Graves’ Disease and the Heart: Severe Reversible Left Ventricular Systolic Dysfunction With Apical Thrombus in a Young Woman With Relapsed Thyrotoxicosis

Graves' disease is a common cause of autoimmune hyperthyroidism and is frequently associated with cardiovascular manifestations, including sinus tachycardia, atrial fibrillation and high-output heart failure.Severe left ventricular (LV) systolic dysfunction complicated by LV thrombus is an uncommon presentation.Recognition may be challenging when concurrent illness and antithyroid treatment complicate the interpretation of thyroid function tests.A 27-year-old woman with Graves' disease diagnosed in 2021 presented in March 2025 with progressive dyspnoea, orthopnoea, profound lethargy, jaundice and generalised oedema.Following relapse in September 2024, carbimazole had been recommenced, but adherence was suboptimal, and heart failure symptoms had developed over several months.Examination revealed sinus tachycardia, diffuse goitre, exophthalmos, hepatomegaly and marked anasarca.Community-acquired pneumonia was also diagnosed.Admission free thyroxine was 8.5 pmol/L (reference range: 8.9-17.3),thyroid-stimulating hormone (TSH) was 0.48 mIU/L (0.30-4.40), and free triiodothyronine was unavailable.This biochemical pattern was interpreted in the clinical context as consistent with non-thyroidal illness.N-terminal pro-B-type natriuretic peptide (NT-proBNP) was elevated at 9,326 ng/L.Electrocardiography demonstrated sinus tachycardia, and transthoracic echocardiography showed LV dilatation with severe global systolic dysfunction and an estimated LV ejection fraction (LVEF) of approximately 10%.Contrastenhanced computed tomography demonstrated an LV apical thrombus and hepatic congestion.Graves' disease-associated myocardial dysfunction was considered an important contributor; however, tachycardiamediated dysfunction, myocarditis and critical illness-related myocardial dysfunction remained potential contributing causes.Management included adjustment of carbimazole, diuresis, bisoprolol, valsartan, spironolactone and dapagliflozin, alongside treatment of pneumonia.Therapeutic anticoagulation was initiated with enoxaparin, followed by intravenous unfractionated heparin and bridging to warfarin.Clinical improvement was accompanied by recovery of LVEF to 36% during admission, approximately 40% in June 2025 and 52%-54% on echocardiography in September 2025.Cardiac magnetic resonance imaging during the same time confirmed normal biventricular size and systolic function, with an LVEF of 54% and no residual intracardiac thrombus.A small area of nonspecific non-infarct-pattern fibrosis could represent previous myocarditis.Definitive thyroidectomy was planned.This case highlights severe but reversible LV systolic dysfunction with apical thrombus in a young woman with relapsed Graves' disease and suboptimal treatment adherence.Although the clinical course suggests a thyroid-related contribution, the myocardial dysfunction may have been multifactorial.The reduction in thyroid-stimulating immunoglobulins (TSIs) alongside cardiac recovery represents a temporal association and does not establish causation.Careful clinical assessment and cardiac imaging are essential to recognising significant cardiac involvement when thyroid biochemistry is complicated by concurrent illness.