Unexpected Cardiovascular Collapse After Radioiodine Therapy in a Patient with Severe Graves' Cardiomyopathy
https://doi.org/10.15605/jafes.041.S1
- Author:
Choon Peng Sun
1
;
Ahmad Affan Bin Hassannuddin
1
Author Information
1. Hospital Teluk Intan
- Publication Type:Journal Article
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):111-112
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:Graves’ disease may lead to thyrotoxic cardiomyopathy,
a potentially reversible condition following restoration of
euthyroidism. Radioiodine (RAI) therapy is commonly
used as definitive treatment for patients with long-standing
Graves’ disease or poor compliance with antithyroid
medications. However, individuals with severe underlying
cardiomyopathy may remain vulnerable to cardiovascular
instability during the peri-treatment period.
Case:We report a 39-year-old male with a 10-year history of
Graves’ disease who had previously defaulted on follow-up
and was admitted with thyroid storm. Echocardiography
during that admission demonstrated severe dilated
cardiomyopathy with global hypokinesia and an ejection
fraction (EF) of 26%. Following treatment with carbimazole
and propranolol, he achieved biochemical euthyroidism
and remained clinically stable (NYHA class I). In view
of his long-standing disease and prior thyroid storm, he
underwent RAI therapy as definitive therapy as per the
guidelines.
One week following RAI, he developed a persistent cough
and progressive dyspnea. Six weeks later, he presented to
the emergency department with hypotension (BP 60/31
mmHg) and new-onset atrial fibrillation (heart rate 100
bpm), requiring intubation and inotropic support for
cardiogenic shock. Laboratory evaluation showed low free T4 (5.31 pmol/L) with normal thyroid-stimulating hormone
(2.1 mIU/L). Repeat echocardiography demonstrated
persistent severe left ventricular dysfunction (EF ~25%)
without new structural abnormalities. The patient
improved rapidly with supportive management and was
successfully extubated after stabilization.
Although RAI is considered a safe and effective definitive
therapy, transient thyroid hormone fluctuations and
inflammatory thyroid destruction may occur following
treatment. In patients with severe pre-existing cardiomyopathy, these physiological changes may precipitate
arrhythmias or acute cardiac decompensation. In this case,
new-onset atrial fibrillation in the setting of markedly
reduced myocardial reserve likely triggered cardiogenic
shock despite biochemical euthyroidism.
Conclusion:This case highlights that patients with advanced Graves’
cardiomyopathy may remain at risk of acute cardiovascular
deterioration following RAI therapy. Careful cardiovascular
risk assessment, optimization of heart failure therapy,
and close monitoring after definitive treatment should be
considered in this high-risk population.
- Full text:2026080508431472020EP_A165.pdf
