This is a case report, titled 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/. It reports on a patient with dilated cardiomyopathy caused by hypothyroidism, 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 and severely depressed systolic function. The past history included hoarseness (a classic hypothyroid symptom), for two years and the Thyroid profile revealed a grossly elevated TSH (thyroid-stimulating hormone) value of 313 μIU/ml. Her FT4 (free thyroxine) was very low, at 0.220 ng/dl.

The authors state (paraphrased, 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 that “T3 modulates inotropic and lusitropic properties of the myocardium, myocardial contractility, and vascular function” and that “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 a 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 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 lady’s cardiomyopathy was caused by T3 deficiency, they did not test for T3 and reverse T3, which would yielded a T3/are T3 ratio, to clinch the diagnosis.

** Synonymous with intracellular (Functional) Hypothyroidism. In my opinion, prescribing slow-release T3 in addition to T4 would have corrected the problem more certainly and more quickly. Also, the short half-life of T3 would have allowed daily reassessment, ongoing monitoring and better control of her life-threatening condition.

*** The hallmarks of intracellular hypothyroidism are very low T3, elevated reverse T3 (T3/rT3 ratio of less than 20) and normal TSH and T4. The T3/rT3 ratio is diagnostic; but a low T3 by itself is very suggestive of IH.

(1) Although no mention was made of the serum T3 level, nor of reverse T3, this patient evidently did not have intracellular hypothyroidism. She had true hypothyroidism, since the T4 and TSH are usually normal in intracellular hypothyroidism unless there is underlying true hypothyroidism. If this patient actually had IH, the T4 with which she was treated would have been converted into reverse T3 and she would not have recovered.

This patient’s therapy therefore was exactly correct, although I do think that if combination T4+T3 had been prescribed, she would have recovered more quickly. In any event, the patient recovered due to treatment with T4, thus proving the premise of the paper. The authors are to be congratulated on their success.

(2) My reason for a blog post based on this paper is that it emphasises that hypothyroidism can be responsible for heart failure. Therefore all patients presenting with CHF symptoms should have a full thyroid profile done, to include TSH, free T4, free T3 and reverse T3. This would permit facile diagnosis of intracellular hypothyroidism (a.k.a. euthyroid sick syndrome, low T3 syndrome, nonthyroidal illness, functional hypothyroidism, etc.), which is easily and safely treated with slow-release triiodothyronine.

Please see the page on THYROID HORMONE, for details re. intracellular hypothyroidism.

I am a Toronto-trained Urologist. I practiced in downtown Toronto, from 1977 to 1997, when I went to Saudi Arabia as chief of Urology at the Armed Forces (teaching) hospital in Tabuk. Returning to Toronto in Y2000, I switched to family practice. In 2007, began to prescribe Hormone Restoration Therapy and in 2012, I became a member of the American Academy of Antiaging Medicine [A4M]. I successfully wrote the A4M's written examination in December, 2013 and In May, 2016 I passed the oral examination, for accreditation as a BHRT consultant. In 2014 I began BHRT practice in Collingwood, Ontario and in January, 2017, joined the Stone Tree Naturopathic Clinic. Now I am 82 and have retired, but it seems wasteful to jettison my learning and experience: the medical establishment knows nothing of BHRT / Functonal medicine and I feel obliged to offer my knowledge in the interest of those who are willing to think outside the box. MY QUALIFICATIONS: MB, BS, (from UWI), 1964. LMCC 1969. FRCSC (Urology), 1974. ECFMG 1984. Florida license 1998 [inactive], ABAARM Certification [A4M], 2016. I am a Member of CSAMM [the Canadian Society for Aging and Metabolic Medicine], the OMA&CMA, SUSO, CUA, RCP&S/C. PRACTICE TO DATE: Consultation in Functional Medicine, including assessment of Chronic Fatigue Syndrome, Fibromyalgia, Andropause, Menopause, Teenage and Postpartum Depression/Panic Attacks, Thyroid Hormone malfunction, Infertility, Sexual Dysfunction and “the Undiagnosable”. ALL ARE WELCOME to read, comment or question!

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