MON-295 - Reversible Severe Right-Sided Heart Failure with Low Cardiac Output in A Patient with Graves Disease and Limited Systemic Sclerosis

Background

Hyperthyroidism commonly causes atrial arrhythmias and high-output heart failure; however, predominant right-sided heart failure with pulmonary hypertension and severe tricuspid regurgitation is less commonly appreciated, particularly with low cardiac output. We present such a case associated with Graves’ disease and coexisting limited systemic sclerosis.

Case Presentation

A 56-year-old woman with recently diagnosed Graves’ disease on methimazole and atenolol presented with two weeks of anasarca, chest discomfort, and dysphonia. She reported a 19-lb weight gain and several months of worsening dyspnea at rest without prior cardiac or pulmonary disease. On presentation, she was hypoxemic, requiring 3 L/min supplemental oxygen. Examination revealed jugular venous distension, diffuse pitting edema, loud P2, and holosystolic murmur at the lower left sternal border. Thyroid examination demonstrated mild enlargement without discrete nodules.

Labs showed suppressed TSH ( < 0.01 uIU/mL), markedly elevated free T4 (>6.8 ng/dL), thyroid peroxidase antibody (551.1 IU/mL), NT-proBNP (779 pg/mL), and normal troponin. Chest radiography showed bilateral pleural effusions. Echocardiography demonstrated moderate right ventricular enlargement with mildly reduced systolic function, severe functional tricuspid regurgitation, interventricular septal flattening, and preserved LVEF 60%.

Imaging was unrevealing for pulmonary embolism or venous thromboembolism. Right heart catheterization demonstrated elevated biventricular filling pressures, mild pulmonary hypertension (48/21 mmHg), and markedly depressed cardiac index (1.7 L/min/m²) consistent with low-output thyrotoxic cardiomyopathy. Autoimmune studies revealed high-titer ANA (>1:2560) with centromere pattern, abnormal nailfold capillaries, and anti-centromere B antibody (>8.0 AI) consistent with limited cutaneous systemic sclerosis. These findings favored thyrotoxic rather than systemic sclerosis-associated etiology.

She was treated with aggressive diuresis, beta-blockade, and antithyroid therapy with marked clinical improvement. At one-month follow-up, she demonstrated significant improvement in functional status from NYHA Class IV to Class II.

Conclusion

Severe right-sided heart failure may represent a highly reversible manifestation of Graves’ disease, even in the absence of typical high-output physiology. Early recognition of thyrotoxicosis as a cause of cardiopulmonary decompensation is essential, particularly when overlapping autoimmune features may confound diagnosis. This case underscores the importance of thyroid function testing in unexplained heart failure with preserved ejection fraction, as cardiovascular complications are a leading cause of mortality in older adults with untreated hyperthyroidism.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*