Thyroid hormones play a pivotal role in cardiovascular regulation, modulating cardiac inotropic and chronotropic function as well as peripheral vascular homeostasis through both genomic and nongenomic mechanisms. In hypothyroidism, the loss of these inotropic and chronotropic effects leads to reduced stroke volume and heart rate, culminating in decreased cardiac output. Although uncommon, prolonged untreated hypothyroidism can lead to cardiomyopathy. We present a case of post-ablation hypothyroidism complicated by hypertrophic cardiomyopathy, which demonstrated reversal following thyroid hormone replacement.

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A 38 year old male with history of primary hyperthyroidism treated with radioactive ablation therapy presented at the outpatient clinic with easy fatigability. There were no other known comorbidities, no history of alcohol or substance abuse. Post-ablation therapy 13 years ago, patient was prescribed Levothyroxine but was eventually lost to follow up with poor compliance to Levothyroxine. On physical examination, noted with blood pressure of 130/80mmHg, heart rate of 64 beats per minute, puffy eyelids, icteric sclerae, and hypercarotenemia. Initial thyroid function tests showed elevated TSH >100 mIU/L, and reduced FT4 at 0.76 pmol/L, FT3 at 0.25 pmol/L. On 2D-echocardiogram at baseline, there was severely increased left ventricular mass index with global hypokinesia and mildly depressed left ventricular systolic function. With continuous levothyroxine therapy, he showed improvement of symptoms with repeat 2DED showing normal resting wall motion and improved ejection fraction after 11 months.

Hypertrophic cardiomyopathy is an uncommon complication of hypothyroidism. This case highlights the need to recognize hypothyroidism as a cause of cardiomyopathy, as timely initiation of thyroid hormone replacement can lead to significant cardiac improvement.