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TXPOTS

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  1. I had POTS for 3 years. It followed a waxing and waning pattern and finally left me completely bedridden. I can recall my heart rate lying down was 60 bpm and would rocket to 200 bpm after standing for 10 minutes or so. Yuck! Yuck! Yuck! I felt like "death". I finally started Florinef, DDAVP, and gradually started an exercise routine. At my peak, I was jogging 8 miles 4-5 times per week, lifting weights, rowing, using the stair master, and a cross trainer. I pumped my blood volume up to elite athlete levels per Dr. Levine. I dropped the Florinef and DDAVP without issue. I still qualified as having POTS based on my resting and standing hear rates, but my standing catecholamine levels were normal, and I very gradually began feeling normal. It has been about 3 years, I think? I feel fabulous with no POTS relapses and exercise like a regular human these days. I have absolutely zero fear of getting POTS again and rarely spend time worrying about the past. The first older cardiologist who diagnosed me said he had two other ladies with the condition who gradually improved and became POTS free. Neither experienced a relapse. Remember that those who have recovered are not hanging out on forums.
  2. I just wanted to pop in and give a quick update. I apologize that I don't frequent the boards anymore. I am still traumatized by my experience with POTS. I find it difficult to read posts that hit so close to home. I have fully recovered from POTS. I even was sick with the flu this summer and was in bed for a week. I'll be getting my flu shot for now on! No relapses post flu. I guess I have been "POTS free" for slightly less than a year. 11 months? I went to Disney World in May. I am back to my regular life and feel healthier and stronger than ever. I can even stand (yes STAND, not sit leaning back in a chair) on the sidelines and watch the kids play soccer. I still exercise daily, as I did prior to getting POTS. I feel extremely lucky that I have recovered from POTS. I probably had the "POTS flavor" that people may recover from over time. I have no clue what caused my POTS. I noticed a few messages where people asked me what I did to recover. It's obviously hard to exercise when you can't even sit up in bed. The volume expansion (Florinef and DDAVP) prescribed by a compassionate endocrinologist helped me get back on my feet. I started gradually exercising and then I turned into an exercise demon. I was really ticked off that I still had POTS when I got up to jogging 8 miles and day and then jumping on the stair master for an hour. At that point, I saw Dr. Levine who confirmed my blood volume was "high", as is normal with athletes. I was able to get off of the Florinef and DDAVP, and then the POTS disappeared. I have no idea if the overly aggressive exercise regimen has any benefit over a more reasonable regimen??? I would venture to say most doctors would advise against this route? The other thing I did differently was that I FORCED myself up. I was in tears and pain everyday for a good year. I would not allow myself to lye in bed unless I was sleeping. I had a recliner and then pushed myself to sit in a regular high back chair. I forced myself to do housework and garden, etc... I started accompanying my family everywhere, even if I felt bad. I would say that I took a very aggressive approach to recovery, not necessarily a gentle approach. It's almost as if I had to retrain my body to be upright again (if that makes any sense). Someone asked if I experienced post-exertional fatigue. YES! especially in the beginning, but it seemed to get better over time Someone asked me if I did tilt training. No. I tried and found it didn't seem to help. Once I accepted that I hd a chronic condition I started to improve. Perhaps the old saying is true. What we resist persists. Best wishes to all. I just wanted to give a little hope. It is possible to improve and even recover.
  3. Any of your docs suggest the saline with albumin?
  4. Julieph85, I haven't been on this forums in maybe over 6 months. For some odd reason, I felt compelled to pop in today, so I thought I would respond to your familiar post. The orthostatic hypertension could certainly be from deconditioning. Your body's reaction to be putting on strict bed rest is "normal". The human body is not meant to lie in bed for weeks on end. The orthostatic hypertension is a sign of a healthy autonomic nervous trying to compensate for a heart that no longer has the ability to pump blood back upstairs. It is a sign of an overactive sympathetic nervous system in response to an under active heart. One would think the changes would "reverse" themselves after you were no longer stuck on bed rest. In my experience, it took 18 months of a very intensive exercise regimen to pull out of POTS. I basically had to build an athlete's heart to pull out of this. Beta blockers are counter intuitive. They lower heart contractility, so it is no wonder they make a good percentage of POTS patients feel worse. I was extremely ill for 3 years with POTS. I have no idea what caused it. I was not deconditioned when the first symptoms hit, but I got myself out of it by graded exercise and refusing to believe that I had an irreversible, scary condition. Best of luck! It is possible to pull out of this., especially with your past history.
