This is a case report, of a patient with dilated cardiomyopathy (DCM) and heart failure, caused by true hypothyroidism (not IH) and cured with T4
“Hypothyroidism-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/, which I first discussed on December 15, 2021.
It concerns a patient with dilated cardiomyopathy (DCM) and heart failure, caused by true hypothyroidism and cured with T4.
Abstract (paraphrased, for brevity)
A young female presented with heart failure and was diagnosed as having DCM. Echocardiography revealed left ventricular global hypokinesia (weak heart muscle contractions) and “severely depressed systolic function” (reduced ability of the heart to pump blood into the aorta).
The past history included hoarseness (a classic hypothyroid symptom), for two years and the Thyroid profile revealed a very high TSH (Thyroid-Stimulating Hormone) value of 313 μIU/ml. Her FT4 (free thyroxine) was very low, at 0.220 ng/dl. No mention was made of her FT3, nor of her reverse T3.
The authors state (paraphrased, for brevity):
”The heart relies mainly on Triiodothyronine (T3): there is no significant deiodinase activity inside myocytes, so the heart muscle cells (myocytes) are unable to convert T4 into T3: T3 is directly transported into the myocyte, from the blood”.
They go on, to explain that “T3 modulates inotropic and lusitropic properties of the myocardium, myocardial contractility, and vascular function” (in other words, T3 enables the myocytes to contract) and that “Hypothyroidism can cause bradycardia (slow heartbeat), impaired contractility, impaired diastolic filling of the heart, increased systemic vascular resistance, diastolic hypertension, and endothelial dysfunction.”
Further, they say, “It has also been demonstrated that Subclinical 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 a normal thyroid gland may have low levels of FT3, with normal T4 and TSH. ** Low serum FT3 in these patients strongly predicts all-cause and cardiovascular mortality. The most consistent cardiac abnormality recognized in patients with overt hypothyroidism is impairment of Left Ventricular 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 young lady’s cardiomyopathy was caused by T3 deficiency, they did not test for FT3 and reverse T3, which would have yielded a low (<20) T3/rT3 ratio, to confirm the diagnosis of LT3S.
* The following are Synonyms, for Subclinical Hypothyroidism:
– Intracellular (Functional) Hypothyroidism (IH),
– Low T3 syndrome (LT3S)
– Euthyroid Sick Syndrome(ESS)
– Non-Thyroidal Illness
Therapy, for IH (LT3S, or “subclinical hypothyroidism”)
In my opinion, prescribing slow-release T3, by itself or in addition to T4, would have corrected this young woman’s problem more certainly and more quickly. Also, the short half-life of T3 would have allowed daily reassessment, with titration of the T3 dose according to the serum concentration of T3, allowing ongoing monitoring and better control of her life-threatening condition.
** The hallmarks of Intracellular Hypothyroidism are low Free T3 and elevated reverse T3, yielding a FT3/rT3 ratio of less than 20, with normal TSH and FT4: The FT3/rT3 ratio is diagnostic; but a low FT3 by itself suggests a diagnosis of IH.
COMMENTS:
(1) The authors are to be congratulated on their success: the patient recovered due to treatment with T4, thus proving the premise of the paper.
(2) The reader should appreciate that this was not Takotsubo-type DCM, which is due to stress-related intracellular hypothyroidism: the high TSH tells us that she had true hypothyroidism. (T4 and TSH are normal in Intracellular Hypothyroidism, unless there is underlying true hypothyroidism).
(3) Had this patient’s problem been due to IH, the T4 with which she was treated would have been converted into reverse T3 and she would not have recovered. Therefore the therapy she received was exactly correct, although I do think that if combination T4+T3 had been prescribed, she would have recovered more quickly.
Why a blog on this subject?
(1) This paper emphasises that Low FT3 can be responsible for heart failure.
(2) All patients presenting with CHF symptoms should have a full thyroid profile done, including TSH, Free T4, Free T3 and reverse T3, to exclude a diagnosis of Takotsubo-type DCM due to stress-related IH: Takotsubo’s DCM is due to stress-related Low T3 Syndrome and requires treatment with slow-release T3, not with T4: The FT3/rT3 ratio permits facile diagnosis of IH (Intracellular Hypothyroidism, a.k.a. the synonyms listed above), which is easily, safely treated with S-R Triiodothyronine.
Caveat
Those familiar with this SUBSTACK will have noted that Intracellular Hypothyroidism is a recurring theme in my posts: the background to this is that IH occurs in all acutely life-threatening and/or chronic conditions. It is found in 100% of people admitted to intensive care units and most people with chronic conditions, Including starvation and obesity.
So if my posts “sound like a broken record”, it is because Intracellular Hypothyroidism is so pervasive that every ill person should be investigated for IH, by checking the FT3/reverse T3 ratio.