HISTORY, CURRENT DISEASE AND PHYSICAL EXAMINATION
We present the case of a 54-year-old woman from Paraguay. She had a history of arterial hypertension treated with diuretics and a probable episode of pulmonary embolism for which she had received anticoagulant treatment in 2013, which the patient described imprecisely. She remained asymptomatic after this episode. However, 4 months prior to the current admission, she began to present symptoms of progressive dyspnoea until she became resting, oedema in the lower limbs and a weight loss of 10 kg, for which reason she consulted a cardiologist in Paraguay.
A transthoracic echocardiogram showed moderate pulmonary hypertension (PSAP 55 mmHg), severe tricuspid insufficiency (TI) and a dilated right ventricle with normal function (TAPSE 24 mm). For this reason, he was prescribed treatment with spironolactone 25 mg, furosemide 40 mg and carvedilol 12.5 mg every 12 hours. At that time, thyroid hormone tests were not performed, although they were recommended, because her health insurance did not cover such tests. A few months later she travelled to Spain on holiday, presenting with diarrhoea for 3 days and colicky abdominal pain, for which reason she went to the emergency department of our centre. On arrival, he presented evident signs of heart failure, predominantly right-sided, with oedema in the legs, jugular ingurgitation and dyspnoea at rest with paradoxical breathing and supraclavicular tugging, for which the coronary unit was notified.
On admission to the coronary unit he had a blood pressure of 137/47 mmHg and heart rate of 42 bpm (in the absence of beta-blockers), temperature of 36 ̊C and oxygen saturation of 96%. Physical examination revealed marked jugular engorgement, a jugular venous pulse with oscillating stop at 5 cm from the angle of Louis and Kussmaull's sign. In addition, a large goitre with palpable thrill and a continuous thyroid murmur, not irradiated and accompanied by bilateral exophthalmos, was documented. Cardiopulmonary examination revealed palpation of the right ventricle in the right parasternal region, as well as a tricuspid regurgitation murmur.
On pulmonary auscultation, the vesicular murmur was abolished in both lung bases. The patient also showed hepatomegaly 3 cm below the costal margin and oedema with fovea up to the root of the lower limbs. After diuretic treatment the signs of congestion improved and bilateral pretibial oedema without fovea compatible with myxoedema could be observed.

COMPLEMENTARY TESTS
Electrocardiogram (ECG) showed a nodal rhythm at 42 bpm, with low voltages in the limb leads and diffusely flattened T's in all leads. Chest X-ray showed right pleural effusion, with deflected hilarity and enlarged cardiac silhouette. At this time, an emergency portable transthoracic echocardiogram was performed showing severe right ventricular dilatation and dysfunction and severe PH (estimated PSAP of 60 mmHg), together with severe tricuspid regurgitation and evidence of peripheral congestion. The patient was admitted under initial suspicion of chronic pulmonary embolism as the origin of the condition. Anticoagulant and intravenous diuretic treatment was started, which resulted in large negative balances and clinical improvement. Analyses showed anaemia (Hb 8.8 g/dl), thrombopenia (93,000 platelets/mcl), cholestasis without hepatic cytolysis (GGT 95 IU; alkaline phosphatase 223 IU, total bilirubin 1.9 mg/dl, normal GOT and GPT and spontaneous INR of 1.7), all compatible with a stasis liver. Impaired renal function (Cr 1.7 mg/dl), hyponatraemia (Na 127) and hyperkalaemia (K 6.4), markedly elevated NT-proBNP values (11,617 pg/ml) were also documented. D-dimer levels were also elevated 2,400 ng/ml.
Antibody tests (ANA, rheumatoid factor, anti-glomerular basement membrane, c-ANCA and p-ANCA, anti-beta2 glycoprotein, anticardiolipin) and serology (HIV, HCV, HBV, syphilis) were also negative. Ultrasound scans of the lower limbs and abdomen ruled out the presence of deep vein thrombosis and revealed ascites and liver stasis, respectively. Given the apparent chronic nature of the condition, and the deterioration of renal function, a ventilation/perfusion scan was requested (instead of CT angiography of the pulmonary arteries), with the aim of establishing the diagnosis of chronic pulmonary embolism.
The result of the test was inconclusive, so pending a definitive diagnosis, anticoagulant treatment was maintained. Computed tomography was not performed as a first choice due to the deterioration of renal function. Once anticoagulant and diuretic therapy had been started, we obtained the following thyroid hormone results: undetectable TSH, T3L 15.79 mlU/l and T4L 59.20 mlU/l. Given these results, the patient was referred to the endocrinology department, who considered the condition to be primary autoimmune hyperthyroidism (Graves-Basedow disease) with secondary hypoaldosteronism and cytopenias, as the first diagnostic possibility. Treatment was started with antithyroid drugs (thiamazole), beta-blockers (propranolol) and corticosteroids (dexamethasone). The results of antithyroid antibodies were positive.
During admission, the patient presented, after the first 72 hours, with a fever of 38 ̊C related to bacteraemia due to methicillin-sensitive Staphylococcus aureus, which was treated with a 10-day course of antibiotherapy with cloxacillin. After completing the course, he again developed fever and retrocardiac pulmonary infiltrate with sputum positive for Rothia mucilaginosa. He was treated with levofloxacin, ceftriaxone and azithromycin with good response and satisfactory resolution of the infectious picture. Once renal function improved, a chest CT scan was performed which definitively ruled out the presence of lung embolism, highlighting the dilatation of the right heart cavities and the presence of significant right pleural effusion.

CLINICAL EVOLUTION
After one month of antithyroid treatment, a repeat transthoracic echocardiogram was performed, which showed complete normalisation of both the function and size of the right ventricle. Normalisation of pulmonary pressure and the presence of minimal tricuspid regurgitation were also documented. The patient was finally discharged once the alterations at the right ventricular level and in the pulmonary circulation had resolved with correction of the significant thyroid disorder. Our patient presented a complete resolution of cardiopulmonary symptoms after normalisation of thyroid hormone levels.

DIAGNOSIS
Right predominant heart failure. Severe right ventricular dysfunction and severe tricuspid regurgitation in the context of pulmonary hypertension. Severe pulmonary hypertension secondary to primary autoimmune hyperthyroidism (Graves-Basedow disease). Primary autoimmune hyperthyroidism (Graves-Basedow disease). Acute renal failure.
