When It Rains It Pours: A Case of Thyroid Storm Presenting as Thyrotoxic Cardiomyopathy

Waqar, Aneeq; Ansar, Aisha; Gudipati, Swapna; Liebo, Max

doi:10.1016/s0735-1097(20)33904-8

Cited by 1 publication

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“… 8 , 9 Additional reports demonstrate the reversible nature of heart failure caused by thyrotoxicosis, highlighting the importance of recognizing thyrotoxic cardiomyopathy. 10 , 11 On the other hand, hypothyroidism has also been shown to have a cardiac impact, as demonstrated in characteristic echocardiograph findings, such as larger left atrial diameter in patients with heart valve disease. 12 Our patient presented with thyrotoxicosis in the setting of possible toxic adenoma complicated by severe TR due to malcoaptation of the tricuspid valve leaflets and moderate MR due to myxomatous changes of the mitral valve.…”

Section: Discussionmentioning

confidence: 99%

Right heart failure in the setting of thyrotoxic valvulopathy: the pathophysiology of an often neglected diagnosis: a case report

Harirforoosh

Cohen

Glovaci

et al. 2022

European Heart Journal - Case Reports

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Background Hyperthyroidism has a significant, well-established impact on the cardiovascular system on both a molecular and circulatory level. The cardiac consequences of thyrotoxicosis are not uncommon, indicated by a 1.2% prevalence of this disorder in the United States. However, our case describes the less widely observed association between thyrotoxicosis and valvulopathy. Case summary A 69-year-old Hispanic male presented with a 3-week history of shortness of breath, intermittent chest pain, and lower extremity swelling. Transthoracic echocardiogram revealed a dilated left and right atrium with severe tricuspid regurgitation, moderate mitral regurgitation, malcoaptation of the tricuspid valve leaflets, and a myxomatous mitral valve. In addition, right ventricular systolic function was moderately reduced. A right and left heart catheterization was performed with findings of normal right heart pressures and normal coronary arteries, respectively. To further evaluate the aetiology of the patient’s heart failure, thyroid studies were sent, revealing a thyroid-stimulating hormone value of <0.010 uIU/mL and a free T4 of 1.96 ng/dL. A 4.9 cm lesion was seen on thyroid ultrasound. We concluded that the patient’s heart failure and notable valvular abnormalities were likely as a result of thyrotoxic heart disease. Furosemide and methimazole were initiated while inpatient, and the patient was discharged with close follow-up. Discussion We demonstrate a unique case of the possible hemodynamic and cellular effects of thyroid hormone on the development of primary and secondary valve dysfunction. This association is important for clinicians to be aware of, as treatment of its underlying aetiology can lead to improvement in a patient’s cardiac outcomes.

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