Some possible explanations, other than their “acidifying” quality, for the beneficial effect of cranberries
On the page entitled “Cranberries will probably do you good anyway" (Link F), I have listed four probable beneficial health effects of cranberries, in addition to any effects on AF, which have been attributed to various identified beneficial components in the fruit other than their “acidifying” qualities. Of course, it is always possible that any one of those components could also be the cause of the apparent beneficial effect on AF, rather than the acidifying quality. That is certainly a possibility, as is the possibility that it is yet some further constituent of cranberries that has the beneficial effect on AF.
Of course, from the point of view of an atrial fibrillation sufferer who gains any relief whatsoever, it is unlikely they would be overly concerned what the exact mechanism is.
But the exact mechanism or active component would be of interest: (a) from a straightforward science perspective; (b) due to the possibility of developing an active concentrate which would then require a much smaller dose and which could therefore plausibly prove effective even in individuals unresponsive to whole cranberries; and, (c) due to the possibility of developing a targeted pharmaceutical having the benefits mentioned in (b), but more strongly so.
With that in mind, the following are comments about possible afib-related effects of the three identified “non-acidifying” cranberry factors listed on the page referred to above (Link F), plus a comment on general anti-inflammatory effects and a comment on quinic acid:
Resveratrol: The content in cranberries is significant, and recently a new, synthetic, resveratrol-related compound has been reported to have some effects on certain “test tube” rhythm-related aspects of isolated atrial cells . However, on the two occasions upon which I reduced my cranberry intake, and subsequently noted ectopic beats reappearing, I had substituted the cranberries with firstly an equivalent weight of blueberries and secondly a 50/50 equivalent weight of blueberries and malbec black wine grapes (including all skins and seeds). These are both fruits with supposedly comparable levels of resveratrol to cranberries, which would argue against resveratrol being the active component.
Oligomeric proanthocyanidins: No effect of these ingredients on AF has been previously reported, and again, both the blueberries and malbec grapes have high levels of these compounds.
Nevertheless, neither the resveratrol nor the oligomeric proanthocyanidin content are probably quite as high in blueberries or malbec grapes as in cranberries; also, assays for all these compounds are imprecise; and seasonal, regional and ripeness variations of these components would be considerable in all three fruits. So the possibility of cranberries’ observed effect on AF being due to either component cannot be ruled out.
Ursolic acid content does not appear to be as high in blueberries or grapes as in cranberries, so the possibility of cranberries’ observed effect on AF being due to this compound cannot be excluded. (As has also been noted above regarding as yet unidentified cranberry components.)
A generalised anti-inflammatory effect may be another possible route of action of the cranberries. However, the general idea of applying a maximally anti-inflammatory dietary approach was not unknown to me, and I have previously tested vast quantities of such things as black grapes, blueberries, turmeric, broccoli and all other cruciferous vegetables, cinnamon, sumac, extra-virgin olive oil, blackcurrants, tomatoes, etc. All showed no detectable effect on afib or ectopics. Nevertheless, although it appears to be the acidifying quality of cranberries which is most sharply distinctive in comparison to all these other foods, some specific anti-inflammatory effect of cranberries cannot be ruled out. They are certainly higher in their content of a whole range of constituents compared to virtually all readily available fruits and vegetables, for reasons discussed elsewhere (Link G).
Quinic acid is related to the known antiarrhythmic drug quinidine, so perhaps some direct antiarrhythmic activity, rather than an action due to its metabolic acidifying effect, is a possibility. However, any such new development would be a very positive one because quinidine has known undesirable effects, whereas quinic acid has been consumed in large quantities, in many fruits, by all humans, over millions of years, so it is unlikely that humans are not genetically adapted to it or that it would be the source of similar adverse effects.
 Baczko, I., Liknes, D., Yang, W., Hamming, K. C., Searle, G., Jaeger, K., ... & Light, P. E. (2014). Characterization of a novel multifunctional resveratrol derivative for the treatment of atrial fibrillation. British journal of pharmacology,171(1), 92-106.