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 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.