So appreciate your sharing all this. Beyond your Toprol XL, are you on any additional beta blocker, ARB (angiotensin receptor blocker), calcium channel blocker, or ACE inhibitor either for your hypertension or AFib?

I ask because after 6 months of unrelenting post-COVID upper respiratory illness with periods of severe coughing, I am finally realizing that several of the medications I have been taking, on a maintenance basis, may have set the stage for my particular form of long COVID. (And btw, I am very close to your age, and I am lately experiencing drug side effects and sensitivities that I never suffered when I was much younger, a phenomenon that may also be affecting you.)

This week, I expect to receive a paid consultation with a terrific pharmacist who provides highly analytical medication therapy reviews, but while I await that appointment, I have learned that my ARB, in particular (losartan), has been found in multiple studies to produce the same risk of angioedema and related symptoms (bronchospasm, e.g.) as ACE inhibitors are already famous for producing, and so job 1 after my consultation is probably going to be replacement of my losartan. (In addition, my beta blocker, carvedilol, unlike metoprolol/Toprol, causes peripheral vasodilation similar to the vasodilation caused by ACE inhibitors and some ARBs, and so that will probably also have to be replaced, because it vasodilation generally contributes greatly to bronchospasm and also to the nasal blockage that is my worst symptom.)

It is well known that the peptide that causes excessive peripheral (non-cardiac) vasodilation (and, in turn, angioedema, bronchospasm, and nasal congestion) is bradykinin. Bradykinin behaves similarly to histamine, btw, but does not respond to the therapies designed to lower levels of histamine in patients with disorders like mast cell activation syndrome or histamine intolerance.

Best of all, my research is uncovering that in the early days of COVID, several important studies explored whether elevation of bradykinin in COVID patients might be contributing to the COVIDś most severe respiratory manifestations, and once this linkage was established across a number of patients, there was apparently some attempt to use bradykinin-reducing medications and supplements to bring levels down as fast as possible. I don´t know whether this line of research has continued and been applied to long COVID, but I would urge you to ask the next doctor whom you find to be clear-thinking and patient whether s/he would consider evaluating you for elevated bradykinin levels (that can then be treated appropriately).

My perfunctory research, so far, tells me that there are some well-established non-pharmaceuticals that can lower bradykinin levels. These appeal to me because once I am safely weaned from the blood pressure drugs that I believe play a big role in my now chronic upper respiratory illness and cough, I will need help in accelerating the normalization of my bradykinin levels, because it takes a while for bradykinin to normalize even after the offending medications are discontinued. The go-to items for this help are ginger, black tea, low/safe doses of Vitamin K, polyphenol-rich foods (like beets and beet root), and small amounts of aloe extract taken orally. (Because you have AFib, any supplementation with K would have to be very, very, very carefully considered, by your physician(s), in the context of the Eliquis you will be continuing and the features inherent in the AFib diagnosis itself.)

Godspeed to you in getting the answers and treatment that you need, and remember always that a hopefulness and even expectation that you will get lots better can do you no harm and could well increase your chances of recovery.