HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
Male, 79 years old.

History
High blood pressure.
Altered basal glycaemia.
Valvular heart disease consisting of severe degenerative mitral insufficiency, severe tricuspid insufficiency and severe pulmonary hypertension. Preserved left and right ventricular function.
Permanent atrial fibrillation.
Moderate-severe chronic obstructive pulmonary disease.
Sleep apnoea-hypopnoea syndrome, in treatment with nocturnal CPAP.
Stage 3a chronic kidney disease secondary to nephroangiosclerosis.
Bronchial carcinoid tumour T2 N0 M0, operated by right lower lobectomy and currently in complete remission.
Polymyalgia rheumatica.
Gouty arthritis.
Usual treatment: telmisartan/hydrochlorothiazide 80/25 mg 1 tablet every 24 hours; furosemide 40 mg 1 tablet at breakfast and half a tablet at lunch; spironolactone 25 mg 1 tablet every 24 hours, amlodipine 5 mg 1 tablet every 12 hours; acenocoumarol 4 mg according to INR; bicarbonate 500 mg every 12 hours; resin calcium 15 mg 1 tablet every 24 hours.

Present illness
Referred from pulmonology for increased dyspnoea on exertion and worsening of functional class in recent months, with a recent admission for decompensated failure. No exertional angina. In stable condition, he reported minimal effort dyspnoea (NYHA class III/IV), orthopnoea on 2 pillows.

Physical examination
At the outpatient clinic:
Blood pressure (BP) 130/65 mmHg. Heart rate (HR) 72 bpm. Baseline SatO2 94%. Afebrile. Good general condition, normohydrated, normoperfused. Jugular ingurgitation. Cardiac auscultation: arrhythmic tones, systolic murmur in mitral focus III/VI. Pulmonary auscultation: preserved vesicular murmur, generalised hypoventilation, no crackles. Abdomen: soft, depressible, non-painful, with no signs of ascites.
Oedema with perimalleolar fovea. Distal pulses present and symmetrical. No signs of deep vein thrombosis in the lower extremities.

COMPLEMENTARY TESTS
Electrocardiogram (in consultations): atrial fibrillation at 74 bpm, narrow QRS with normal axis, flattened T wave in inferolateral face without other repolarisation alterations.
Chest X-ray: post-surgical alterations with volume loss in the right hemithorax and fracture calluses of the costal arches (history of right lower lobectomy). No pulmonary consolidations were observed. Cardiothoracic index (CTI) increased. No pleural effusion.
Transthoracic echocardiogram: absence of pericardial effusion. Left ventricle slightly dilated (DTD 67 mm, VTD 142 ml) with normal wall thickness and normal systolic function (LVEF 67%), without alterations of segmental contractility. Severe dilatation of both atria. Dilated right ventricle (tricuspid annulus 52 mm, basal diameter 4C 57 mm) with preserved systolic function. Trivalve aortic valve with leaflet sclerosis and adequate opening movements. Mild-moderate aortic insufficiency. Mitral valve with thickening of the anterior leaflet without clear atrial prolapse by this technique and restrictive systolic motion of the posterior leaflet; calcification of the posterior portion of the annulus and the subvalvular apparatus. Mitral insufficiency that appears severe with a very eccentric jet in a postero-lateral direction, significant coanda effect, up to the atrial roof, ORE estimated by PISA of 0.50 cm. Tricuspid valve with large central coaptation defect.
Massive tricuspid insufficiency allowing an estimated PSAP of 63 mmHg. Aortic root (43 mm) and ascending aorta (41 mm) slightly dilated. Severely dilated inferior vena cava (31 mm) with abolished inspiratory collapse.
Transesophageal echocardiogram (pre-procedure): moderate calcification of the mitral annulus with normal opening. Restrictive systolic movement of the posterior leaflet, with a maximum length of 13 mm and associated prolapse of the anterior leaflet (A2 scallop) with an image of probable rupture of the chordae tendineae at this level. Severe mitral insufficiency codne codne eccentric pansystolic regurgitation that runs along the lateral wall of the left atrium, reaching its roof and causing inversion of the S wave in the pulmonary veins.
Contracted vein of 7 mm, ORE by PISA 0.81 cm. No image of ruptured cord is visualised. Mitral annulus 34 mm. Trivalve aortic valve with slightly thickened leaflets, normal opening and mild insufficiency. Tricuspid valve with normal structure and large dilatation of the annulus (55 mm), causing a large central coaptation defect with severe insufficiency. Normal pulmonary valve. No intracavitary masses and/or thrombi are visualised. Thoracic aorta of normal dimensions with some small uncomplicated atherosclerotic plaque. Septum intact. Rest of the study unchanged with respect to the transthoracic echocardiogram.
Transesophageal echocardiogram (haemodynamic monitoring): transseptal ultrasound-guided puncture was performed without incident. A first clip was implanted in a central position that clearly limited the eversion of the A2 scallop, with moderate residual insufficiency persisting in the medial region. It was decided to implant a second clip medial to the first, with good results. The overall insufficiency after the procedure was considered grade II (mild-moderate), with gradients of around 3 mmHg, without haemodynamically significant stenosis. After removal of the material, an atrial septal defect with diameters of 11 x 5 mm was observed by 3D planimetry, with predominant right-to-left Doppler shunt, which was finally sealed with a 12 mm Amplatzer device, leaving a residual, non-significant intradevice minimohunt. Good left ventricular systolic function after the procedure, with no pericardial effusion.
Transthoracic echocardiogram (pre-discharge): severely dilated left atrium. Severely dilated right atrium. Mitral valve closure by means of two mitral clips that behaves as a double residual lesion: mild-moderate mitral insufficiency and mild mitral stenosis. The right ventricle is moderately dilated with preserved systolic function. Left ventricle with moderate hypertrophy, not dilated and with hyperdynamic contractility (LVEF 73%). Ascending aorta slightly dilated. Double aortic valve lesion mild. Severe tricuspid insufficiency. Moderate pulmonary hypertension. Closure of atrial septal defect (ASD) secondary to intervention by means of Amplatzer percutaneous device without residual shunt. No pericardial effusion.

