An 85-year-old female patient with prior history of hypertension, was urgently admitted to an outside institution with symptoms of progressive dyspnoea and malaise of ∼1 week duration. The patient later revealed all symptoms being preceded by an episode of persistent substernal chest discomfort that she managed at home without contacting her primary physician. In the emergency department, she was found with electrocardiographic evidence of a recent acute myocardial infarction (Q in precordial leads V1–V4 with ST elevations and T-wave inversions). She was diagnosed with an anterior ST-elevation myocardial infarction, pretreated with aspirin 325 mg, and clopidogrel 600 mg and urgently underwent coronary intervention with a drug-eluting stent to an occluded intermediate artery. The rest of the coronary arteries were without stenoses. Echocardiography 24-h later showed akinetic anterior and lateral wall with an estimated ejection fraction of 40%. After initial clinical improvement, the patient abruptly deteriorated on the third day with onset of acute pulmonary oedema and cardiogenic shock. At this time, the electrocardiogram did not show any dynamic changes of the ST-T segments or any arrhythmias. Repeat coronary angiography was without any further stenosis and re-evaluation with echocardiography revealed new severe mitral regurgitation and no other abnormalities that could lead to shock, such as pericardial effusion—tamponade or ventricular septal defect (VSD). Clinical examination at the time revealed an elderly female in moderate distress, requiring supplemental oxygen (60% FiO2) for maintenance of a saturation of 92–93%, with orthopnoea, jugular venous distension, and bilateral inspiratory crackles on lung auscultation. There was a two out of six systolic apical murmur, without evident gallop rhythm and mild peripheral oedema. The patient was transferred to our institution for further management and possible surgery. Upon transfer, she was in New York Heart Association (NYHA) Class IV with persistent pulmonary oedema despite high doses of intravenous furosemide (180 mg/24 h), on high dose supplemental oxygen (60% venturi mask), and on dobutamine infusion at 3 μg/kg/min. A transoesophageal echo exam (TOE) revealed partial rupture of the anterolateral PM with flail anterior (A1 and A2 scallops) and posterior leaflet (P1 scallop) (, , Videos S1 and S2). This PM rupture and flail mitral valve produced severe acute mitral regurgitation, pulmonary oedema, and cardiogenic shock. The patient was evaluated by the heart team and was considered at prohibitive surgical risk [log EuroSCORE 43% (85-years-old female, critical preoperative state/cardiogenic shock, EF 30–50%, recent myocardial infarction) and STS score 13%]. Indeed, she was in intractable heart failure, despite maximal intravenous diuretics, with dyspnoea at rest, radiographic appearance of bilateral pulmonary oedema, and in need of intra-aortic balloon counterpulsation for stabilization. She was thus referred for emergency transcatheter mitral valve edge-to-edge repair with MitraClip (Abbott Vascular, Santa Clara, CA, USA), (, , Video S3). Two clips were implanted at the central and lateral part of the valve. The first clip was implanted at the A2–P2 scallop towards the lateral aspect of the valve. Due to the significant remaining regurgitation coming from the flail anterolateral commissure (, Video S4), a second clip was implanted lateral to the first within the commissure. The final result after implantation of these two clips was with an effective reduction of mitral regurgitation from torrential to mild-moderate, while creating a single orifice valve (‘zipping’ of the lateral commissure) with an estimated (with use of three-dimensional echocardiographic multiplanar reconstruction) residual valve area of 2.1 cm2 and a mean transmitral gradient of 6 mmHg (, , Video S5). Subsequent to the MitraClip procedure, the patient was weaned off both intra-aortic balloon counterpulsation and inotropic support (dobutamine and dopamine infusions). The patient was also switched to oral diuretics and had reduced supplemental oxygen demands. The post-procedural course was uneventful. She was discharged home a week later on standard heart failure therapy including metoprolol, ramipril, furosemide, spironolactone, and ivabradine. At the 20-month follow-up, she remains in stable clinical condition in NYHA class II, and no further interventions were required on the mitral valve. Echocardiography revealed moderate mitral regurgitation and a mean transmitral gradient of 6 mmHg.
An 80-year-old female patient with a prior history of hypertension, hyperlipidaemia, diabetes, and ischaemic heart disease with a prior inferior MI and PCI with drug-eluting stent placement to LCX, 3 years prior to her current admission. She was admitted with respiratory failure due to pulmonary oedema and pneumonia.\nThe patient was conscious, intubated, and ventilated with remarkable tachypnoea, her blood pressure was 80/50 mmHg and her pulse 100 b.p.m. There were decreased lung sound in both bases, heart sounds were irregular and fast, periphery was cold and dry.\nInitial TTE upon admission showed normal size LV with normal global systolic function, severe ischaemic MR (posteriorly directed wall jet), and no stenosis. After a 10-day period with improvement of infectious status, but no improvement in her CHF signs and inability to wean from mechanical ventilation due to continuous pulmonary congestion, a decision was made to perform urgent mitral clipping as salvage therapy. Prior to the procedure, TOE was performed that showed severe MR with a posteriorly directed jet, severe malcoaptation mainly resulting from posterior leaflet immobility, and no evidence of papillary muscle rupture or new VSD. Mitral valve measurements were based on TOE prior to the procedure: average annular diameter was 40 mm and average coaptation surface length was 2.9 mm. An IABP was inserted 3 days prior to the procedure as means of haemodynamic support and aim of altering LV geometry to optimize the chances of success of MC by improving leaflet coaptation surface length and annular diameter. Transoesophageal echocardiography after insertion of IABP showed an average annular diameter of 36 mm and average coaptation surface length was 5.2 mm. Two MCs were implanted (one medially and one laterally to the prominent calcification). Mitral regurgitation improved from severe to moderate and atrial V-wave decreased from 60 to 25 mmHg, with no immediate post-procedural complications.\nFollowing the procedure there was an initial improvement in in her respiratory condition, the IABP was kept in situ to allow better haemodynamic and vulemic support. Unfortunately 7 days after the procedure, she developed ventilator associated pneumonia and sepsis with multiorgan failure, she died 10 days following the procedure.