Recently, abnormal thyroid function was shown to be common in patients with Takotsubo syndrome (TTS), being classified into “endocrine-type” and “stress-type” responses. The aim of this study was to investigate the association between thyroid homeostasis and TTS in a larger international registry.
Methods
In total 288 patients with TTS were enrolled through the GEIST multicentre registry from Germany, Italy and Spain. Thyrotropin (TSH), free T4 (FT4) and free T3 (FT3) concentrations were analysed at admission. Data were collected both retrospectively and prospectively from 2017 onwards. Primary endpoints included in-hospital and all-cause fatality, determined by cluster analysis using an unsupervised machine learning algorithm (k-medoids).
Findings
Three clusters were identified, classifying TTS with low (TSLT), high (TSHT) and normal (TSNT) thyroid output, based on TSH and FT4 levels in relation to the median thyroid’s secretory capacity (SPINA-GT). Although TSH and FT4 concentrations were similar among survivors and non-survivors, these clusters were significantly associated with patient outcomes. In the longitudinal Kaplan–Meier analysis including in- and out-of-hospital survival, the prognosis related to concentrations of TSH, FT4, and FT3 as well as SPINA-GT, deiodinase activity (SPINA-GD) and clusters. Patients in the TSHT cluster and with cardiogenic shock had a lower initial left ventricular ejection fraction (LVEF).
Interpretation
This study suggests that thyroid hormones may impact the evolution and prognosis of TTS. The findings indicate that thyroid-derived biomarkers may help identify high-risk patients and pave the way for novel personalized and preventive therapeutic options.
Funding
This research was not funded by any public, commercial, or not-for-profit agencies.
#SPINA_GT, #SPINA_GD and Jostel's TSH index (#JTI or #TSHI) are predictors of survival in patients with #Takotsubo syndrome (#stress #cardiomyopathy), as recently demonstrated in the international GEIST registry.
Written by
helvella
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Gosh this is beginning to make sense of my mother's untimely death from a heart attack at age 64....50 years ago!
Possible Takotsobu Syndrome or broken heart syndrome! I doubt it was known about 50 years ago!
If I may explain why I jumped in here...
Looking back I'm now sure my mother had several symptoms of hypothyroidism....but she was never diagnosed.
I had no idea back then about thyroid disease... or about what the future held for me
She died very suddenly, less than 3 months after my father died following several years of heart related problems.
Again, looking back, I think my father also had symptoms of a thyroid problem, there is now some evidence of this.
A few years ago I discovered that I have the Dio2 polymorphism inherited from both parents....so both my parents had impaired T4 to T3 conversion and very possibly low T3
We always thought, given their absolute devotion to each other, that our mother died of a broken heart.....perhaps she did have low ( cellular) T3 and developed TTS
Some members know that I need high dose T3-only to function....background in my bio.
They also know that I write frequently about the importance of T3....which has prevented my body from shutting down.
This forum has enabled me to identify my thyroid condition and also to discover that my younger son has a failing thyroid.
Thank you TUK.
With apologies, this is rather a personal journey which I hesitated to write about but perhaps it serves as an example of how this study suggests that thyroid hormones may impact the evolution and prognosis of TTS and the importance of novel personalized and preventive therapeutic options.
Both FT4 and FT3 must be tested if we are to make any progress
My view is your reply is absolutely on topic, highly relevant, and potentially of great value.
Sometimes we get the best understanding by having both an explanation and an example available side by side.
There are so many stories of loving couples - one dying shortly after the other. I think we have tended to imagine some sort of pining away (not meant to be dismissive - just don't want to misuse psycho-babble). To see that there might be a direct and clear physiological/biochemical basis truly up-ends the classical "story" view.
We know that the heart needs a great deal of T3, so by lumping it in "clusters' rather than focussing on it as the active thyroid hormone within the cluster they appear to have missed the significant clue to solving their problem.
Yet again the importance of T3 to the entire body in general, and to the heart specifically, has been lost.
I've long come to the conclusion that T3 terrifies the medical profession....and I think it is more than the price hike of a few years ago that they appear to hide behind.
Without a high dose of T3 that sends medics running for the hills, and which stopped my body from shutting down, I would not be here regularly ranting about the importance of T3... in a therapeutic dose large enough to contradict current guidelines
I don't think it needs blue sky thinking to clarify this issue.....just open minds and an understanding that testing/ investigating T3 is key.