CLINICAL EVOLUTION
This is a patient under cardiological follow-up for his valvular heart disease, consisting of severe mitral insufficiency, who was referred to our clinic preferentially due to worsening functional class and recent admission for heart failure. At this time, mitral valve treatment is being considered. Taking into account the patient's comorbidities (moderate surgical risk, EuroSCORE II 4.46%) and history of pulmonary resection with severe chronic lung disease, he was considered the best candidate for percutaneous mitral valve treatment.
Thus, the patient is admitted on a scheduled basis for the procedure. It is performed in the cath lab under general anaesthesia and monitored by transesophageal echocardiography. Two mitral clips are released with reduction of the mitral regurgitation grade to mild-moderate (grade II/IV), maintaining a good opening area without significant increase in valve gradients (mean gradients of 3 mmHg). The procedure was terminated, but when the catheter was removed, the patient presented significant desaturation with hypoxaemia in the arterial blood gas analysis, with the rest of the vital signs remaining stable. The transesophageal echocardiogram showed that the mitral clips had not embolised, biventricular systolic function was good and there was no pericardial effusion. However, a significant right-to-left Doppler flow was observed at the level of the atrial septal defect secondary to the transseptal puncture. The decrease in left atrial pressure as the degree of mitral regurgitation decreased, together with the very high right atrial pressures due to severe pulmonary hypertension and tricuspid regurgitation, explains this phenomenon. Since the patient persisted with hypoxaemia despite 100% oxygen concentrations on the ventilator, it was decided to percutaneously close the atrial septal defect with an Amplatzer device. The patient's oxygenation improved and he was transferred to the post-surgical critical care unit where he was extubated without incident.
In the following days, the patient evolved favourably and did not present any complications at the vascular access level or deterioration of renal function or clinical signs of heart failure. A control echocardiogram was performed which showed good placement of the mitral clips, mild to moderate insufficiency and normal gradients. The patient was discharged from hospital on the fourth day of admission. On subsequent cardiology reviews, he remained clinically stable, in NYHA II/IV with mild heart failure predominantly on the right, which was controlled with a daily tablet of furosemide 40 mg.

DIAGNOSIS
Severe organic, degenerative mitral regurgitation, effectively treated percutaneously with the implantation of two mitral clips (MitraClip). Residual mitral regurgitation grade II (mild-moderate).
Significant right-to-left atrial septal defect and secondary hypoxaemia. Effective closure of the defect with Amplatzer device.
Severe tricuspid regurgitation. Severe pulmonary hypertension. Preserved left ventricular function.
Permanent atrial fibrillation.
