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AF Symposium 2015
Dr. Prashanthan Sanders
Obesity Produces Fibrosis, But Getting Lean Reverses Fibrosis (in Sheep)
by Steve S. Ryan, PhD
In a fascinating experimental study with sheep, Dr. Prashanthan Sanders from Royal Adelaide Hospital in Australia, overfed sheep so that they developed sustained obesity for 72 weeks. Their fibrosis increased. Their atria were damaged by fibrotic tissue replacing normal atria muscle. As the sheep moved from being overweight to obese, it was progressively easier to induce A-Fib.
Then Dr. Sanders made the sheep lose weight. With a 30% weight reduction, the fibrosis was no longer present! The sheep were similar to the lean sheep controls.
Dr. Sanders used activation mapping to show that in the obese sheep there was an increased delay in activation suggesting delayed conduction. It took a longer time to activate the atria. But when the obese sheep lost weight, conduction became normal. Also there were improvements in left atrial pressure, inflammatory cell counts and fibrosis, atrial TGf beta 1 and reversal of connexin-43 and ETR-beta (which contribute to fibrosis).
Hypertension and A-Fib in Sheep
Dr. Sanders also stimulated sheep into progressive hypertension for 15 weeks. As with the obese sheep above, these hypertensive sheep developed fibrosis. And activation mapping again showed delayed and abnormal conduction.
Sleep Apnea and A-Fib in Animals
Citing other research, including from Dr. Andrea Natale’s group, repetitively blocking off breathing as in sleep apnea developed increased fibrosis as well as slowed atrial conduction, increased atrial size, and induced more atrial fibrillation.
More Risk Factors Lead to Persistent A-Fib
Dr. Sanders pointed out that A-Fib patients with cardiovascular risk factors like obesity, hypertension, and sleep apnea are more likely to progress to persistent A-Fib than individuals with few or no risk factors.
Fibrosis Produces More Fibrosis
Fibrosis (interstitial fibrosis) is the main factor in changing the atrial substrate. Voltage maps of fibrotic atria show large areas of low voltage, increased areas of scarring, and a more complex electrogram resulting in abnormal conduction. According to Dr. Sanders, fibrosis produces more fibrosis. “There is clear evidence that A-Fib feeds back on itself to remodel this process, and there is even a suggestion that it may induce further atrial fibrosis.”
Editor’s Comments:
(Readers of this report may also want to read Dr. Jose Jalife’s similar experimental sheep studies where, among other findings, he proved that pacing sheep into A-Fib produces fibrosis. See Experiments in Atrial Remodeling in Sheep and the Transition From Paroxysmal to Persistent A-Fib.)
In a previous report Dr. Sanders described the great results he is achieving by having his overweight A-Fib patients lose weight, buy into the program and keep the weight off. Sometimes this life style change alone makes them A-Fib free. But not everyone can lose weight and keep it off. Other risk factors like hypertension and diabetes are more difficult to permanently change. And once A-Fib is well established, life style changes aren’t as effective. Though life style changes certainly do improve overall health and heart health.
Fibrosis is Usually Permanent and Irreversible
Unlike some of Dr. Sanders results with sheep, fibrosis in general is considered permanent and irreversible.
Life Style Changes Usually Not Effective in Lone A-Fib
Approximately half of people with A-Fib have no risk factors or co-morbidities (which used to be called “Lone A-Fib.”) I, for example, developed A-Fib at age 54 when I was in perfect health, running track and 5ks, lifting weights, etc. Life style changes aren’t always effective in cases of Lone A-Fib.
Risk Factors lead to persistent A-Fib
Why do some people with A-Fib stay Paroxysmal for years while others progress rapidly to Persistent A-Fib? Perhaps Dr. Sanders has discovered the reason. Risk factors or co-morbidities like obesity, sleep apnea, hypertension, diabetes, etc. make people more likely to transition from paroxysmal to persistent A-Fib. Patients with A-Fib risk factors should be warned of this danger.
Fibrosis Produces More Fibrosis
Here’s yet another scary thought for anyone with A-Fib. According to Dr. Sanders, fibrosis may feed upon itself producing yet more fibrosis.
Though this isn’t normally done today, anyone diagnosed with A-Fib ought to have a heart MRI to measure exactly how much fibrosis has developed in their heart and how much and how fast it is progressing.
This danger of fibrosis progression is yet another incentive to consider a catheter ablation in order to be A-Fib free with no further progression of fibrosis.
Return to: AF Symposium: Steve’s In-Depth Reports Written for Patients
Last updated: Friday, March 6, 2015
