When TSH Suppression Becomes Harmful: Thyroxine Over-Replacement Driving Cardiovascular Decompensation in Advanced Heart Failure
https://doi.org/10.15605/jafes.041.S1
- Author:
Ahmad Syahmi Yusof Zaki
1
;
Nur Izat Muhamad
2
;
Ezelea Elwina Walter Sandosam
2
;
Wan Mohd Izani Wan Mohamed
2
Author Information
1. Faculty of Medicine, University Sultan Zainal Abidin;Department of Internal Medicine, School of Medical Sciences, University Science Malaysia
2. Department of Internal Medicine, School of Medical Sciences, University Science Malaysia
- Publication Type:Journal Article
- MeSH:
Thyroxine;
Heart Failure;
Thyrotropin
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):116-
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:Thyroid stimulating hormone (TSH) suppression following
differentiated thyroid carcinoma is widely recommended
to reduce recurrence risk. However, this strategy assumes
cardiovascular tolerance to supraphysiologic thyroid
hormone exposure. In patients with advanced structural
heart disease, this assumption may fail, exposing a critical
limitation of guideline-directed TSH suppression.
Case:We report a 71-year-old male with end-stage renal failure
on hemodialysis and severe ischemic cardiomyopathy
(ejection fraction 23%) who presented with acute
decompensation characterized by dyspnea, rapid atrial
fibrillation, and non–ST-elevation myocardial infarction.
He had a history of papillary thyroid carcinoma treated
with total thyroidectomy and radioactive iodine over
20 years prior and was maintained on levothyroxine 200
mcg daily for TSH suppression. Despite biochemically
euthyroid indices (TSH 1.8 mIU/L, free thyroxine 4 17
pmol/L), he developed recurrent arrhythmia with heart
failure decompensation.
This case highlights a dissociation between biochemical
euthyroidism and tissue-level thyrotoxicity in a structurally
compromised myocardium. Papillary thyroid carcinoma
after definitive therapy typically follows an indolent course
with low short-term mortality. In contrast, in severe left
ventricular dysfunction, excess thyroid hormone increases
adrenergic sensitivity and myocardial oxygen demand,
precipitating arrhythmia and ischemia. This risk is amplified
in end-stage renal disease, where altered hormone handling
renders biochemical indices less reliable.
Conclusion:Biochemical euthyroidism does not equate to physiological
safety. In patients with advanced cardiovascular disease,
thyroid hormone therapy should be titrated to cardiovascular tolerance rather than oncologic targets alone, and
routine TSH suppression may be inappropriate.
- Full text:2026080509311070571EP_A173.pdf
