Case Presentation: A 74-year-old female presented to the ED with two days of shortness of breath and fatigue. She reported a past medical history of heart failure with reduced ejection fraction, chronic kidney disease, and essential hypertension. Medications included Lisinopril, Amlodipine, Furosemide, Atorvastatin, Aspirin, Famotidine, and Warfarin. She denied tobacco, alcohol, and illicit drug use. Family history was notable for coronary artery disease in her mother and liver cancer in her father. On exam, she was ill-appearing. Temperature was 37.1°C, pulse 89 bpm, blood pressure 136/93 mm Hg, respiratory rate 17 bpm, and SpO2 96% while on a non-rebreather mask with FiO2 of 70%. She was alert and oriented to person, place, and situation. Cardiac exam was notable for a normal rate, a regular rhythm, and no murmurs, gallops, or rub; there was no jugular venous distention. Her lungs were clear to auscultation with good air movement and no crackles, wheezes, or rhonchi. There was 2+ pitting edema in the legs, and 1+ edema in the upper extremities. Labs were significant for a BNP of 35,000 pg/mL, creatinine of 2.43 mg/dL, lactic acid of 4.5 mmol/L, AST of 328 IU/L and ALT of 460 IU/L. CT scan of the chest revealed interstitial and alveolar edema with moderate bilateral pleural effusions. An echocardiogram revealed biventricular heart failure with a left ventricular ejection fraction of 25-30%. Diuresis was initiated with IV furosemide. Over the next several days, the patient became progressively hypotensive and lethargic, and she continued to be volume overloaded. Further investigation revealed that the patient had a history of hypothyroidism. She had been prescribed levothyroxine previously, but had not been taking it. Thyroid studies were obtained and revealed a TSH of 331 mU/L, total T4 of 1.6 mcg/dL, and total T3 of 29 ng/dL. IV Levothyroxine was initiated. Over the next several days, her volume status and hemodynamics improved. She was discharged several days later in stable condition.
Discussion: A low level of thyroid hormone leads to decreased cardiac contractility and heart rate, which causes a fall in cardiac output. While it is unusual for hypothyroidism to be the sole cause of an acute heart failure exacerbation, the hypothyroid state can increase the severity and resistance to typical treatment. Identifying hypothyroidism as a contributor to heart failure requires careful evaluation, as the two conditions are not typically associated and hospitalized patients commonly exhibit abnormal thyroid studies. However, when thyroid levels are severely low and the patient fails to improve with standard heart failure treatment, the clinician’s suspicion should be raised. Management involves IV thyroxine replacement, which rapidly corrects the cardiovascular changes induced by the hypothyroid state. Checking thyroid levels should be standard practice for patients who present with an acute heart failure exacerbation as not to overlook this uncommon but important association.
Conclusions: Hypothyroidism is an uncommon driver of heart failure but should be kept on the differential of every heart failure presentation, especially those that fail to respond to appropriate diuresis and hemodynamic support.