A 74-year-old female patient with a prior history of hypertension, hyperlipidaemia, diabetes, asthma, chronic renal failure, and ischaemic heart disease. Two months prior to her admission, she was treated in the cardiac intensive care unit for inferior-lateral ST-elevation myocardial infarction and underwent percutaneous coronary intervention (PCI) to the left circumflex (LCX) artery.\nOn examination, she was in respiratory distress (25 breaths/min) and her oxygen saturation was 86% on room air. Upon auscultation, she had a clear audible systolic murmur radiating to her left axilla, had diminished lung sounds in the bases and crackles suggestive for pulmonary oedema.\nThe patient did not improve despite maximal medical therapy and remained in NYHA Classes III–IV. Transoesophageal echocardiography showed severe MR with practically no leaflet coaptation (‘Free MR’), and other causes for severe MR (VSD/papillary muscle rupture, etc.) were excluded. Prior to the procedure an IABP was placed for 48 h to help maintain clinical stability and euvolemic status, and to achieve LV geometry alteration thus allowing better leaflet coaptation to optimize MC success. Mitral valve measurements using TOE showed an average annular diameter of 42 mm, and coaptation surface length of 1.9 mm. After insertion of IABP, the average annular diameter was 34 mm and the average coaptation surface length was 4.4 mm (Figure); see , Videos S3 and S4). The patient underwent implantation of three MCs, with a good overall results and improvement of the MR from severe to mild-moderate.\nFollowing the MC procedure for 48 h, the patient was weaned from the IABP after assuring stable haemodynamic status. The patient was discharged a few days later in good condition, with major improvement in NYHA symptoms and no additional episodes of pulmonary oedema. Three months after discharge, the patient was stable at NYHA Class II. Follow-up TTE showed moderate MR with moderately reduced LV function (EF 40%).
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.