Permanent atrial fibrillation in heart failure patients as another condition with increased reverse triiodothyronine concentration

Don't know abou tyou, but I am not convinced that the reverse T3 is quite so innocent as simply being a novel sign appears to imply. Unfortunately, for now, this appears under the "That's all folks!" banner.

Neuro Endocrinol Lett. 2016 Sep 18;37(4):337-342. [Epub ahead of print]

Permanent atrial fibrillation in heart failure patients as another condition with increased reverse triiodothyronine concentration.

[No authors listed]

Abstract

OBJECTIVE:

To fully investigate the thyroid hormonal function in patients with the most common arrhythmia - atrial fibrillation.

MATERIALS AND METHODS:

120 patients (aged 55-85 yrs) with symptoms of congestive heart failure exacerbation and no other concomitant disorders (inclusion criteria: normal cardiac troponin T at admission and 12 hours after, normal renal, hepatic and respiratory function; exclusion criteria: inflammatory state, history of myocardial infarction). Depending on the presence of permanent atrial fibrillation (PAF), patients were divided into two groups: PAF (34 females, 26 males) and regular sinus heart rhythm (43 females, 17 males), the groups did not differ in terms of heart rate, blood pressure, presence of overt/subclinical thyroid dysfunction, and medical therapy used. In all subjects thyroid stimulating hormone, free thyroxine, free triiodothyronine, reverse triiodothyronine were measured; echocardiography was performed.

RESULTS:

PAF group showed higher FT4 and rT3 (1.41 vs. 1.27 ng/dl, p=0.0007; 0.61 vs. 0.32 ng/ml, p<0.0001, respectively). With ROC curve analysis the biochemical thyroid related factor of the highest prognostic value for PAF occurrence (with the highest sensitivity and specificity: 77% and 72%, respectively) was rT3 with the cut-off of above 0.3 ng/ml. Also, a positive correlation between rT3 levels and left ventricular posterior wall diameter was observed (Spearman's correlation coefficient 0.33, p=0.0093).

CONCLUSIONS:

PAF is another condition where an increase in rT3 is observed. rT3 concentration above 0.3 ng/ml may be a novel biochemical sign associated with the presence of PAF in patients with chronic heart failure.

PMID: 27857052

[PubMed - as supplied by publisher]

ncbi.nlm.nih.gov/pubmed/278...

15 Replies

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  • Or, could it not be that because the T4 was converting to rT3, levels of FT3 were low, and that's what caused the AF? I don't trust studies that ignore FT3.

  • On the basis that FT3 is a standard test (even if often not performed even when desirable) it is utter folly to ignore it when performing such investigations as above.

    And to ignore it because it wasn't measured, whether because the lab refused, the medics didn't request, or any other reason, does undermine the investigators themselves.

    I'd certainly rather like to know what happens to T2 levels when there is high rT3 - especially if T3 levels are acceptable.

  • What if t3 has nothing to do with it? I mean there is a reason why t4 converts to rt3, whatever the reason is ,it happens because something is wrong.

    Something could be wrong before the t3 dropped.

    Something else happens first, which causes our body to hit the alarm button and force you to slow down and rest.

    I have always thought that rt3 has sort of a big role. To me it makes sense it is a response to something that is wrong and doesn't have to be related to thyroid issues at all as thyroid hormones drop during any illness to try to tell us to rest.

    Over here in finland they do say rt3 has sort of protective role and one should not interfere it by taking T3 unless you know why rt3 is high. By protective it means it slows down your body functions for reason so you would rest. But in these cases it is temporary of course, after healing rt3 should decrease.

    Just wanted to say that doesn't necessarily mean t3 would be ignored, it just simply isn't always the cause?

    Ofc I didn't read the article so shoot me if it was said t3 has role at all :P

  • Like so much in thyroid medicine, clarity is almost entirely absent!

    Again, like so much in thyroid medicine, we need to distinguish between high rT3 in those who have no thyroid issues and those with such issues - whether the rT3 is high at least partly due to exogenous levothyroxine, or excess endogenous T4 production, or something else...

    We are very much lacking a decent set of factors which control the balances of the whole thyroid system. Though we do know some factors which upset them.

  • Totally agree with everything you say. rT3 is a form of protection, it is natural and necessary, and does mean there's something wrong in the body. And, it would make sense that if you have heart problems, you would have high rT3, to force the body to rest. But this paper seems to be implying that the rT3 is responsible for the AF.

