I had no difficulties. My first ablation failed at six days, I was hospitalized with a runaway atrial rate, 180+, and had to go on amiodarone for 10 weeks. A second ablation, same EP, came seven months later and this time he got 'er done. Whew! I knew I was in AF, while some patients have no idea. Same for flutter...I knew full well I was in arrhythmia, whereas two people I know hadn't a clue.

Everyone is different. Each EP is different. How you recover, and what subsequently becomes part of your daily experience, is unknown and unpredictable. I know of one person who had migraines. Some get flutter and need yet another ablation. Some only get some PACs or SVT. It's not a crapshoot in terms of stemming the AF if that was the original problem, but what happens after that won't be known until some time into the 'blanking period' of about 10 weeks that follows, after which you'll get a Holter monitor or some kind of measuring device that can track your heart rhythm, usually worn for an afternoon, over night, and you return it to the issuing party next day by about noon-ish. You get the results days, two weeks later...whatever the local rate is.

PFA is currently only used for the standard PVI (pulmonary vein isolation). That location is where something like 80% of all paroxysmal AF originates. The shape of the mechanical 'head' is designed to be placed at the ostia of the pulmonary veins and then energized. It currently cannot be used in the coronary sinus, for example, nor in the left atrial appendage.

About drugs: I was issued with both Eliquis, a DOAC (direct oral anti-coagulant) and metoprolol tartrate (the slow acting version). The risk of stroke when, and after (yes, after it stops!!!) fibrillating is at least six times as high as previously, generally, on average. So, your cardiologist should have you on a DOAC immediately. You can refuse, but then the cardiologist wonders what kind of a patient he/she is dealing with. If he/she just shrugs, go away happy, but with six times the risk. Metoprolol is a beta blocker:
https://www.webmd.com/drugs/2/drug-8814-2372/metoprolol-succinate-oral/metoprolol-succinate-extended-release-capsule-oral/details
Note that metoprolol can help with incipient hypertension, but in this case it is meant as a 'rate' control medicine that keeps the heart from beating too fast when it is in arrhythmia. Ideally, you should not have a heart beating at more than 100 BPM for more than 24 hours. Note also, that too much metoprolol can put you into bradycardia where your heart beats too slowly. If it drops below 45 BPM regularly when you're awake, I would question my cardiologist soon about it.

My last point, still about drugs: they tend to lose efficacy over time, and this because the disorder, itself, evolves over time. The disorder progresses, and not in the right direction. So, you'll need more of the same drugs, or you'll have to find another that works. Many do not tolerate all the various anti-arrhythmic drugs, and amiodarone is moderately toxic...you don't want to be on it more than a few months ideally. So, my real point is that if the drugs are losing ground for you, a mechanical fix is all that's left. Except, there isn't one. The closest you can come to 'fixing' a fibrillating heart is to ablate the locus or re-entrant point where the extra signal is getting in and forcing the atrium to contract. If it works, the ablation dams, literally, or places a stockade, of fibrosis/scarring around the affected area, and that scarring prevents the electrical impulse from moving outward and causing the contraction. Literally, ablation is the process of damming the area to prevent the signal from spreading. No signal spread, no contracting atrium. (Picture Mr. Burns with his evil look and saying, 'Eeexxcellennntt...').

There is a lot more to say, but it's already a book I've typed. You can google all related topics and read for another three hours easily.