A 56-year-old woman with a 3-year history of Hashimoto’s thyroiditis presented with hypothermia (35°C), hypotension (66/49 mmHg), bradycardia (53 b.p.m.), psychomotor dysfunction (Panel A, Supplementary data online, Video S1A), irritability, fatigue, polyneuropathy, diplopia, weight loss (10 kg in 6 weeks), and dizziness with several falls and brief loss of consciousness. She had discontinued L-thyroxine substitution a year ago over medication concerns.
Cranial magnetic resonance imaging (MRI) revealed discrete exophthalmos and ruled out ischaemia and haemorrhage. Free thyroxine (<1.3 pmol/L) and free triiodothyronine (fT3 < 0.6 pmol/L) were undetectable, while thyroid-stimulating hormone was significantly elevated (84.6 mIU/L), indicating severe primary hypothyroidism. Mild hyponatraemia, mildly elevated high-sensitivity cardiac troponin T, and NT-proBNP were noted, and an electrocardiogram (ECG) showed low-voltage signs (Panel B, Supplementary data online, Table S1, Figure S1A and B). Echocardiography and cardiac MRI revealed concentric left ventricular hypertrophy with normal global and regional function (Panel C). Tissue characterization showed elevated myocardial extracellular volume (Panel D), along with anasarca, bilateral pleural effusion, and a small pericardial effusion (Panels C and E).
These findings were consistent with a myxoedema coma due to non-adherence, complicated by myxoedema heart disease. Thyroid hormone replacement (levothyroxine 150 µg/days) was initiated immediately. At follow-up 7 months later, the patient was in a good condition with improved neurological status, normalization of laboratory values, ECG, and left ventricular hypertrophy (see Supplementary data online, Video S1B, Table S1, Figure S1C).
The diagnosis of myxoedema coma is primarily clinical.1 A proposed scoring system for myxoedema coma with a score of 60 or higher being diagnostic showed our patient scored 105 points (see Supplementary data online, Table S2).2
Supplementary data are available at European Heart Journal online.
The authors declare that there is no conflict of interest.
Supplementary Material
Contributor Information
Philip Haaf, Department of Cardiology, Cardiovascular Research Institute Basel, University Hospital Basel and University of Basel, Petersgraben 4, CH-4031 Basel, Switzerland.
Julia Beck, Department of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland.
Michael Mayr, Medical Outpatient Department and Hypertension Clinic, ESH Hypertension Centre of Excellence, University Hospital Basel, Petersgraben 4, 4031 Basel, Switzerland.
This manuscript was prepared without any funding.
References
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