    If you're doing research, it doesn't make any sense to measure the rT3 and T4 only, and ignore the FT3. And I was just talking about this paper, not rT3 in general. That's another discussion entirely.

  • I know you meant rt3 in this context, but I just rambling about it.

    I do not believe it's rt3 causing the issue but something else which leads to high rt3 , therefore level of t3 would be meaningless as the damage was done already. So low t3 was not the cause.

    But i find most of these studies failing to separate all possible scenarios which then leads to possibly false results. Tho if the study would prove that conversion issue is real then next step would be obvious and it would just show what we already know of importance of t3.

  • But, we all know that low T3 can cause heart problems, that was my point. Therefore, it is ludicrous to do a study on heart problems, and ignore the FT3. The heart needs T3, therefore, in an unhealthy heart, it seems logical to me to check that it's getting enough T3.

    What is more, as helvella says, it's rubbish science to research anything that involves the thyroid without taking the active hormone into consideration.

  • I know and I agree, but if the damage was done before t3 dropped then it had nothing to do with it.

    I know you are passionate about T3 and it's not wrong , we know how important it is and we all hope it would be admitted rather sooner than later.

    I am just trying to say what if the importance of t3 was irrelevant either because the cause of high rt3 was somewhere else in the beginning. I think it takes a bit time before the rt3 affects t3 or your body reacts to it. OR the relevance of t3 doesn't bring anything new as this could point out the mechanism of poor conversion is the culprit. T3 might not even drop that much it just doesn't enter the cells.

    Now as we know most doctors consider rt3 humbug. These type of studies could point out it really does provide important information. Next step is to figure out how to use it and how to separate different conditions from each other.

    Complexity of thyroid function should be torn in pieces and create a "map" of all different variables to show how many different types of point of views there are, not just T4 all. This study could even provide some needed information of harm of T4 only for those who convert it to rt3.

    Dunno. Just trying to see a bigger picture.

  • No, I'm not passionate about anything. I just know the difference between good science and bad.

  • Pffft. I don't mean passionate in negative way. Most of us who truly understand the importance of t3 are passionate about it. That's why we keep hanging here and share information over and over again.

    We keep brining up the safety of t3 while doctors try to judge it.

  • I didn't know there was a negative way to be passionate.

    The point is, good science covers all the bases, doesn't just ignore half the data. Of course the heart problems could be nothing to do with thyroid whatsoever, and the rT3 is just a consequence of ill health. But we already know that happens, why waste a whole research project on it? It is just what you would expect if you know anything about thyroid. So, I don't see that this study advances us in any way whatsoever. But they should still have done all relevant measurements, and they didn't, they didn't measure the FT3, and therefore, for me, it's bad science, and to be ignored. That's all I was saying.

  • HI I am new here but certainly not to thyroid issues . I disagree that rT3 is necessary. I believe it is a leftover from our hunter gatherer days. No longer needed but not gone yet. Back then, when we were injured or ill, RT3 could save your life by lowering your metabolic rate so you didn't starve while incapacitated for hunting. It is also present as part of a hibernation cycle of certain mammals to lower their metabolism while they hibernate. Now we no longer are in danger of starving when ill, nor do we hibernate. RT3 can be a huge issue for people, with and without other thyroid issues. It can go too high in a Diabetic person if their glucose commonly goes over 140 on their meter. It can also be caused by toxins in our food and water. Fluoride and chlorine are two such toxins we consume almost daily. To my knowledge there is no way to insure lower RT3 levels other than taking straight T3. I am currently on only 50mcg of T4 and 90mcg T3 and my RT3 is beginning to build again. I do best on only T3 all the time. I have congestive heart failure that only acts up when my T3 levels are too low and RT3 high.

  • We have seen all too many cases of starvation over my lifetime. It is very definitely not something of the distant past for those in regions of famine, war, and other events.

    In my view, the evidence on rT3 is still inadequate.

  • I know some who had functional hypothyroidism caused by strict diet which then corrected by itself after consuming enough calories (even upto 5000 )So high rt3 was a response to poor nutrition which could be fixed without medication. But it doesn't work for everyone of course.

  • We used to think the appendix was just a relic of the past. Now we know better.

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