And cured with T4: this is a case report, titledHypothyroidism-induced reversible dilated cardiomyopathy; ,
by P Rastogi, A Dua, S Attri, and H Sharma, J Postgrad Med. 2018 Jul-Sep; 64(3): 177–179. doi: 10.4103/jpgm.JPGM_154_17, PMCID: PMC6066629PMID: 29992912 , https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6066629/
This paper reports on a young female with DILATED CARDIOMYOPATHY CAUSED BY HYPOTHYROIDISM and cured with T4.
Interestingly, the authors state (I have paraphrased this, for brevity):
”The heart relies mainly on Triiodothyronine (T3) because there is no significant deiodinase activity inside myocytes: T3 is directly transported into the myocyte”.
They go on, to explain “T3 modulates inotropic and lusitropic properties of the myocardium, myocardial contractility, and vascular function”………….. and
“Hypothyroidism can produce bradycardia, impaired contractility, impaired diastolic filling, increased systemic vascular resistance, diastolic hypertension, and endothelial dysfunction.” 
Further, they say ………….
“It has also been demonstrated that subclinical (intracellular) Hypothyroidism ** may lead to heart failure.”
“Studies have shown that as in the sick-euthyroid syndrome **, which occurs in nonthyroidal illnesses like sepsis, patients with heart failure who have normal thyroid gland may have low levels of T3 with normal T4 and TSH”.
“Low serum T3 in these patients strongly predicts all-cause and cardiovascular mortality”. “The most consistent cardiac abnormality recognized in patients with overt hypothyroidism is impairment of LV diastolic function characterized by slowed myocardial relaxation and impaired early ventricular filling.”…………
In spite of their recognition of T3 as a prime mover in myocardial function, their appreciation of hypothyroidism as a cause of heart failure and their freely admitted realisation that this lady’s cardiomyopathy was caused by T3 deficiency, they still treated her with T4 instead of T3 !
MESSAGE: ** These terms are synonymous with Functional (INTRACELLULAR) Hypothyroidism and in my opinion prescribing oral, slow-release T3 would not only have corrected the problem more certainly and more quickly, but the short half-life of T3 would have allowed daily reassessment, ongoing monitoring and better control of her life-threatening condition.
Fortunately, the patient recovered due to treatment with T4, thus proving the premise of the title of their paper.
See the page on THYROID HORMONE, for details re. functional, intracellular hypothyroidism.
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