Abstract

Hyperthyroidism often leads to heart failure when left untreated, specifically high output heart failure and left ventricular (LV) hypertrophy. A very minimal portion of those develop severe LV dysfunction. We report a case of a 65-year-old male who presented with signs and symptoms of heart failure and was found to have hyperthyroidism, severe systolic dysfunction, and severe dilated cardiomyopathy.The patient is a 65-year-old African American male with a history of hypertension (HTN) who presented with complaints of dyspnea on exertion and bilateral lower limb edema of one-week duration. A review of systems revealed paroxysmal nocturnal dyspnea, orthopnea, palpitations, fatigue, and weight loss. Physical exam showed tachycardia but otherwise no exophthalmos, no thyromegaly, no thyroid nodules, clear lungs, normal heart sounds, regular heart rhythm, normal reflexes, and 2+ edema of bilateral lower extremities up to the knees. Labs showed elevated B-natriuretic peptide, severely suppressed thyroid-stimulating hormone, elevated free triiodothyronine (FT3), and free thyroxine (FT4). Electrocardiogram (EKG) revealed sinus tachycardia, incomplete left bundle branch block, and non-specific T wave abnormality. Echocardiography revealed abnormal (LV) structure and function, with moderate to severe dilatation without LV hypertrophy, severe LV systolic dysfunction with ejection fraction (EF) 30-35%, and an abnormal LV diastolic function.The patient was managed with diuresis for acute onset heart failure and with beta-blocker and methimazole for symptomatic hyperthyroidism.Thyroid assessment is an important step in evaluating any patient with suspected heart failure. This case highlights the balance that should exist between treating hyperthyroidism symptoms and managing disease states such as acute heart failure.

Highlights

  • Thyrotoxicosis is defined as a clinical state that ensues due to high thyroid hormone levels exerting their effect on tissues

  • Hyperthyroidism is a form of thyrotoxicosis that is due to inappropriately elevated synthesis and secretion of thyroid hormones by the thyroid gland [1,2]

  • We present the case of a 65-year-old male who presented with signs and symptoms of heart failure and was found to have hyperthyroidism

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Summary

Introduction

Thyrotoxicosis is defined as a clinical state that ensues due to high thyroid hormone levels exerting their effect on tissues. The patient is a 65-year-old African American male with a history of hypertension (HTN) and normal thyroid studies (thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), and free thyroxine (FT4)) two years prior to this presentation who presented with complaints of exertional dyspnea and bilateral lower limb edema of one-week duration. Laboratory work Hemoglobin (g/dL) Mean Corpuscular Volume (MCV) (fL) Creatinine (g/dL) BUN (mg/dL) Albumin (g/dL) Troponin (ng/mL) B-natriuretic peptide (ng/mL) Thyroid Stimulating Hormone (TSH) (mIU/mL) Free triiodothyronine (FT3) (pg/mL) Free thyroxine (FT4) (ng/dL) Iron (ug/dL) TIBC (ug/dL) Ferritin (ng/mL) Iron saturation (%). He remained tachycardic despite the metoprolol with a heart rate in the low 100s (110-120) He was closely monitored and on day 3 of admission, the patient had resolution of his bilateral lower limb edema with significant improvement in his dyspnea on exertion, paroxysmal nocturnal dyspnea, and orthopnea.

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Kravets I
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