SUN-307 - Reversible Hypothyroid Cardiomyopathy in Myxedema Coma: A Diagnostic and Therapeutic Challenge

Background:
Myxedema coma is the most severe and life-threatening manifestation of decompensated hypothyroidism. It is a clinical diagnosis defined by multisystem organ dysfunction rather than the presence of coma alone or a specific thyroid-stimulating hormone (TSH) threshold. Cardiovascular complications include low cardiac output, conduction abnormalities, and, rarely, reversible cardiomyopathy. Mortality remains high, ranging from 25–60%, emphasizing the need for early recognition and aggressive treatment.

Clinical

Case:
A 73-year-old man with paroxysmal atrial fibrillation (on apixaban), chronic heart failure with preserved ejection fraction, hypertension, and hypothyroidism presented after being found unresponsive at home. He reported several days of progressive dyspnea, generalized weakness, and medication nonadherence to levothyroxine. On arrival, he was hypoxic (SpO2 78%), hypotensive (99/55 mmHg), somnolent but arousable, with dry scaly skin and bilateral pulmonary crackles. Laboratory evaluation revealed TSH 33.25 mIU/L, free T4 0.77 ng/dL, lactate 3.4 mmol/L, proBNP 1229 pg/mL, leukocytosis, and severe vitamin B12 deficiency. ABG demonstrated severe hypoxemia. ECG showed sinus tachycardia, prolonged QT, and low voltage complexes. Chest radiograph demonstrated marked cardiomegaly with interstitial opacities. The Popoveniuc myxedema score exceeded 60, strongly supporting myxedema coma.

He was treated emergently with IV hydrocortisone 100 mg followed by IV levothyroxine 200 mcg loading dose and 100 mcg daily prior to transition to oral therapy. Echocardiogram revealed new systolic dysfunction with LVEF 35–40% (previously 50%) and grade II diastolic dysfunction. Ischemic evaluation was negative. Ambulatory rhythm monitoring demonstrated low atrial fibrillation burden, supporting hypothyroid cardiomyopathy as the etiology of reduced ejection fraction. Cardiac function improved with thyroid hormone replacement.

Discussion:
Severe hypothyroidism can precipitate reversible cardiomyopathy through impaired myocardial contractility, increased systemic vascular resistance, and reduced cardiac output. Myxedema coma is a clinical diagnosis characterized by organ dysfunction, not solely elevated TSH or overt coma. Prompt IV thyroid hormone replacement with stress-dose glucocorticoids is critical and may reverse systolic dysfunction.

Conclusion:
Hypothyroid cardiomyopathy should be considered particularly in elderly patients with new systolic dysfunction and medication nonadherence. Early recognition of myxedema coma can be lifesaving and may result in recovery of cardiac function.

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