Low-T3 syndrome and angina

When deprived of T3 hormone, the heart suffers

Low-T3 Syndrome—associated with angina or myocardial infarction: Although studies on Low-T3 syndrome usually focus on patients with “normal” thyroid glands and explicitly exclude patients with thyroid disease and/or on T4-therapy, the dysfunction of thyroid hormone equilibrium is also relevant to patients who suffer from Low-T3 while on T4-therapy despite having a normal TSH.

NOTE: The following review involves ethical copying of limited content from journal articles within Canadian Copyright Law. See the Wikipedia article “Fair dealing in Canadian copyright law” or the Law itself, at http://laws-lois.justice.gc.ca/eng/acts/c-42/page-18.html

Low-T3 and Angina articles

Kim, B.-B., Ku, Y.-H., Han, J.-Y., & Ha, J.-M. (2013). Relation of Triiodothyronine to Subclinical Myocardial Injury in Patients With Chest Pain. The American Journal of Cardiology, 111(8), 1087. http://doi.org/10.1016/j.amjcard.2012.12.039


Why the study was done: “Heart dysfunctions have been shown to be associated with altered concentrations of thyroid hormones. However, the relation between thyroid hormones and subclinical myocardial injury in those without clinically apparent coronary heart disease is not well-established.”
[ … ]After adjusting for traditional risk factors, the odds ratio for an elevated hs-cTnT level (‡0.014 ng/ml) for patients with T3 <74.6 ng/dl was 6.95 (95% confidence interval 3.09 to 15.66) compared to patients with T3 ‡74.6 ng/dl.
In conclusion, the T3 levels were negatively related to hs-cTnT levels among patients without clinically obvious coronary heart disease.


“A total of 365 consecutive patients with chest pain, whose thyrotropin (TSH), free thyroxine (FT4), triiodothyronine (T3), and hs-cTnT levels had been measured in the emergency room or outpatient department of the cardiovascular center of Chosun University Hospital from November 2011 to January 2012 were included in the present study.” (p. 1087)

“Of these 365 patients, 250 were included in the present analysis, because patients who were diagnosed with CHD or overt hyperthyroidism were excluded.” (p. 1087)


The mean TSH, T3, FT4, and hs-cTnT levels for the overall study population were

  • TSH 5.97 ± 15.0 mIU/L (median 1.92, interquartile range 1.02 to 3.31),
  • T3 84.9 ± 36.1 ng/dl (median 81.7, interquartile range 58.1 to 110.0),
  • FT4 1.18 ± 0.42 ng/dl (median 1.15, interquartile range 0.98 to 1.38), and
  • hs-cTnT 0.014 ± 0.020 ng/ml (median 0.003, interquartile range
    0.003 to 0.017), respectively.

    • A total of 115 subjects (46%) had measurable hs-cTnT levels (>0.003 ng/ml).
    • Of the participants, 28% had high hs-cTnT levels (0.014 ng/ml).

We found a moderate, but significantly negative, correlation between T3 and hs-cTnT levels (r = 0.428, p <0.001). The TSH and FT4 levels were not associated with the hs-cTnT levels.” (p. 1088)

Table 1. Low T3 group (<74.6 ng/dl) data:

  • Triiodothyronine [T3] ng/dl = 51.0 ± 15.7
  • High-sensitivity cardiac troponin T (ng/ml) = 0.023  ± 0.027 (p. 1089)

