A 48-year-old man came to the emergency department of a regional hospital referred from his local health centre due to progressive dyspnoea, asthenia, orthopnoea and cough in the last 24 hours.

History, current illness and physical examination
History: No known drug allergies. No DM, no hypertension, no dyslipidaemia. Sporadic smoker (1 pack/day at weekends) and regular drinker (3-4 beers daily, with other drinks at weekends). Severe mitral stenosis of probable rheumatic origin (no reports), mitral valve replacement in April 2011 with Carbomedics No 27 metal prosthesis using a minimally invasive technique (Heart Port). Transthoracic echocardiography (TTE) at discharge: Normally functioning mitral prosthesis. Mild aortic regurgitation. Mild atrial dilatation. Normal ejection fraction (EF). Permanent atrial fibrillation secondary to his valvular pathology. Previous surgical interventions: 'Cervical' (no reports).
Usual treatment: Sintrom 4 mg, pitavastatin 2 mg, bisoprolol 2.5 mg every 12 hours, digoxin 0.25 mg every 24 hours without rest, lansoprazole 15 mg, lorazepam 1 mg occasionally. The patient had no chest pain or other symptoms apart from those mentioned above. In the following hours, during his stay in the Emergency Department of the regional hospital, the patient suffered a progressive deterioration of his general condition, with increasing dyspnoea until he became resting, pink expectoration, pallor and diaphoresis. He was transferred to the observation ward with acute pulmonary oedema (APE) requiring non-invasive mechanical ventilation (NIV), presenting haemodynamic instability, and entering AF with RVR around 140-150 bpm. The patient continued with poor respiratory mechanics despite NIMV, with refractory hypotension and oligoanuria, so orotracheal intubation (OTI) was performed, connection to mechanical ventilation (MV) and noradrenaline and furosemide were started in p.c. Given the rapidly unfavourable evolution of the patient, an urgent TTE was carried out at the regional hospital, and the report from the aforementioned centre showed that the mitral prosthesis had not opened. The suspicion of prosthetic thrombosis was reinforced by the finding of an INR of 1.12 in the ED analysis. It was decided to perform fibrinolysis with 10 mg of rTPA as a bolus and then 90 mg of rTPA in pc for 90 min, simultaneously initiating anticoagulation with a bolus of 4,000 IU of sodium heparin and p.c. of the same at 800 IU/h.
The patient was transferred by ambulance to the ICU of our centre for urgent assessment. On admission to the ICU of our centre, the patient was sedoanalgesiated (midazolam at 0.2 mg/kg/h, morphine chloride at 1 mg/h), under OTI and connected to MV with 100% FiO2 according to standard parameters, maintaining 100% SatO2. Haemodynamically he maintained BP around 130/60 mmHg with amine support (noradrenaline at 0.3 μg/Kg/ min), in AF rhythm with RV around 90-100 bpm. Preserved diuresis with support of furosemide in p.c. at 40 mg/h, which was subsequently lowered to 20 mg/h. Diuresis on admission 300 cc. Anticoagulated with sodium heparin at 10 mg/h (10,000 IU/h). Physical examination on admission: BP 110/60 mmHg, HR 90 bpm, O2 sat 98% baseline. Conscious, oriented, reactive, perceptive. No palpable lymphadenopathies.
Cardiac auscultation: Rhythmic heart tones at 85 bpm, pansystolic murmur of intensity III/VI at mitral focus level, radiating to the axilla. Pulmonary auscultation: preserved vesicular murmur. Abdomen: soft, depressible, not painful on palpation, no masses or megaliths palpable. Lower extremities: No oedema or signs of deep vein thrombosis. Auscultation showed arrhythmic tones at about 100 bpm, no murmurs or extratonos, with audible prosthetic click in the mitral focus. Vesicular murmur was preserved bilaterally, with crackles in both lung bases. Abdomen without findings. Lower limbs without oedema or signs of DVT.
The patient was assessed by on-call Cardiology, and a new TTE was performed followed by transesophageal echocardiography (TEE) which confirmed the diagnostic suspicion, showing thrombotic release to the left chambers and the existence of a severely depressed LVEF (see images and description in the complementary tests).
Urgent catheterisation was subsequently performed, as described in the evolution.


Additional tests
- ECG: AF with RV at about 120 bpm. Normal electrical axis. BIRDHH. ST depression of 1.5 mm in inferolateral face (II, III, aVF, V4-V6).
- Blood gases: pH 7.25, pCO2 56, HCO3- 24, EB -2.1, Hb 18.4, SvO2 70%, ions normal, lactic 2.1.
- CBC on admission to ICU: Creatinine 1.50 (previous normal), urea 37, ions normal, glucose 135, total bilirubin 1.49, direct bilirubin 0.83, CRP 39, 19,060 leukocytes, 85.9% PMN, Hb 16.9, platelets 192,000, INR 2.08, TPTA: No clotting.
- Urgent TEE: Non-dilated LV with severely depressed EF with global hypokinesia. Normofunctioning trivalve aortic valve. Autocontrast in LA with images of scattered thrombi, in atrial appendage, interatrial septum and anterior portion of the mitral annulus. Mitral prosthesis with fixed anterior disc and posterior disc with preserved mobility. Peak transprosthetic gradient of 7 mmHg (AF at 100 bpm). Mild regurgitation. The ventricular side of the anterior disc shows images compatible with the presence of thrombus adhered to it. From the bicave plane, autocontrast and mobile thrombus can be seen at the mouth of the inferior cava (which is not seen again later in the study). RV not dilated with systolic function at the lower limit of normality.
Conclusions: Mitral prosthetic thrombosis that does not cause significant stenosis. Multiple thrombi in LA. Severe LV dysfunction (coronary embolism?).

Clinical course
In view of the TEE findings, on-call Cardiac Surgery was notified and it was decided to perform coronary angiography (due to the contractility alterations and ECG changes) and then urgent surgery, both procedures being carried out in the following hours. Catheterisation showed no angiographically significant coronary lesions, and once again the non-mobility of one of the prosthetic discs was confirmed. During the surgical procedure, a large amount of LA thrombus and thrombus causing occlusion of the aforementioned disc was observed. Remnants of the posterior mitral leaflet that may have contributed to the occlusion were observed. It was decided to remove the prosthesis and implant a new one. During CPB, with the heart at low preload, marked LV hypocontractility was observed, mainly at the expense of the middle and apical regions (septum and basal region with good mobility). He was connected to an epicardial pacemaker for sinus bradycardia. Times: ECC 138 min. Anoxia 78 min. Temperature 32 oC. He left the operating theatre with significant inotropic support (dobutamine at 10 μg/kg/min + noradrenaline at 0.3 μg/kg/min + adrenaline at 0.3 μg/kg/min + levosimendan at 0.05 μg/kg/min), maintaining AMT around 80-85 mmHg. He also presented a significant coagulation alteration, which was controlled with transfusion of blood products (800 cc plasma + 1 pool of platelets + 4 g of fibrinogen + 2 red blood cell concentrates). In the immediate postoperative period he presented abundant bleeding through the drains and anaemisation, which again required transfusion of blood products. The patient is currently still in the ICU, under sodium heparin p.c. and with good prosthetic function. In the last few hours he has been extubated and has no neurological deficits on examination, and is progressing favourably.

Diagnosis
- Mitral prosthetic thrombosis in a poorly anticoagulated patient. Urgent fibrinolysis partially effective with thrombotic release to the left chambers.
- Severe LV dysfunction with alterations in contractility and ECG changes in this context, with no evidence of coronary embolism.
- Impaired renal function secondary to low output, now resolved.
