It is a vicious cycle. AF it is responsible of myocardial fibrosis but atrial fibrosis increases the risk of AF occurence, recurrences and persistence.

Many studies based on atrial strain or on LE CMRI have confirmed that the more fibrosis the higher the risk of AF.

Atrial Fibrosis leads to atrial fibrillation and atrial fibrillations leads to collagen turnover and degradation resulting in atrial and ventricular remodeling, congestive heart failure and atrial fibrillation.  Reports of increased Galectin-3 in patients may trigger ventricular remodeling leading to CHF and atrial fibrillation.

Hi Uğur, 

When you look at the risk factors for atrial fibrillation (age, hypertension, obesity, diabetes and Cv diseases) they will all contribute to fibrosis of ventricles and of atriae.  t can be simple. Rapid firing from the PV will irritate the atriae but will in most cases not bring the system out of balance and cause atrial fibrillation.  Let us phrase it as in the 2010 ESC guidelines: 

TRIGGER

Focal activity of pulmonary vein cells

Triggered activity and re-entry

This leads to extrasystoles and runs of extrasystoles. 

SUBSTRATE

Any kind of structural heart disease may trigger a slow but progressive process of structural remodeling in both the ventricles and the atria

WAVELETS

The impulse no longer progresses as a wavefront but as multiple small wavelets (> 350 pm) with micro-re-entry

On top of that atrial fibrillation and other expressions of cardiovascular diseases (infarction, heart failure, valvular heart disease) will exacerbate this fibrosis. 

So it is not a chicken and the egg story, it is rather an "AND" "AND" story.

This is how I look at this problem. What about you?

Best regards,

Thierry 

Ugur why am I thinking that you know very well the answer ???

Both are the case: cause and result

Hi, Ugur

Good question and good answers abobe. My recommendation: Atrial Remodeling and Atrial Fibrilation. Recents Advances and Translational Perspectives. Nattel and Harada, JACC  Vol 63 N 22  2013

All the best

 Hi Ugur, I agree with most answers above: both cause and effect (no paradox there). The relationship between the amount of fibrosis and the degree of conduction disturbance is not straightforward, though, as was explained well by Burstein and Nattel JACC 2008;51:802.

We probably have to be more careful in the distinction of types of fibrosis (reactive (endomysial and/ or perimysial) fibrosis versus reparative/ replacement fibrosis), as was done in some older literature (e.g. Weber et al JMCC 1989;21:121). We ourselves have shown that in an animal model, AF itself leads to a small amount of endomysial fibrosis in the outer millimeter of the atrial free wall, which still seems to have a major impact on fibrillatory conduction (Verheule et al Circ AE 2013;6:202-211). 

Best regards,

Sander.