Slow resting pulse and gout
Fouryears ago I was prescribed Atenolol(Tenormin) for PVCs(palpitations)at 25 mg daily. My doctor and cardiologist said the PVCs are benignbut since they bother me the atenolol was prescribed to slow themdown. My resting pulse plummeted from around 80 bpm to 50 bpm whichis the norm for atenolol usage. Not too long after I starteddeveloping gout slowly (took a couple attacks over the years fordiagnoses). Can the fact that my heart is beating slower(less bloodcirculating) cause more uric acid to settle into joints instead ofkeeping flowing in the blood with a stronger faster heart beat?Maybe my physiology is all screwed up here but was just wondering?Does not hurt to ask!
Terrance Molock on April 13th, 2007
Both ends brother.BOTH of these theories have been bandied about. The theory that less circulation allows the uric acid to “pool” inthe area..perhaps contributing to the problem of it super-saturatingthere. The b/p theory that high blood pressure allows some “leakage”allowing the uric acid to get “forced” across the interstitialcellular membrane into the joint area.
At this juncture in time there is NO co-relation between poorcirculation,high b/p and gout.
However it IS known that allo DOES reduce b/p.Reduced mine whichwas never high anyway.
Here is what IS known..uric acid travelling in the plasma..theclear part of the bloodstream..SOMEHOW(ABSOLUTELY NOTHING!! on theresearch horizon(from what I come across)as to thehow/why/mechanism..REALLY SURPRISING! is that even authorites on goutdon’t even have ANY ides!) crosses the interstitial cellular membraneinto the joint area.Too much of it ends up there.ONCE there..it isVERY,VERY hard to get it back to where it came from!!
Me personally.. my humble .02 cents is that it is a hormonalissue.We do know that the gout process basically starts in puberty(in males).We ALSO know that women get it..and almost in the samenumber as men AFTER menopause when their estrogen level drops.Theexperts say because the lower estrogen level cause blood uric acidlevels to rise slightly.SO??..we have pretty much eliminated theblood uric acid level issue in men..so why does this happen withwomen? We also know that uric acid is a “scavenger”..doing a LOT! of goodwork..cleaning up..free radicals etc. along it’s route. It is now known that there isn’t really any actual crystalizationof the u/a in the blood..some say they have found microscopicevidence.Experts disagree with this. I had guessed at the “recombinant” issue that somehow..COMPONENTSof uric acid had left the bloodstream and then combined/re-combinedwith OTHER components to form the actual uric acid on the OTHER sideof the interstitial cellular membrane..on their way to the joint area. Long shot and tough sell as the u/a in the blood and the u/a inthe joint fluid is the same.