The patient was an 85-year-old woman with a biological aortic valve prosthesis and double coronary artery bypass graft who was admitted to the Cardiology hospital ward for acute heart failure. The echocardiogram showed a rupture of one of the prosthesis leaflets with severe aortic insufficiency.

HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

Personal history
Intolerance to calcium antagonists due to oedema.
No toxic habits.
Hypertension, dyslipidaemia and type 2 diabetes under treatment.
Sclerodegenerative aortic valve disease and common trunk disease, undergoing aortic valve replacement surgery for biological aortic prosthesis (Perimount 21) and double aortocoronary bypass (AMI-DA, SF-Cx) at a private centre in 2001. Subsequent check-ups by cardiologist, asymptomatic.
Last echocardiogram (June/2015): non-dilated LV with severe concentric hypertrophy and preserved global and segmental systolic function. Severe calcification of the mitral valve, without significant stenosis. Mild-moderate mitral regurgitation.
Carpentier Perimount 21 biological prosthesis with calcified, degenerated leaflets.
Slightly elevated gradients. Normal RV. Normal pulmonary pressure.

Usual treatment: gliclazide 30 mg (0-1-0), sitagliptin 100 mg (1-0-0-0), ASA 100 mg (0-1-0), doxazosin 8 mg (0-0-1), carvedilol 25 mg (1-0-1), candesartan/HCTZ 32/12.5 mg (1-0-0), pravastatin 40 mg (0-0-1).

Present illness
An 85-year-old woman was admitted to the emergency department of our hospital for progressive dyspnoea over the last month, which had been increasing until it became minimal effort. She reported orthopnoea and episodes of paroxysmal nocturnal dyspnoea. He also has increased oedema in the lower extremities up to the knees and decreased diuresis. She has increased the dose of diuretic with little improvement. Afebrile and with no other associated symptoms.

Physical examination
BP 150/50 mmHg, HR 110 bpm, Ta 36.5°C, baseline SO2 85%.
Conscious and oriented. Tachypnoea and respiratory work. Afebrile. Good hydration and perfusion status.
Chest: mid sternotomy scar.
AC: rhythmic, fast, systolic-diastolic murmur (V/VI) in aortic focus.
PA: crackles in the lower half of both hemithoraxes.
Abdomen: globular, soft and depressible, not painful on palpation, with no signs of peritoneal irritation.
Lower extremities: oedema with bilateral fovea up to the knees. No signs of deep vein thrombosis. Pedial pulses present. Saphenectomy scar.

COMPLEMENTARY TESTS
ECG on admission: sinus rhythm at 60 bpm, known LBBB with secondary repolarisation alterations.
Chest X-ray on admission: cardiomegaly, bilateral perihilar alveolar infiltrates, compatible with pulmonary oedema.
Laboratory tests on admission: arterial pH 7.41, PaCO2 56 and PaO2 59 mmHg, bicarbonate 35.5 mEq/L, SatO2 88 %, glucose 167, urea 79 and Cr 1.35 mg/dl. Na 137 and K 5.07 mEq/l. CRP 10.8 mg/l. NT-proBNP 10195 pg/ml. Troponin T 62 ng/L. Leukocytes 9200/mm3, Hb 11.3 g/dl, Hto 39 %, MCH 26 pg, MCHC 29.2 g/dl, platelets 94000/mm3. T. Prothrombin 76 %, INR 1.19, APTT 30 sg.
Transthoracic echocardiogram on admission: non-dilated LV with severe concentric hypertrophy and preserved global systolic function. Severe annular calcification of mitral valve without significant stenosis. Moderate central MI. Dysfunctioning, degenerated Perimount 21 biological aortic prosthesis, with moderate transprosthetic gradient and severe new onset aortic insufficiency possibly related to rupture of one of the leaflets. Moderately dilated RV with mild systolic dysfunction. Moderate TR. Severe PH.
Transesophageal echocardiogram: dysfunctional Perimount 21 biological aortic prosthesis, with degenerated leaflets, calcified and with one of the leaflets broken, which protrudes into the left ventricular outflow tract in diastole, leading to very severe aortic insufficiency. Severe mitral annular calcification, with moderate central mitral insufficiency. Moderate tricuspid insufficiency due to annular dilatation (39 mm). Severe pulmonary hypertension. Mildly dilated right ventricle, with moderate global systolic dysfunction.
Coronary angiography: common trunk: severe ostial lesion. Anterior descending: irregular borders, without significant stenosis. Circumflex: irregular borders, without significant stenosis. Right coronary: dominant. Minimal irregularities, without significant lesions. Grafts: IMA to LAD: patent. Saphenous to OM: patent.
Angio-CT aorta: thoracic aorta of normal calibre and morphology with slight atheromatous changes.
Abdominal and iliac aorta of normal calibre and morphology with mild-moderate atheromatous changes, predominantly in infrarenal abdominal aorta and proximal common iliac aorta, at postbifurcation level. Discrete focal eccentric calcification in the right common femoral artery prior to bifurcation.

