MON-432 - Infiltrative Cardiomyopathy Secondary to Severe Hypothyroidism from Medication Nonadherence: A Case Report

Background
Background
Hypothyroidism is a common endocrine disorder resulting from thyroid hormone deficiency that affects multiple organ systems, particularly the cardiovascular system. Thyroid hormone receptors are expressed in myocardial and vascular tissues; even subtle hormonal changes may influence cardiovascular physiology through genomic and nongenomic mechanisms. Cardiovascular involvement may include dyslipidemia, endothelial dysfunction, or myocardial structural and functional changes.
Case Report
We describe the case of a 75-year-old woman with a history of long-standing but poorly controlled hypothyroidism. The patient was brought to the emergency department after being found unresponsive on the floor at home for an unknown duration. She lived alone, with concern for medication non-adherence. On arrival, her blood pressure was markedly elevated at 253/119 mmHg, with otherwise stable vital signs. Cardiac auscultation revealed a systolic murmur. The myxedema coma score was calculated at 40, indicating severe hypothyroidism. Laboratory studies showed TSH level of 111.56 μIU/mL and a free T4 level below 0.25 ng/dL, and severe dyslipidemia (total cholesterol 379 mg/dL, LDL 247 mg/dL, HDL 87 mg/dL, triglycerides 225 mg/dL). The EKG demonstrated low-voltage complexes. Echo showed a small LV cavity with hyperdynamic systolic function (EF >80%). The left ventricular walls were markedly thickened with a granular, resembling an amyloid-like “sparkling” myocardial echotexture, raising concern for infiltrative cardiomyopathy. After excluding other causes of infiltrative cardiomyopathy, including cardiac amyloidosis via a negative technetium-99m pyrophosphate (PYP) scan, the presentation was attributed to hypothyroidism-associated cardiomyopathy. Levothyroxine was started intravenously due to impaired oral intake, then transitioned to oral dosing under endocrinology guidance. She showed progressive clinical improvement, with follow-up labs indicating partial biochemical improvement. At one month, thyroid function normalized (TSH 2.1, FT4 1.6) with improved functional capacity, and at one-year follow-up, lipids normalized (TC 135, LDL 61, HDL 56, TG 88), confirming hypothyroidism-associated dyslipidemia.
Conclusion
Severe, untreated hypothyroidism can cause significant and potentially reversible cardiac dysfunction, including cardiomyopathy and hypothyroidism-associated dyslipidemia, reflecting both structural and metabolic consequences of thyroid hormone deficiency. This case emphasizes the need to consider hypothyroidism in the differential diagnosis of unexplained cardiac dysfunction and highlights how social determinants of health, including social isolation and limited support systems, may contribute to medication non-adherence and delayed recognition of clinical deterioration.

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