A 75 year-old man presented with one month of leg swelling and early satiety. He had a history of coronary artery disease and atrial fibrillation (managed with amiodarone for the past 2 years). He recently initiated furosemide treatment but had no history of symptomatic heart failure. Physical exam showed elevated jugular venous pressures, an irregularly irregular heart rhythm, abdominal distention with fluid wave, and bilateral lower extremity edema. An echocardiogram revealed tricuspid regurgitation and a left ventricular ejection fraction of 65%. Lab results included potassium of 2.9 mmol/L, creatinine of 2.3 mg/dL, brain natriuretic peptide of 600 pg/mL, and troponin of 0.06 ng/mL. Despite having no hyperthyroid symptoms, the patient’s thyroid stimulating hormone, triiodothyronine, and thyroxine levels were 0.02 mIU/L, 9.8 pg/mL, and 5.5 ng/dL, respectively. Sonography revealed normal thyroid architecture with diminished vascularity. Thyroid tissue exhibited decreased sestamibi uptake on scintigraphy. Prednisone was started, and amiodarone was stopped; beta blockade was used for rate control during diuresis.
Discussion:
Decompensated heart failure is frequently encountered by the hospitalist. While management relies primarily on diuresis, underlying precipitants must be addressed to optimize short-term management and long-term outcomes. Common precipitants include ischemia, hypertension, dietary or medication nonadherence, chronic obstructive pulmonary disease, and pneumonia. In this patient, the precipitating cause was likely amiodarone-induced thyroid dysfunction.
Amiodarone is a class III antiarrhythmic agent with potential side effects of both hypo- and hyperthyroidism. Due to amiodarone’s beta blocking activity that can conceal hyperthyroid side effects, providers must have a low threshold for possible thyrotoxicosis, which can develop in up to five percent of users. This thyrotoxicosis is classified into two types. In type I, the drug’s high iodine content increases production of thyroid hormone; this typically occurs within six months of starting therapy and tends to affect patients with preexisting goiter in iron-deficient areas. Type II, as seen in our patient, is more common in the United States; amiodarone causes a destructive thyroiditis that can develop over a longer time course, even years after therapy initiation. Sonography and scintigraphy can differentiate the two based upon thyroid blood flow and sestamibi uptake; both are increased in type I and decreased in type II. Thyroid radioiodine uptake test is not reliable due to competition between the test tracer and amiodarone-released iodine. Type I is managed with thionamides while type II is managed with corticosteroids. Once treatment is initiated, amiodarone use is ceased unless required for control of life-threatening arrhythmias. Since amiodarone inhibits conversion of triiodothyronine to thyroxine, premature cessation may initially cause worsened thyrotoxicosis.
Conclusions:
To optimize management of decompensated heart failure, physicians must negate precipitating triggers, such as thyroid dysfunction. Thyrotoxicosis is a common side effect of amiodarone with two different mechanisms requiring separate treatment approaches.