  5. Oh brother... There are hundreds of people dropping dead every day of poor lifestyle choices, including a sedentary lifestyle with poor diet. I don't know many people who have exercised themselves to death. I'll have my husband pop on here and let everyone know if I drop dead anytime soon after a life of intense physical activity minus the year I spent in bed with POTS. It doesn't count if one of my neighbors inadvertently runs over me during one of my jogs. After a year and 5 months of exercise (above and beyond Dr. Levine's protocol), I no longer fit the clinical description of POTS. Finally after 3 years of ****, I seem to have pulled out this mess. I am left with residual crummy posture from hunching over all the time in my POTS induced stupor, resulting in neck pain and muscular problems that I did not have when POTS first hit. The next step is to work with a PT to correct my horrible posture. My heart rate and blood pressure is finally completely normal when upright, even when I stand still after 10 minutes. I don't know what in the heck caused POTS in my case. I was in great shape when I got POTS and do not recall having a virus. However, I can say without a doubt that exercise was the number one factor in pulling me out of this. I think father time also played a factor, but I bet money that I would still be ill if I chose to stay in bed or lead a cautious, sedentary lifestyle. I tried taking walks every on, and they were not helpful. Tachycardia at rest is not accomplishing the same thing as exercise. Exercise strengthens your heart muscle, resulting is a more efficient heartbeat over time. I have a life again. In fact, I am taking my kids to Disney World next week. I am running in a half marathon this October. I am not a Dr. Levine worshipper. You will not see me on you tube or blogging about my success. I saw him in January and found him minimally helpful as someone already exercising beyond his protocol. He's a little brash and recommended a couple medications that did not help. I do think his exercise protocol is a good option. There is no way he is selling this protocol. I am sure that is NOT his intention. Seriously, how much money would he make with the TONS of POTS patients out there? Right. I am sure there are more lucrative ventures, such as developing a drug for more well known chronic conditions. The IEEM at Presbyterian is a first rate research and teaching facility. As far as I know, Vanderbilt and Mayo also recommend exercise as a first line treatment for POTS. To play the devil's advocate, I think a researcher would have to cherry pick to find subjects willing to dedicate themselves to a high level exercise protocol, even in the healthy population, let alone people who can barely stand. By the way Sue, I agree with your conjecture.... regarding catecholamines, pheo, and blood volume. I have discussed this with 2 POTS specialists and my endocrinologist. It is a nasty cycle. I can tell you that I went from low blood volume to high blood volume by incorporating exercise. Best of luck to all. I believe this may be my last post on dinet. Life calls. Just to clarify... I am not biking in the Tour de France or practicing for the Olympics, or even running the Boston Marathon. I can certainly see the benefits of moderation. I don't think Dr. Levine's protocol comes even a tiny bit close to the exercise level athletes engaged in when referring to the studies on fibrosis and ventricular arrhythmias in lifelong athletes.
  6. Another possibility is Gilbert's syndrome. This is a benign condition that effects about 3% of the Caucasian population. Bilirubin in the blood is elevated, but not from liver disease. The elevated bilirubin is of the unconjugated form and is from a mild deficiency in the enzyme that converts unconjugated bilirubin to conjugated or direct bilirubin. Bilirubin levels can vary with Gilbert's and are affected by fasting and stress. My eyes always have a slight yellow ting, but at times they look more yellow than others. My own physician has the same thing. It is so common that he does not specifically mention it to patients with Gilbert's because it is not considered a disease. A simple blood test can rule out liver problems. I would make a visit to your physician, but don't freak out until then. There are certainly other possibilities than dreaded liver disease. People with Gilbert's start getting the elevated bilirubin in their mid 20s. This is an average.
  7. I have the lovely, mystery, partial DI syndrome and was diagnosed by an endo with a clinical interest in DI and went through the full hospital administered water dep study. DI or not DI? They settled on partial DI. However, I do not have hyperadrenergic POTS if we define that by upright catecholamine levels. I sometimes have orthostatic hypertension, but usually not in my everyday life. This can be induced on the tilt table. My upright catecholamines are completely normal (NE a bit under 300). I've had polyuria for 20 years, but I've only had POTS for 3 years. I only need the DDAVP in the morning. The frequent urination at night suddenly stopped and seems to have correlated with an improvement in my POTS. I agree that the polyuria could have something to do with catecholamine levels or constriction at the level of the kidney. If the kidney thinks we are hypertensive, we will start dumping salt and fluid. There is feedback loop involving AVP that goes from RAAS to the pituitary. Who really know though? Enough to make the brain spin. I concur. Oh, I do take a small dose of Florinef in the mornings.
