A 69-year-old female patient with a prior history of hypertension, diabetes, hyperlipidaemia, and ischaemic heart disease, who suffered a recent non-reperfused posterior wall myocardial infarction (MI). Transthoracic echocardiography (TTE) showed mildly decreased LV systolic function [LV ejection fraction (EF) 45–50%], moderately dilated left atrium, severe MR with apically tethered leaflets, other causes for decompensation, and murmur including ventricular septal defect (VSD)/papillary muscle rupture, etc. were excluded. She continued suffering from congestive heart failure (CHF) symptoms: rest dyspnoea, no physical capacity, diuretic dependence, and pulmonary congestion.\nOn examination, she was with severe respiratory distress, her respiratory rate was 30 breaths/min, and her lung examination was suggestive for pulmonary oedema, heart sounds were rapid and a harsh pansystolic murmur was audible.\nAlthough the patient was not an optimal candidate for MC and in this effort, an IABP was inserted and left in situ for 24 h in order to optimize haemodynamic status, with the aim of altering LV geometry and to optimize the chances of success of MC by improving the coaptation length. On TOE, the baseline average annular diameter calculated in two orthogonal views, namely the mitral commissural (MC) and long axis was 37 mm. The coaptation surface length calculated in two orthogonal views was 3.9 mm. After insertion of IABP, the average annular diameter decreased to 35 mm and the average coaptation surface length increased to 5.5 mm (Figure; , Videos S1 and S2).\nShe underwent the procedure with no major complications. Two clips were implanted with a decrease of MR grade from +4 to +2 and no evidence of mitral stenosis.\nThe IABP was removed 12 h following the procedure after assuring stable clinical and euvolemic status. The patient was discharged few days later in good condition, with no additional episodes of pulmonary oedema. Three months after discharge, the patient was stable at New York Heart Association (NYHA) functional Class II. Transthoracic echocardiography showed only mild MR with borderline LV systolic function (EF 50%).
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.