Abstract Background Chronic severe functional mitral regurgitation (FMR) is common in patients with HF as it reflects left ventricle dysfunction and portends poor prognosis. Case report A 42 years old man with cardiovascular risk factors (former smoker, obesity) but without previous cardiological history presented anterior ST-elevation myocardial infarction (STEMI) treated with primary PCI of the anterior descending artery. He developed severe ventricular dysfunction leading to congestive heart failure (HF) requiring early re-hospitalization for pulmonary edema. Despite optimal medical therapy patient remained symptomatic (NYHA class III, INTERMACS 6) with persistence of left ventricle ejection fraction (LVEF) depression, therefore he received an implantable cardiac defibrillator for primary prevention and was referred to our institution for further evaluation. Trans-esophageal echocardiography showed severe left ventricle dilatation and disfunction (EDD 6.9 cm, iEDV 113 ml/m2, LVEF 24%) and presence of severe FMR with EROA 37 mm2 and RV 44 ml. Right heart catheterization (RHC) revealed combined pulmonary hypertension (mean PA pressure 43 mmHg, PCWP 32 mmHg, PVR 4.6 WU) with severely reduced cardiac index obtained (CO 3.4 l/min, CI 1.9 l/min/m2). After infusion of inodilator (enoximone) a decrease of PA pressure and PVR was reported, concluding for reversible pulmonary hypertension. After screening for non-cardiac contraindications, the patient was listed for heart transplantation. Chances to get a donation with a short waiting list time were low because of patient's high BMI and blood group B. Therefore, after Heart Team evaluation, transcatheter edge-to-edge repair of the mitral valve (TEER) was performed as bridge to transplant. A single NTR clip was used, placed centrally between A2-P2 segments, reducing regurgitation from severe to mild. Patient was discharged on heart transplantation waiting list. At three months follow up he presented clinical improvement with reduction of NYHA class from III to II. RHC was repeated and showed normal filling pressures, reduction of pulmonary pressure (mPAP 20 mmHg) and increased cardiac output (CO 5.2 l/min, CI 2.5 l/min/m2). According to his preferences, the patient was suspended from the waiting list with indication to continue outpatient follow-up. At 1-year control he was stable in NYHA II class and the daily diuretic dose had been reduced, echocardiography showed severe LVEF depression (28%) with mild to moderate residual mitral regurgitation. Conclusions TEER recently emerged as an option for patients with FMR who are not suitable for surgery. Latest guidelines suggest its use in presence of specific criteria (LVEF 20-50%, ESD < 7 cm, sPAP <70 mmHg, hemodynamic stability, absence of right ventricle disfunction and severe TR) rarely fulfilled by patients with advanced HF requiring evaluation for transplant. On the other hand, access to surgical strategies for end stage HF is limited by scarce availability of donors and by temporary or definitive contraindications. Evidences are emerging that in this population TEER can improve hemodynamic profile and lead to reduction of pulmonary hypertension, providing temporary stability before definitive treatment or allowing candidacy. In this setting, TEER might be performed to reduce symptoms. Considering TEER as bridge strategy to transplant, candidacy or decision can expand the number of patients suitable for heart transplantation or delay urgency.
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