HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

PERSONAL HISTORY
This is a 75-year-old male patient with a history of smoking, hypertension, insulin-dependent diabetes mellitus and obesity.
His cardiological history includes ischaemic heart disease in dilated phase with surgical revascularisation and mitral valve replacement with mechanical prosthesis due to severe mitral insufficiency in 2005. Single-chamber pacemaker implantation with atrioventricular node ablation was performed due to multiple admissions for acute myocardial infarction (AMI) type 2 in the context of atrial fibrillation with rapid ventricular response. In 2000 he underwent amputation of the right foot and right femoral-popliteal bypass and in 2008 exclusion of the left iliac and femoral aneurysm. The last echocardiogram in May 2018 showed severe left ventricular dysfunction, mitral prosthesis with mean gradient of 4 mmHg without periprosthetic insufficiency and moderate aortic insufficiency.
Standard treatment: sacubitril/valsartan 97/103 mg (1 tablet at breakfast and 1 tablet at dinner), metoprolol 100 mg (1 tablet at breakfast and 1 tablet at dinner), furosemide 40 mg ( 1 tablet at breakfast and 1 tablet at lunch), acenocoumarol according to haematology guidelines, insulin lantus 20 IU at breakfast, eplerenone 25 mg (1/2 tablet at lunch), atorvastatin 20 mg (1 tablet at dinner), salmeterol/fluticasone 25/50 mcg 1 inhalation every 12 hours, chronic home oxygen.


CURRENT ILLNESS
Admitted in February 2019 for critical right lower limb ischaemia due to right femoro-popliteal bypass thrombosis, right anterior femoro-tibial bypass was performed. During this admission, acenocoumarol was withdrawn and anticoagulation with low-molecular-weight heparins (LMWH) was prescribed, with poor compliance by the patient. In usual functional class III/IV, he was admitted to internal medicine with progressive worsening of the same until presenting dyspnoea at rest, paroxysmal nocturnal dyspnoea, orthopnoea, oliguria and oedema in the lower limbs. No chest pain or other symptoms of interest. Treatment was intensified with diuretics and vasodilators without improvement. He presented with an episode of acute pulmonary oedema and was transferred to the coronary unit.

PHYSICAL EXAMINATION
Blood pressure 147/66 mmHg. Heart rate 80 bpm. Oxygen saturation 91% with nasal goggles at 4 litres, jugular venous pressure elevated.
Cardiac auscultation: rhythmic heart sounds with prosthetic click.
Pulmonary auscultation: crackles up to midfield.
Abdomen: globular, depressible, with non-painful hepatomegaly 3 cm below the costal margin.
Lower extremities: oedema up to the knees with amputation of the right foot.

COMPLEMENTARY TESTS
Electrocardiogram: atrial fibrillation. Ventricular stimulation at 70 bpm, without sensing or capture failures.
X-ray: increased cardiothoracic index (CTI), with vascular cephalisation, Kerley's B lines.
Blood tests:
Biochemistry: urea 91 mg/dl, creatinine 1.45mg/dl, glomerular filtration 47 ml/min, NT-proBNP 6,587 pg/ml, procalcitonin 0.096 ng/ml, C-reactive protein 96.5 mg/l.
Basal venous blood gases: pH 7.38, PCO2 44.5 mmHg, PO2 37.6 mmHg, bicarbonate 24.6 mmol/l, oxygen saturation 65.4%.
Haemogram: leukocytes 8,300/mm3, leukocyte formula normal, haemoglobin 12.7 g/dl, platelets 161,000/mm3.
Coagulation: INR 1.76, prothrombin time 47%, activated partial thromboplastin time 36.2 seconds.
Transesophageal echocardiogram: bidisc mitral mechanical prosthesis with immobility of the anterolateral disc in semi-closed position and incomplete mobility of the other disc, with two symmetrical small jets of intraprosthetic regurgitation, with image of thrombus in hinge and prosthetic ring without relevant mobile images. Mean transmitral gradient of 19 mmHg.
Coronary CT angiography: mechanical prosthesis in mitral position, showing a soft tissue density of low attenuation (hypodense), located between the two valve discs and extending along the atrial and ventricular side of the posterior disc, which remains immobile throughout the cardiac cycle. This lesion has a low attenuation (Hounsfield units between 60-80), which is compatible with valvular thrombus and, given its attenuation values, probably responds well to fibrinolytic treatment.
Radioscopy: immobility of the anterolateral disc and incomplete mobility of the other disc of the mechanical mitral prosthesis.
Transthoracic echocardiogram after two fibrinolysis: decrease in transmitral gradient of 7.8 mmHg after two consecutive fibrinolysis.

CLINICAL EVOLUTION
In the coronary unit, antithrombotic treatment was intensified with sodium heparin, acenocoumarol and clopidogrel. After failing to resolve the thrombus and in view of the worsening clinical condition, it was decided to present the case at a medical-surgical session, and the patient was rejected for valve replacement surgery due to multiple comorbidities and a high risk of mortality (around 90%). Fibrinolytic treatment was decided, in our case with alteplase, taking the coronary angio-CT result as a predictor of a favourable outcome after fibrinolysis. Twenty-four hours after treatment with alteplase, the patient showed substantial improvement in congestive signs and symptoms, with adequate diuresis with intravenous furosemide, stable haemodynamic parameters and a decrease in the mean mitral transprosthetic gradient from 20 to 10 mmHg. Despite the decrease in the gradient, it was still high, so a second fibrinolysis was decided 96 hours after the first dose, presenting a transmitral gradient of 7 mmHg 48 hours after this second therapy. As a haemorrhagic event, he only presented self-limited haematuria with no significant decrease in haemoglobin levels.

DIAGNOSIS
Severe mitral stenosis due to very late mitral valve prosthetic thrombosis related to non-compliance with anticoagulation therapy.
Decompensated chronic heart failure, NYHA functional class IV/IV, stage C AHA/ACC.
Good response after two consecutive fibrinolysis.
