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Everything posted by vxmike

  1. If one truly has autoimmune POTS antibodies I would *assume* some kind of immunosuppression or plasmapheresis would be a treatment, but thus far I've not read any papers or recommendations of such. It's such a new avenue for POTS. I believe frequent plasma donation will actually accomplish the same thing as plasmapheresis on a lighter scale assuming the body doesn't regenerate the antibodies quicker than one can dump their antibodies via the donated plasma. I'd try this but losing volume from donation isn't exactly a viable option for a POTS patient! Too bad the donation centers won't replenish you with a couple liters of saline afterwards.
  2. Hello everyone, Now that we are aware of several studies suggesting that autoimmunity alpha and beta antibodies are often found in POTS patients that don't fall under the Hyper or primary neurogenic categories, I am curious if anyone here has tried plasmapheresis as a treatment to remove antibodies? I'm fairly certain my etiology is autoimmune. I was on prednisone for almost 15 years for skin conditions but was otherwise perfectly healthy. After receiving proper Derm care and stopping the Pred my health has fallen apart. My POTS came on 2 years after stopping Prednisone. I have multiple conditions suggesting autoimmune disease: POTS not Hyper or neurogenic Sicca/Sjogrens syndrome - dry eyes/mouth resulting in corneal damage, lacrimal gland atrophy seen on CT Likely IgG4 related disease with all relevant positive serum markers plus positive PET CT scan I likely need systemic immunosuppressant therapy especially Rituximab, but I'm curious to try Plasmapheresis to see if clearing my antibodies will temporarily ameliorate my POTS. All my issues were not present or kept under control while on Prednisone. I'd merely start the Pred again but once I do that further investigation is impossible and Pred is a poor lifetime medication. Ultimately I likely need Rituximab or other steroid-sparing immune suppression. Plasmapheresis anyone?
  3. I did not find Midodrine helpful solo (just no effect at all) but I think it helps in combination with Ivabradine for me. I have no theories why.
  4. Dr. Grubb didn't mention resting HR at all as an issue. In the few days I've been able to do some testing my supine heart rate has been around 55-65 with Ivabradine on board. Without it my supine rate was usually 60-70, so it's a fairly minor difference that doesn't worry me at all. My only concern is that I want to decrease my supine BP at night. My daytime BP is abnormally high due to Mididrine plus my body's natural attempts at compensatory vasoconstriction, and that's not a great thing for my heart long-term especially with the Mitral Prolapse that was found incidentally in my workups. I had great BP usually 100/60 before all this mess started two years ago. I'm a little worried to try something like Clonidine before bed if I already have Ivabradine in my system too. I don't have regular access to a POTS physician willing to be creative (Dr Grubb visits are few and far between as I am not local and he immensely in demand), so I'm in the experimental camp personally...thus far I haven't found a suitable vasodilator that doesn't also reduce heart rate. Even if you have hypovolemia instead of blood pooling POTS I suspect the effect would be similar. Neither of our hearts are completely filling with blood even if the underlying reason is different. If my blood is in my legs and yours doesn't exist it might as well be the same when we're standing!
  5. I think the cause of hyper-POTS is even more elusive than the other variants, unfortunately. What were your upright catecholamine values? These for the most part can diagnose or rule out hyper POTS.
  6. What dose are you using? I just purchased a bunch of pheneylephrine but I'm not certain what a good dose for POTS might be.
  7. I think you ought to reconsider Ivabradine if your physician is offering it. I recently saw the renowned Dr Grubb and he started me on Ivabradine. His explanation is that at a certain the increased heart rate is inefficient and offers no benefit. The baroreceptors sense they don't have enough blood, so the body naturally increases HR. In our case, however, due to blood pooling there is no blood to actually pump. The heart is working like crazy (using tons of energy/oxygen) to rapidly pump dry. If you can lower the HR without decreasing BP (which only Ivabradine can do) then the heart will rest longer between beats and fill with more blood resulting in a higher output per beat. Im close to labeling Ivabradine a miracle drug for me. I'm using it with Midodrine and my standing HR went from 140-155 down to the 90-115 range within 48 hours, and I've had massive symptom reduction. Midodrine was ineffective solo. I'm certainly not "cured" and definitely still impaired, however I've improved at least 50%. Beta blockers decrease BP which negates the benefit from reducing HR. It probably slows the heart but causes even worse blood pooling. Ivabradine is a genius solution for some POTS patients that respond well.
  8. Sounds like you don't have primary neurogenic POTS or autonomic failure. That's good! You're on a beta blocker, so maybe that's why your tachycardia isnt testing positive on the TTT? The last part suggests you might have hyper-POTS. Probably should seek out a cardiologist who specializes in this.
  9. Me too. I was in excellent shape too before the sickness, and I did a 120 mile trek at 15,000+ elevation in Peru three months before I started getting dizzy just sitting at work or in the car. Looking back I was abnormally exhausted and my performance wasn't quite what I expected so I think my blood pooling was starting and the symptoms didn't really manifest as noticeable for a while.
  10. I think this explains it right here. +29 is right on the edge of a POTS diagnosis. Even if you do have POTS your HR is far lower than most people here who experience 40-80+ beat increases. I went from 68 to 148 on my last poor man's TT. I'm not discounting your symptoms or condition at all but your HR increase is at the very low end of the POTS spectrum. I do think there could be something to the male/female differences, however. Anecdotely it seems to me women report greater degrees of disability from POTS. I'm also the rare male with POTS and even with my 70-80 typical increase I can still work full time and even do moderate hikes outside. Men have a higher cardiac output to begin with, larger blood volume, and a higher hematocrit on average so we have more tools in the body's arsenal to fight POTS. There may be other physiological differences in the various blood pressure, RAAS, and vasoconstrictive responses in the body between the two sexes. POTS is like 90%+ female so it's interesting to hear from other guys.
  11. Hi Kim, Thats exactly how Dr Grubb explained it to me as well. The increased heart rate simply becomes less efficient as it pumps faster without sufficient blood to pump. It's literally pumping a fraction of the normal blood volume each beat. By itself the cardiac muscle uses a lot of energy and oxygen itself, so I'm sure it contributes to fatigue and shortness of breath. I recently started on Ivabradine, and it's been a wonder drug so far. It slows the HR without the accompanying reduction in blood pressure that a beta blocker delivers. Essentially my heart has more time to fill up with blood between beats and isn't wasting energy pumping inefficiently. My standing HR went from 140-155 down to the 90-115 range in addition to strong symptom reduction. I too want to try EPO to deliver more oxygen per unit of blood delivered to tissue. My hematocrit is 40% and I feel like a boost to 50% would aid me greatly. Unfortunately there is no way my insurance will pay for it in this case, and it's indeed quite expensive
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