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AF Symposium 2017
Links Between Inflammation, Oxidative Stress and A-Fib
Predicting and Preventing A-Fib
David Van Wagoner, PhD
One of the most important frontiers of A-Fib research is trying to determine why and how Atrial Fibrillation develops. Dr. David Van Wagoner of the Cleveland Clinic, Cleveland, OH talked about the mechanistic links between inflammation, oxidative stress, and A-Fib.
Oxidative Stress
Oxidative stress can cause oxidants to interact with lipids and proteins and cause previously functional proteins to become dysfunctional. Proteostasis, the process of processing dysfunctional proteins, is impaired as in diseases like Alzheimer’s.
A-Fib hemodynamic stress or ‘stress activated’ changes (for example, by stressors like hypertension or obesity) produce reactive oxygen species (ROS) generation which can cause oxidized proteins to form amyloid aggregates like the tau proteins that accumulate in the Alzheimer’s brain. Stressors like sleep apnea and obesity impact arrhythmia substrate changes such as atrial hypertrophy and fibrosis.
Fibrosis/Inflammation
These stress activated changes also promote myofibroblast activation (fibrosis), inflammatory cytotine production, and heat shock endoplasmic reticulum (ER) stress.
Atrial Ectopy (extra beats)
Hemodynamic stress increases sympathetic nerve activity which promotes ectopy (extra beats) that trigger the onset of A-Fib.
Recommended Further Study
Dr. Van Wagoner recommends targeting and researching certain pathways in order to treat and even prevent A-Fib:
• Atrial Ectopy
• Atrial Fibrosis
• Proteostasis Modulation
He suggests that further study of these mechanistic pathways may help us both predict and prevent A-Fib. For example, monitoring for atrial ectopy can be a powerful predictor of future A-Fib.
Second Dr. Van Wagoner Presentation: Prevention of A-Fib
In a second talk, Dr. Van Wagoner built on his earlier presentation and laid out a game plan for research priorities to prevent Atrial Fibrillation:
1. Find the mechanisms underlying ectopy (extra beats). Why does ectopy predominately result in A-Fib in older people?
2. Identify the genes. signaling pathways, and mechanisms that impact the risk of A-Fib. How are they modifiable?
3. Determine the stages in A-Fib progression where reducing risk factors (obesity, sleep apnea, etc.) can reverse remodeling or prevent A-Fib progression.
4. Develop preventive strategies based on A-Fib mechanisms (atrial ectopy, oxidant stress, proteostasis, fibrosis, etc.)
What A-Fib Patients Need to Know
Being able to predict who will develop A-Fib would be a major advance for patients. (See how research shows that, as Dr. Van Wagoner discusses, ectopic beats do predict the development of A-Fib: FAQ: Coping with A-Fib PVCs & PACs.)
But an even more important step in A-Fib research would be to develop ways to prevent A-Fib. Further study of Dr. Van Wagoner’s mechanistic pathways of A-Fib may bring us closer to actually preventing A-Fib.
Return to 2017 AF Symposium reports
If you find any errors on this page, email us. ♥ Last updated: Monday, September 12, 2022