EVOLUTION
The patient is an 85-year-old woman, with a biological aortic valve prosthesis and double coronary artery bypass grafting who was admitted with acute pulmonary oedema and severe aortic insufficiency was detected on echocardiography due to rupture of one of the leaflets of the biological aortic prosthesis. The patient was admitted in severe heart failure, requiring high doses of intravenous diuretics. After clinical stabilisation, a transesophageal echocardiogram was performed which confirmed the rupture of one of the aortic prosthesis leaflets, resulting in very severe aortic insufficiency.
Given the severity of the valve disease, the case was presented at a medical-surgical session. Given the patient's advanced age and previous cardiac surgery in 2001, it was decided to implant an aortic valve prosthesis inside the previously implanted prosthesis, percutaneously from femoral access (TAVI valve in valve).
Coronary angiography showed no new lesions and aortic CT angiography showed favourable femoral accesses for the procedure.
By means of a catheter introduced through the left femoral arterial access, the correct right femoral arterial access is checked, through which it is passed by means of an Extra-Stiff guide. The Ewards Sapien 3 No 23 expandable prosthesis is advanced over this guide. It is expanded in the aortic position, remaining slightly under-expanded at the level of the ring of the previous Perimount prosthesis (Video 3 and 4).
Transesophageal echocardiography is used to verify the normal position of the valve, the absence of regurgitation and the transvalvular gradients (max 37 mmHg). The absence of aortic regurgitation and absence of leakage after Prostar closure of the right femoral access is verified by angiography. The left femoral access is closed with Angio-Seal.
After the procedure, the patient was admitted to the Coronary Unit extubated, haemodynamically stable, with initially fair O2 saturations in the context of sedation after the procedure and signs of mild pulmonary congestion, which evolved well with diuretic treatment. He also presented with acute renal failure prior to the procedure, with a creatinine peak of 2.2 which resolved during admission (urea 122 at discharge, creatinine 1.06).
He remained in his own rhythm during admission (sinus with LBBB and long PR, already present before the procedure), with no other arrhythmic events in telemetry, so the transient jugular PM was removed.
On the hospital ward, he had a very good clinical evolution. Congestion data disappeared, remaining stable at all times. A control echocardiogram showed residual moderate aortic stenosis after the procedure, without aortic insufficiency. Good appearance of the femoral arterial accesses, with slight haematomas, without major complications. In good clinical condition, she was discharged home.

DIAGNOSIS
Acute heart failure due to severe aortic insufficiency.
Biological aortic prosthesis with severe insufficiency due to leaflet rupture.
Implantation of Edwards Sapien 3 (valve in valve) percutaneous valvular aortic prosthesis.
LV function borderline-slightly depressed.
Acute renal failure, resolved.