Takotsubo is referred to as a syndrome...a collection of symptoms
Although TSH and FT4 concentrations were similar among survivors and non-survivors, these clusters were significantly associated with patient outcomes.
"Significantly associated" suggests they mean "correlated". But if that is what they meant why didn't they say so?
It would suggest to me that the strength of any association is not that high, despite the use of the word "significantly".
I've heard many times that "correlation" doesn't mean "causation".
But I also thought "association" was less strong than "correlation".
Are the authors trying to encourage people to make this connection just with words?
Another thing I notice is that the first sentence I quoted above doesn't mention Free T3, so I assume it wasn't "significantly associated" with patient outcomes, which is surprising in this context because Free T3 is the active hormone.
If I was going to investigate Takotsubo Syndrome I would have firstly tested Cortisol levels, and secondly Adrenaline levels before considering thyroid. But then I'm not a doctor.
Really this paper yet again emphasises the effect of lack of T3 in particular on the heart. There is so much information now on this it should be understood by every blooming doctor on the planet, not just (but most especially) endocrinologists.
The information is in fact overwhelming! I am collecting the papers to inform my GP who seems to be dawdling over a referral to Dr Salman Razvi, a UK doctor presently doing a research programme into T3 and heart failure . helvella has recently provided information on this research too.
The chief endo in my area is one of the prominent endos in the country holding back on using any new research which does not suit him. He has even managed to get his name on this research that he Pooh poohs (T3) at every turn. I suppose he is covering his back by doing that, should the whole world’s view on T3 suddenly change and move away from his scandalous behaviour and influence.
I have often wondered about my possibly having suffered this very condition. I was already suffering hugely from stress (aka low T3) when my husband was involved in an emergency landing, when an engine exploded on his plane shortly after take off. Within a fortnight I had an MI. Pretty classic. And pretty much whatever you call it but basically Low T3.
In the absence of ‘proper’ diagnosis and help on this journey, for many of us it’s our only option. Hence our presence here on the Forum. It makes us vulnerable and maybe appearing to be suffering from mental health issues, in some quarters.
Thank you for this important information! I’ll add my related anecdote: in 2022 until Jan 2024 I had an acute myocarditis and was very sick. My GP of course at the very beginning said I should stop taking T3. (This GP always resisted my T3-only therapy and would predict dire things and try to blame any issue on it.) I asked the cardiologist, a well-known figure in my region, who said “NO! Absolutely keep taking your T3: thyroid hormones in proper balance are essential for the heart. We will measure them every visit to be sure all is well.” I’m completely healed now but at least there’s one cardiologist who knows this!
I suffered aTakotsubo having been informed of my son’s sudden death over the phone . 5 hours later I was taken to hospital. The ambulance driver recognised it when they first got to me , it took blood test etc to confirm. I was in hospital for 9 days and recovered on ,
Can you explain , is it because of lack of t3 ? Or too much ?
That is an awful way to learn of the worst possible news. How lucky you were it was recognised!
In my case I had no ‘enzymes’ in my blood or too few for a normal MI. They were scratching their heads - it was twenty plus years ago! I can’t be sure what happened. I now call it a MINOCCA. Myocardial Infarction No Occlusions …..something.
I have continued to have symptoms but no repeat, so far, of whatever it was. My T3 levels however are getting lower and lower and I am getting more persistent symptoms. However I have survived a very long time since.
So too much or too little T3? I think too little BUT I have found myself ‘over sensitive’ to T3 when attempting to take it. (In fact over reactive to T4 too). Hence my pretty desperate pursuit of Dr. Salman Razvi, a lone voice in the U.K. endocrinology as far as I know, with a genuine interest and acknowledgement of the connection.
I viewed this page in Apple Safari using their translation feature so I could read it in English and it was close to perfect. I imagine similar results in other browser translations but it is better you choose how to translate than me make that choice.
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Never delay seeking advice or dialling emergency services because of something that you have read on HealthUnlocked.
TSH is just the 'opinion' of your Pituitary about your dose ~ but your Pituitary's 'opinion' is a bit warped once you take Thyroid Hormone.
Mathematical modeling of the pituitary-thyroid feedback loop: role of a TSH-T3-shunt and sensitivity analysis
