I did not have that conversation, but what he and I discussed would have led him to understand that I had done my homework and was fairly conversant with the problem and its treatment.

The heart's substrate has become disordered when someone develops an arrhythmia. It cannot be reversed...at least not that I have ever read or seen in amazing news. It can be controlled to an extent, but the point is that the disorder is progressive....slow or fast, or middlin', it progresses.

It gets worse if the arrhythmia is not controlled, and it can accelerate. If the arrhythmia persists, and becomes permanent, the entire time it is in arrhythmia is time where the heart remodels itself. Collagen gets deposited in the substrate and fibrosis appears there as well. In time, the mitral valve is going to sag or lose its tone and you'll get mitral valve stenosis. Note that this is predicted as likely, not absolutely in all cases.
https://www.ahajournals.org/doi/full/10.1161/JAHA.123.032215
Here, below, they discuss the results of a study where they measured EF and enlargement in patients, some who were cardioverted early and stayed in apparent NSR for five years, and the others were in and out of AF. The latter had much more enlargement, and those who were successful at staying in NSR even had some modest reduction (they use the term 'reverted') in atrial size...bonus!
https://pubmed.ncbi.nlm.nih.gov/15860382/
Note, also, that hypertension is mentioned. If the patient is in NSR, but still largely hypertensive, then atrial enlargement is going to be much more prevalent.

I couldn't find a study hazarding an estimate of the probability that any one heart will succumb to heart failure when in AF and left there long enough. My guess, if you insist, is that it's close to 80%.