HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
Male, 61 years old.

BACKGROUND:
Arterial hypertension. Dyslipidaemia. Dilated cardiomyopathy of ischaemic origin with moderate ventricular dysfunction, non-revascularised chronic ischaemic heart disease. Permanent atrial fibrillation (AF) anticoagulated with acenocoumarol. Rheumatic mitral valve disease with mechanical prosthesis implantation in 1977 and subsequent replacement in 2001.
Medical treatment: telmisartan 40 mg/day, bisoprolol 2.5 mg/day, eplerenone 25 mg/day, digoxin 0.25 mg/day, acetylsalicylic acid 100 mg/day, omeprazole 20 mg/day, atorvastatin 40 mg/day, ranolazine 375 mg/12 hours, acenocoumarol according to controls.

CURRENT DISEASE:
She attended the emergency department of our hospital in February 2015 due to an increase in her usual dyspnoea from moderate to minimal exertion, in the last week. She denied cough, fever or other concomitant symptoms. She was admitted to cardiology with a diagnosis of acute pulmonary oedema.

PHYSICAL EXAMINATION:
Blood pressure (BP) 140/60 mmHg. Heart rate (HR) 110 bpm. Jugular venous pulse (PVY): normal. Cardiac auscultation: arrhythmic tones with mitral opening click and pansystolic murmur in mitral focus. Pulmonary auscultation: preserved vesicular murmur (VCM) with crackles up to the middle third of both lung fields. Lower extremities: no oedema.

COMPLEMENTARY TESTS
ANALYTICS: Cr 1.23 mg/dl. CK 3 U/L. Total bilirubin 1.37 mg/dl. Direct bilirubin 0.36 mg/dl.
Indirect bilirubin 1.01 mg/dl. LDH 1.086 U/L. Sodium 137 mmol/l. Potassium 4.4 mmol/l. CRP 3.7 mg/l. Haptoglobin 3 mg/dl. Hb 9.4 g/dl. Hcto 28.2%. MCV 84.1 fl. Leukocytes 7,670 u/l. Platelets 163.000 u/l. APTT 50.6 s. T. protombin 35.2%. INR 3.3. Fibrinogen 598 mg/dl.
Admission electrocardiogram (ECG): AF with ventricular response at 140 bpm, LBBB with secondary repolarisation alterations.
Transthoracic echocardiography (February 2015): dilated left atrium and left ventricle with mild-moderate ventricular hypertrophy with mild inferior hypokinesia, preserved remaining segmental contractility and slightly depressed systolic function (LVEF 47%). Mitral mechanical prosthesis with mild-moderate obstruction (mean gradient 5-6 mmHg, AVM per THP 1.4-1.45 cm2). Trivalve aortic valve, slightly thickened with mild regurgitation. Ascending aorta slightly dilated. Structurally and functionally normal pulmonary valve.
Structurally normal tricuspid valve with trivial regurgitation. Very dilated inferior vena cava. Absence of pericardial effusion.
Transesophageal echocardiography (June 2015): paraseptal periprosthetic dehiscence in A3-P3 of 6 mm in diameter causing moderate-severe mitral regurgitation with jet directed towards the interatrial septum, reaching the roof of the left atrium.
CARDIAC CATHETERISM (February 2015): right dominance. Left common trunk without lesions. Lesion of 90% in the middle anterior descending artery. Lesion of 90% in bisector. Long lesion in middle circumflex artery. 90% lesions in proximal, middle and distal right coronary artery.
After this, the third cardiac surgery is performed, with closure of the leak and coronary revascularisation.
Transesophageal echocardiography (June 2015 - after surgical repair): periprosthetic paravalvular dehiscence of 6 mm in diameter, which caused moderate to severe mitral regurgitation with a jet directed towards the interatrial septum reaching the roof of the atrium.
CARDIAC CATHETERISM (September 2015): percutaneous closure of periprosthetic leak with retrograde transfemoral arterial approach.
Transesophageal echocardiography (September 2015 - in the periprocedural haemodynamics room): the device is correctly implanted with new appearance of another periprosthetic leak.
3D Transesophageal Cardiac Echocardiography (September 2015 - in the periprocedural cath lab): the device is correctly implanted with the appearance of another periprosthetic leak.

CLINICAL EVOLUTION
During admission, transesophageal echocardiography revealed a mitral periprosthetic leak at A3-P3, leading to severe mitral regurgitation. Coronary angiography showed 3-vessel disease, so after clinical stabilisation with diuretics, he was accepted for surgery, with triple bypass and closure of the leak with four stitches, with a good result on postoperative echocardiography.
During the following months, the patient presented several admissions for decompensated heart failure (HF) and haemolytic anaemia that required several periodic transfusions. Transesophageal echocardiography showed the presence of a new periprosthetic paravalvular dehiscence of 6 mm in diameter, causing moderate-severe mitral regurgitation with a jet directed towards the interatrial septum reaching the roof of the atrium.
Given the high surgical risk due to previous cardiac surgery and associated comorbidities, percutaneous closure of the periprosthetic leak with retrograde transfemoral arterial approach was chosen. During implantation of the Amplatzer device, a new paravalvular leak appeared showing mild to moderate mitral regurgitation with a central jet, making it impossible to approach during this procedure (videos 5 and 6). It was therefore decided to discharge the patient and monitor his progress.
In the following months and progressively, he presented poor ambulatory functional class, requiring several admissions for decompensated HF secondary to the appearance of this last periprosthetic dehiscence close to the severe Amplatzer device (21 x 37 mm).
Thus, we are dealing with a young patient with recurrent paravalvular dehiscences, who presents a high surgical risk and requires a safe intervention with a high success rate. Accordingly, despite the need for a thoracostomy and apical puncture, the transapical approach was the best option for the patient. A rectangular Occlutech PDL device was implanted in the appropriate position under transesophageal echocardiography guidance.
Control transesophageal echocardiography showed that the paravalvular leak was sealed with minimal residual regurgitation. The patient was discharged 4 days after the procedure and the post-procedure course was uneventful during the 2-year follow-up.

DIAGNOSIS
Ischaemic heart disease. 3-vessel coronary artery disease with surgical revascularisation.
Mild systolic dysfunction and left ventricular (LV) dilatation.
Rheumatic valve disease with mitral involvement. Valve replacement by mechanical prosthesis on two occasions. Multiple recurrent periprosthetic mitral leaks, treated with surgical suture and percutaneous closure.