  8. Here is a copy and paste from "Acetylcholinesterase Inhibition Improves Tachycardia in POTS" in the journal Circulation from Raj et al. regarding possible mechanism of action. The mechanism of the salutary action of pyridostigmine is not entirely clear, but we propose a model based on neurotrans- mission in the autonomic nervous system (Figure 4, top). Acetylcholine is the primary neurotransmitter in the auto- nomic ganglia in both the sympathetic and parasympathetic nervous systems. The parasympathetic nervous system uses acetylcholine again as the neurotransmitter at the postgangli- onic synapse. This results in an inhibitory effect on heart rate. In contrast, the sympathetic nervous system uses norepineph- rine as the postganglionic synaptic neurotransmitter. This results in a direct increase in heart rate and blood pressure (Figure 4, solid lines); however, the increase in blood pressure is modulated by the baroreflex, which leads to a reduction in sympathetic tone, an increase in parasympathetic tone, and a subsequent decrease in heart rate (Figure 4, dashed lines). In the presence of an acetylcholinesterase inhibitor (Figure 4, bottom), synaptic acetylcholine is increased in the auto- nomic ganglia of both the sympathetic and parasympathetic nervous systems, which results in increased cholinergic transmission in both limbs. At the postganglionic synapse of the parasympathetic nervous system, the augmented level of acetylcholine (due to both increased transmission and de- creased acetylcholine degradation) has a strong inhibitory effect on heart rate. Because the sympathetic nervous system uses norepinephrine as the postganglionic neurotransmitter, the acetylcholinesterase inhibitor has no effect at this level. There is slightly more sympathetic nervous system traffic (thicker lines) as a result of the ganglionic acetylcholine augmentation. The resulting increase in blood pressure leads to augmented baroreceptor activity, which also contributes to a restraining effect on heart rate. In support of this model, there are recent data that pyridostigmine has been found to increase baroreflex sensitivity in both a murine model22 and in patients with POTS.23 It is likely that the major effect of acetylcholinesterase inhibition in patients with POTS is the reduction in heart rate through augmentation of parasympathetic tone. It is possible, however, that other mechanisms also play a role in the apparent benefit of acetylcholinesterase inhibition. Jacob et al11 have reported that some patients with POTS have a “partial dysautonomia,” with focal impairment of sympa- thetic tone in the lower extremity, which leads to impaired vasoconstriction. Stewart et al6 have shown that intravenous phenylephrine, an -1 adrenoreceptor agonist, acutely im- proved orthostatic tolerance through peripheral vasoconstric- tion in a cohort of patients with POTS. Augmentation of sympathetic tone due to ganglionic acetylcholinesterase inhi- bition might increase peripheral vascular resistance through -1 receptor stimulation. It is tempting to speculate that this “non–heart rate” mechanism may play an important role in the symptomatic improvement seen with acetylcholinesterase inhibition in POTS; however, vascular resistance was not measured in the present study. The augmentation in sympathetic tone with acetylcholines- terase inhibition has proven clinically useful in patients with orthostatic hypotension. We found that peripheral acetylcho- linesterase inhibition increased blood pressure among pa- tients with autonomic failure in a dose-dependent fashion.8 Singer et al9 reported that pyridostigmine decreased ortho- static hypotension in patients with neurogenic orthostatic hypotension by increasing the peripheral resistance in re- sponse to head-up tilt and consequently improved their orthostatic symptoms.
  9. The approved indication is myasthenia gravis, which as we know may cause profound skeletal weakness. I don't know if Mestinon is used to treat myopathy of the GI tract, though it definitely may increase peristalsis by ramping up parasympathetic activity. One word of caution Mestinon can actually cause muscle weakness (the very thing it is used to treat). The dose has to be carefully tailored to the patient.
  10. Sue- Mestinon may be especially good if you have gastroparesis or slow movement of the GI tract. This is one of the reasons I am opting out of Mestinon for now. I think it's one of those things that you just have to try and judge for yourself. What I personally don't like about Mestinon is it's broad mechanism of action, especially if POTS is a partial dysautonomia.
  11. Dr. Ben Levine (the exercise guy) in Dallas thought the mechanism of my POTS was parasympathetic withdrawal and recommended that I try Mestinon as a next step. I also have postural hypertension (no hypotension) with completely normal catecholamines supine and then after standing and high/ normal overall blood volume. I still haven't taken the leap because I have been feeling much better lately. I'm not 100%, but I am a happy 70%, so I don't want to rock the boat.It may be a good option for select patients.
  12. Diagnosis of Parkinson's is made by clinical symptoms and evaluation by a neurologist, as well as response to levodopa. There is no quantitative lab test or scan. The dopamine blood and urine tests are not diagnostic for Parkinson's. Looking forward to the results of this study. Keep the faith.
  13. I don't know that a blood draw for dopamine or 24 hr urine collection translates well into the amount present at the kidney. Parkinson's patients have low dopamine in the brain, but the blood and urine tests are not useful for diagnosis, because dopamine levels are only effected in the brain. Plus, a dopamine level < 20 pg/ml is considered normal. They are manipulating dopamine levels peripherally with carbidopa, but I don't think they actually know what the specific kidney dopamine levels are. Issie- Thanks for bumping the old post. Funny that we are still going round and round.
  14. http://clinicaltrials.gov/ct2/show/NCT00685919 I look forward to a future interpretation by the Vanderbilt team.
  15. Vanderbilt has an ongoing study looking at kidney dopamine and POTS.
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