What does the community think about this paper on AF?

Please share your thoughts and comments.

Fibrosis and Atrial Fibrillation: Computerized and Optical Mapping; A View into the Human Atria at Submillimeter Resolution

Full article at [www.ncbi.nlm.nih.gov]

Some teasers from the paper:

Recent studies strongly suggest that the majority of atrial fibrillation (AF) patients with diagnosed or subclinical cardiac diseases have established or even pre-existing fibrotic structural remodeling, which may lead to conduction abnormalities and reentrant activity that sustain AF.

Atrial fibrosis is directly correlated with age of patients, which is mirrored by the increasing incidence of AF in the elderly(1,2). Structural cardiac diseases, such as hypertension(14) and heart failure(15), have been shown to have both an increase in atrial fibrosis and an increase in the occurrence of AF compared to healthier hearts. Recently, Kottkamp(9) has coined the phrase fibrotic atrial cardiomyopathy to denote the structural remodeling that accompanies or even precedes AF which is independent of other co-morbidities.

Based on recent ex-vivo experimental results and multiple clinical studies, we hypothesize that one of the primary mechanism driving AF in diseased human hearts is a limited number of localized intramural reentry within patient-specific 3D microanatomic tracks composed of fibrotically-insulated myobundles.



Edited 1 time(s). Last edit at 07/30/2020 09:15AM by NotLyingAboutMyAfib.

Fibrotic structural remodeling as the basis for AF has been well accepted for a number of years now. Nothing new in the first two paragraphs of the quote. The last paragraph perhaps adds new low-level details, but it's only hypothesis at this point.

Quote
NotLyingAboutMyAfib
Recent studies strongly suggest that the majority of atrial fibrillation (AF) patients with diagnosed or subclinical cardiac diseases have established or even pre-existing fibrotic structural remodeling, which may lead to conduction abnormalities and reentrant activity that sustain AF.

Atrial fibrosis is directly correlated with age of patients, which is mirrored by the increasing incidence of AF in the elderly(1,2). Structural cardiac diseases, such as hypertension(14) and heart failure(15), have been shown to have both an increase in atrial fibrosis and an increase in the occurrence of AF compared to healthier hearts. Recently, Kottkamp(9) has coined the phrase fibrotic atrial cardiomyopathy to denote the structural remodeling that accompanies or even precedes AF which is independent of other co-morbidities.

This is why I am interested in starting Modified Citrus Pectin (MCP) - a Galectin-3 inhibitor. Studies indicate it may be able to reverse cardiac fibrosis, caused by Galectin-3. If so, that would be a big part of undoing the structural remodeling that accompanies afib. We shall see!

My echo of 6 months ago showed "both atria are mildly dilated." (Left is "borderline enlargement", right is "enlarged".) Maybe after using the MCP for a while, I will get another echo to see whether that has changed.

Carey, Kim, thanks.

Kin - this ? [www.ncbi.nlm.nih.gov]

Does Dr. Natale use this technology or similar to help him target where he ablates? (maybe Shan knows)



Edited 1 time(s). Last edit at 07/30/2020 12:01PM by NotLyingAboutMyAfib.

This isn't even a paper per se, but a blog post about Dr. Jose Jalife's presentation titled “Searching for the Holy Grail: Upstream Therapy to Prevent AF Progression.”

[a-fib.com]

Persistent AF was induced in sheep. Half were then given the Galectin-3 inhibitor Davanat. Half were given saline.

The Gal-3 inhibitor:

*Lessened A-Fib-induced atrial dilation
*Reduced fibrosis by 50%
*Reduced the increase in dominant frequency
*Prevented the shortening of action potential duration in both atria
*Increased the percentage of sheep spontaneously terminating their persistent A-Fib during treatment

The Galectin-3 inhibitor available to most of us at a non-pharmaceutical retail level is Modified Citrus Pectin (MCP). It may not be identical in performance to the Davanat used by Dr. Jose Jalife. But I believe it could have a similar effect on cardiac fibrosis. There is a certain amount of research saying MCP can do this (mainly from the PectaSol-C manufacturer - but legitimate studies nevertheless published in peer-reviewed medical journals).

[www.sciencedirect.com]

This study (by creator of PectaSol-C) makes reference it it improving various types of cardiac fibrosis: [www.ncbi.nlm.nih.gov]

Quote
NotLyingAboutMyAfib
Does Dr. Natale use this technology or similar to help him target where he ablates? (maybe Shan knows)

No, not likely. He targets where to ablate based on where the AF is actually originating from, and that's not necessarily going to be areas with more fibrosis.

NLAMAF - In the archived posts, there are numerous entries on the fibrosis topic...and one summary report in the Conference Room Archives... You may find something relevant to your questions there. I definitely became convinced of the potential connection.

Jackie

[www.afibbers.org]

[www.afibbers.org]

Thank you Jackie - very good info. I made a new post because it sounds like I am on the right track.

[www.afibbers.org]



Edited 2 time(s). Last edit at 07/31/2020 03:52PM by NotLyingAboutMyAfib.

Dr Natale doesn't directly target fibrosis for ablation. His group tried that approach many years ago, but it' never proved to be a reliable target and simply did not make any difference trying to ablate the actual fibrotic scars.

However, one beneficial thing that they discovered from detecting an increase in atrial fibrosis, is a definite correlation to increased Non-PV triggers as well ... not surprisingly. And thus, targeting those associated Non-PV triggers can, indeed, improve durable ablation outcome!

Take care,
Shannon