A 39-year-old African man was admitted to our department within a four days symptoms of short of breath, cough, tachycardia and lower limb edema. He also complained headache for about a month. He denied fever, chest pain and loss of consciousness. Clinical and family history were unremarkable.
Blood tests showed moderate microcytic anemia ( Hb 9.6 g/dl, MCV 93.3 fL), hypoalbuminemia ( Albumin: 3.20 g/dl) , elevated levels of LDH ( LDH: 246 U/L), mild C-reactive protein (CRP) and pro-Brain Natriuretic Peptide (pro-BNP) increase (CRP: 1.14 mg/dl); (PRO-BNP: 1133 pg/mL) and negative troponin. Given the clinical picture suggestive of heart failure, we immediately started diuretic therapy with benefit. Chest-x ray revealed a modest thickening of the pulmonary interstitium, electrocardiogram (ECG) a sinus rhythm and early repolarization changes. Chest CT highlighted a bilateral apical-basal pleural effusion, a bilateral hilar ectasia and interstitial markings due to stasis. He underwent an ultrasound of the abdomen that was normal. Thyroid function tests showed high levels of thyroid hormones with suppressed TSH and elevated levels of Ab anti-receptor TSH ( FT3: 8.73 pg/mL; FT4: 2.35 ng/dL; TSH<0.01 mUI/ml; TRAB: 3.62 UI/L). Thyroid ultrasound showed a multinodular goiter. The patient began therapy with Tapazole. Echocardiogram didn’t show any evidence of acute heart disease and systolic function was normal. After discharge he performed a heart MRI with evidence of no alteration of global systolic function, of regional left and right ventricular kinetics or of pathological areas of delayed enhancement in relation to myocardial edema/fibrosis/necrosis.
Hyperthyroid patients can show signs and symptoms of heart failure that are due to the hyperdynamic circulatory state and/or to the frequent pulmonary arterial hypertension and our case report demonstrates that this clinical status tends to improve with the restoration of euthyroidism, but if left untreated, can worsen over the time leading to heart failure.