HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

PERSONAL HISTORY
69-year-old male with no known allergies.
Cardiovascular risk factors (CVRF): high blood pressure (HBP), overweight, ex-smoker.
Sleep apnoea-hypopnoea syndrome (SAHS) under treatment with continuous positive airway pressure (CPAP).
Diagnosed with oesophageal spasms with manometry, following an admission to cardiology in 2007 for chest pain without structural heart disease.
Glomerulonephritis in infancy labelled as post-streptococcal.
Uncomplicated cholelithiasis.
Surgical interventions: cataracts, retinal detachment, varicose veins, tonsillectomy, haemorrhoids.

CURRENT ILLNESS
She came to the emergency department with dyspnoea, asthenia, anorexia and weight loss of two months' duration.
No clear orthopnoea or oedematisation of the lower limbs. No syncopal episodes or palpitations. When assessed in the emergency department, atrial fibrillation with ventricular response at 100 bpm was detected. In view of this finding, the worsening of functional class and the elevation of NTproBNP, the patient was diagnosed with heart failure and admitted to the cardiology department.

PHYSICAL EXAMINATION
Blood pressure 145/80 mmHg. Heart rate 100 bpm. Basal saturation 95%.
Temperature 37.4 ̊C.
Height 175 cm, weight 86 kg, body mass index (BMI) 28.
No palpable adenopathies or skin lesions. Conscious, oriented, normal colour.
Cardiac auscultation: arrhythmic, no significant murmurs.
Pulmonary auscultation: normal ventilation.
Abdomen soft, not painful, no masses or megaliths, persistalsis preserved.
Lower extremities: no oedema.
No ulcerative lesions in the upper airways.

COMPLEMENTARY TESTS
Blood tests: biochemistry: glycaemia 91 mg/dl, urea 44 mg/dl, creatinine 0.86 mg/dl, triglycerides 135 mg/dl, LDL 87 mg/dl, sodium 138 mEq/l, potassium 4.3 mEq/l. NT-proBNP 2606 pg/ml. Thyroid function: TSH 1.49 mIU/l, T4 1.17 ng/dl. Haemoglobin 10.2 g/dl, haematocrit 30.8%, leucocytes 6,700/mm3, platelets 350,000/mm3. Anti DNA and antiENA negative. pANCA 1459.7. ESR 91.
Urinalysis: microalbuminuria 3.03 mg/dl, microhaematuria +.
Chest X-ray: global cardiomegaly. Pulmonary hyperinflation. Residual impingement of the left costophrenic sinus. No pulmonary parenchymal infiltrates.
ECG on admission: atrial fibrillation with rapid RV at 110x ́, complete left bundle branch block (LBBB) and low voltages.
Transthoracic echocardiogram: slightly dilated atria. Left ventricle (LV) of normal size. Mild left ventricular hypertrophy (LVH). Global contractility preserved, without observing segmental alterations.
LVEFbp 60%. No criteria for elevated left ventricular end-diastolic pressure (LVEDP). Trivalve aortic valve (VAo) with sclerosis of the leaflet cusps and calcification on the NC leaflet. It maintains adequate opening, with no regurgitant flows. Mitral valve (MV) with normal appearance and function. Cava and suprahepatic valves not dilated, without flow reversal and normal inspiratory collapse. Normal PPs. Mild-moderate pericardial effusion without haemodynamic involvement, with leaflet separation (2 mm over the anterior sac and over the roof of the right atrium (RA), 7 mm in the posterior, 10 mm in the lateral LV and 7 mm over the lateral RV). Fibrin tracts with partially organised effusion on the lateral aspect of the RV and the apex of the right ventricle (RV) are observed (without increased movement on the lateral aspect of the RA and RV and normocolapse of the cava).
Thoracoabdominal CT: no axillary lymph nodes. Subcentimetric right paratracheal, bilateral prevascular and subcarinal mediastinal nodes, as well as right bronchopulmonary nodes, all of them with a reactive appearance.
Bilateral laminar atelectasis. Discrete left pleural effusion with passive atelectasis of the underlying lung parenchyma, showing an aerial image that could correspond to a bulla in the collapsed parenchyma vs. bubble at the level of the pleural fluid (assess history of manipulation). Pericardial effusion with a maximum thickness of 27 mm in the lateral region of the left ventricle. Homogeneous liver, normal size and morphology, with a millimetric hypodense lesion in the dome, unspecific due to its small size. Cholelithiasis. Bile duct of normal calibre. Pancreas and spleen without alterations. Slight bilateral adrenal thickening with hyperplastic appearance.
Kidneys of normal size and morphology, with good bilateral and symmetrical function.
Bilateral simple cortical cysts, the largest of 53 mm in the upper pole of the left kidney and 52 mm in the upper third of the right kidney. No excretory tract ectasia. The bladder is scarcely replete, with no obvious parietal alterations. Prostate with a transverse axis of 44 mm. Sigmoid diverticulosis with no signs of complication. No significant intra-abdominal adenopathy or intraperitoneal free fluid. Bone degenerative signs.
Electroneurogram: study compatible with sensory-motor polyneuropathy (PNP) in the lower limbs, of severe degree.


CLINICAL EVOLUTION
On questioning the patient again, he reported asthenia, anorexia and weight loss (about 10 kg) in the last 3 months, which he attributed to the start of a hypocaloric diet from primary care.
He also reported left cervical adenopathy that disappeared after taking ibuprofen together with erythematopapular lesions, which improved with topical corticosteroids, two months before his current admission; migratory arthralgias (in the elbows and right shoulder), persistent afternoon fever of 3 months' duration, haematuria and proteinuria in urine with normal renal function (confirmed in a general analysis at his primary care centre several weeks earlier).
Episode of rhinitis and epistaxis two months earlier, resolved with intranasal corticosteroids.
An echocardiogram was performed which showed no significant valvular heart disease, slight pleural effusion and moderate pericardial effusion without repercussions.
In view of the significant general and systemic involvement, acute phase reactants and autoimmunity tests were requested, with significant elevation of CRP, ESR and positive P-ANCA and C-ANCA autoantibodies. Given the high suspicion of vasculitis with renal involvement, a discussion was held with the nephrology department, who did not consider a renal biopsy to be indicated at the present time, and with the internal medicine department (autoimmune diseases).
The study was completed with an electroneurogram which showed data compatible with severe polyneuropathy of the lower limbs.
Given the diagnosis of C-ANCA-positive vasculitis, treatment with corticoids was started, in agreement with the autoimmune unit, with significant improvement in general condition and reduction of pericardial effusion, which at discharge was only slight-moderate in the posterior sac.
From the cardiovascular point of view, he remains in atrial fibrillation with adequate heart rate control with beta-blockers. Initially, given that he has not completed 4 weeks of anticoagulation and that the main problem is his autoimmune pathology, a strategy of rate control is advocated, considering elective cardioversion on an outpatient basis according to clinical evolution.
Clinically and haemodynamically stable, he was discharged from hospital with the following treatment: methotrexate 20 mg (one injection weekly), folic acid 5 mg (1 tablet weekly after methotrexate injection), prednisone 30 mg (2 tablets at breakfast), bisoprolol 5 mg (at breakfast) and 2.5 mg (at dinner), apixaban 5 mg (at breakfast and dinner), simvastatin 40 mg (at dinner), omeprazole 20 mg (fasting) and furosemide 40 mg (at breakfast).

DIAGNOSIS
Vasculitis C-ANCA positive.
Pleuropericardial effusion of autoimmune aetiology.
Atrial fibrillation of uncertain onset with controlled ventricular response at discharge, CHADSVASc 2, HASBLED 1.
