The misfolded protein amyloid fibrils that have alresdy accumulated in heart/other internal organs, or in and around your autonomic and peripheral nervous systems, are not in any way helped by Vyndamax or Attruby.
Those amyloid fibrils are proteotoxic which means that they very, very slowly interfere with or destroy the ability of your heart muscle cells to serve as conductors of the electrical signals that allow your ventricles to contract to pump blood to your body. Heart Arrhythmias such as AFIB and AFLUTTER, Premature ventricular contractions, and bradycardia(slow Heart rate) or tachycardia (fast Heart rate) are caused by the damage already done by the extracellularly deposited broken-up Transthyretin proteins.
So, there is zero reduction of symptoms from the existing damage to your heart, nerves, lungs, liver, etc, from the use of Vyndamax or any stabilizer drugs. That is even true of silencer drug therapy with Eplontersen or Amvuttra use.
There is some evidence that Amvuttra in 22% of patients on that silencer drugs have shown some small amount of regression of heart thickening or heart symptoms. Too soon to know.
Hi Sheldon,Nice to hear from you.You know your stuff.Take care ,Joe
Vyndamax never improves your symptoms or clinical status. It stablizer the tetrametic ( the term means 4) structure of the Transthyretin protein (actually, 4 identical Thyretin proteins that are bound together).
The other interventions such as diuretics, antiarhymia drugs, pacemaker, etc., are what ameliorate your symptoms. Anyone thinking Vyndamax "saved their life" or improved their symptoms is incorrect.
False attribution about Vyndamax, a drug hat helps limit further depositing of misfolded broken-upTTR, is an incorrect understanding of the drug's purpose and benefits. If you are diagnosed early for any disease your survival odds may be optimized but if you were diagnosed late in the disease progression, you are not receiving much benefit from Vyndamax.
My short answer is no. Everything you read states that the drug will SLOW the disease process and EXTEND life. It has done that in my case. I probably not be here if not for vyndamax. I continue to have new challenges pop up.
In the overall assessment of this disease, there is a lot that is not known, but things have come a long way since I was diagnosed in 2019. You have to keep abreast, work with your doctor and never give up!
Vyndamax (tafamidis) works by attaching to the TTR protein and stabilizing it, which helps prevent it from forming the amyloid deposits that damage organs like the heart. So while it doesn't reverse existing damage, it can slow down the progression of the disease. Research has shown some encouraging results with tafamidis:
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