at all when discussing the various manifestations of CSVD.
This suggests that Afib is not highly associated with CSVD.

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@harveywj

"So many confounders, it is hard to know where AF begins and CSVD ends, or how the sequelae of a catheter ablation may contribute to brain function.'

Searching the literature on PUB MED reveals a paucity of articles combining the search of CSVD and Afb. CSVD which occurs independently of Afib shows that Afib is a multiplier of morbidities and not a primary driver of the brain disease. When searching "CSVD Burden" that appears in many articles Afib is not mentioned at all when discussing the various manifestations of CSVD.
This suggests that Afib is not highly associated with CSVD.

Jump to this post

It’s a sticky wicket. Several referenced articles (on Perplexity) point to shared mechanisms underlying brain changes in AF and CSVD. The AF-related brain changes have a “significant relationship” with those found in CSVD.

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