Their Discussion

The main finding of the present study was the independent association of low T3 levels with subclinical myocardial injury, as assessed by elevated hs-cTnT levels in patients with chest pain and without clinically evident CHD. The association was comparable to the predictive significance of age, left ventricular hypertrophy, and renal dysfunction.” (p. 1089)
“A possible mechanism by which low thyroid function induces myocardial damage is impairment of coronary blood flow, because thyroid hormones influence the vasoreactive properties of vessels. Other mechanisms include myocardial fibrosis and a gene program resembling that of pathologic hypertrophy.” (p. 1090)
“Our outcomes suggest that [low] T3 is an indicator of subclinical myocardial injury compared to TSH or FT4.” (p. 1090)
“Apart from the existence of thyroid hypofunction, and in contrast to other organs, the heart is particularly susceptible to diminution in biologically active T3 in plasma, because cardiomyocytes have little ability to produce T3 from locally converted precursor T4.” (p. 1090)
“Thus, once circulating T3 is low, the myocardium could become relatively hypothyroid.”
“Hypothyroid hearts demonstrate poor substrate usage of glucose, lactate, and free fatty acids by mitochondria. Accordingly, the cardiac oxygen expenditure, as measured by positron emission tomography 11C acetate, is reduced in hypothyroid patients; however, cardiac work is more compromised than the oxidative metabolism. This leads to decreased cardiac energetic efficiency of the hypothyroid human heart.” (p. 1090)
Review commentary by Healthy Researcher Blog: As for the exclusion of thyroid-treated patients, I just want to start by mentioning that they, too, experience “Low-T3 syndrome” (see Midgley, et al, 2015) due to being poor converters of T4 to T3 (like myself). 
This article is unique. In most studies of cardiac Low-T3 syndrome, they study patients who already have overt heart disease. This study actually included people who did NOT have clinically evident heart disease. Therefore, they were able to see if low-T3 predicted heart disease… and it did.
They even go so far as to suggest that “T3 is an indicator of subclinical myocardial injury” because “once circulating T3 is low, the myocardium could become relatively hypothyroid”– tell that to your doctor if you have Low-T3 in your lab results. 
Sigh. I have had low T3 showing up in my lab results since 2013 and no alarm bells rang. How many people on thyroid treatment aren’t even tested for T3 levels?

Pavlou, H. N., Kliridis, P. A., Panagiotopoulos, A. A., & Goritsas, C. P. (2002). Euthyroid sick syndrome in acute ischemic syndromes. Angiology, 53(6), 699.

Total 114 patients.  “Exclusion criteria included age less than 20 or greater than 90 years; patients with any thyroid dysfunction; or patients receiving treatment with thyroid hormones, glucocorticoids, medications known to alter liver or renal function, oral contraceptive drugs, or amiodarone for 4 months or less before admission.”(p. 700)

“As shown in Figures 1 and 2, a statistically significant decrease (p < 0.05) of T3 and an increase of rT3 [Reverse T3] were observed during the first 5 days of the acute phase in the group of patients with myocardial infarction and in the group of patients with unstable angina.” (p. 701)

Table 1. T3 and rT3 [Reverse T3] hormone levels (mean ±SD) in 19 patients with unstable angina on days 1 through 5 (acute phase) and levels at 1 month after admission.

  • T3 (ng/mL) Day one:  0.68; Day two  0.54;  Day three 0.46; Day four 0.51; Day five 0.55; Day thirty 1.76
  • Reverse T3 (ng/dL) Day one:  62; Day two  69;  Day three 77; Day four 72; Day five 88; Day thirty 31

“Our data demonstrating a clear decrease in T3 and increase in rT3 during the first 5 days of the acute myocardial infarction are in agreement with results of previous reports. Furthermore, our results show the occurrence of this syndrome even in patients with UA [Unstable Angina]. Although UA has a milder clinical presentation than AMI, it seems sufficient to produce similar disturbances in thyroid hormones.” (p. 705)

“The degree of T3 decrease is proportional to the severity of cardiac damage and may have a possible prognostic value. Thus, T3 and rT3 blood levels may contribute to the elaboration of an AMI severity index.” (p. 706)

Review commentary by Healthy Researcher Blog: Although this makes the case that ischemic syndromes cause Low-T3 syndrome within days, the article begs for research that investigates whether the causation could also be reversed (Low T3 —> ischemic syndromes). 

Also, the exclusion of hypothyroid patients is troubling, since they also may experience heart attacks and angina.  What happens specifically to Low-T3 hypothyroid patients on Synthroid therapy after they have a heart attack or angina? Does their T3 get even lower and Rt3 get even higher by Day 5? Are they more likely to die? Is it harder for them to recover by Day 30?


Midgley, J. E. M., Larisch, R., Dietrich, J. W., & Hoermann, R. (2015). Variation in the biochemical response to l-thyroxine therapy and relationship with peripheral thyroid hormone conversion efficiency. Endocrine Connections, 4(4), 196.


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