Emily Tat

Mitral annular calcification is not associated with decreased procedural success, durability of repair, or left ventricular remodelling in percutaneous edge-to-edge repair of mitral regurgitation.

AIMS Mitral annular calcification (MAC) negatively influences outcomes in surgical mitral valve (MV) repair for mitral regurgitation (MR). However, there are no data on whether MAC impacts on outcomes of MitraClip percutaneous MV edge-to-edge repair. This study sought to investigate whether the presence of MAC impacts on the procedural success and durability of percutaneous transcatheter repair of MR using the MitraClip. METHODS AND RESULTS One hundred and seventy-three patients undergoing MitraClip repair for significant MR were studied. Patients with moderate-or-severe MAC (n=28) were compared to those with no-or-mild MAC. Post-procedural MR severity was not different (p=0.642) and MR reduction to moderate-or-less was equally high in patients with moderate-or-severe MAC (100%) and those without (96.7%), p=1.000. At one year, MR severity was not different (p=0.831), and there was no difference in the repair durability when comparing patients with moderate-or-severe MAC (93.8%) to those without (90.6%), p=1.000. All patients with moderate-or-severe MAC assessed at one year were in NYHA functional Class I-II and had haemodynamic improvements with a decrease in pulmonary artery systolic pressure (-6.5±13.1 mmHg), p=0.021, and end-diastolic left ventricular internal diameter (-3.9±6.5 mm), p=0.034, not different to those achieved by patients without MAC (both p>0.100). CONCLUSIONS Moderate-or-severe MAC scored by echocardiography and confirmed on fluoroscopy was not associated with decreased procedural success or durability of repair. Patients with moderate-or-severe MAC had improvements in clinical symptoms and haemodynamics, as well as decreased left ventricular dimensions.

Not Your Typical Hole-in-the-Wall: Percutaneous Closure of an Acquired Post-Myocardial Infarction Ventriculoatrial Gerbode Defect.

A 58-year-old male patient presented with an inferior ST-segment elevation myocardial infarction complicated by a ventricular septal defect (VSD). The VSD was surgically repaired, but basal extension of necrotic tissue obligated a second repair 2 weeks later. Subsequently, he again presented in