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A previously non-described cause of mitral regurgitation is presented. An asymptomatic 50-year old male who was casually diagnosed of mitral valve Barlow's disease underwent cardiac surgery due to severe mitral regurgitation. In the operating theatre, a longitudinal fissure of 1.5-2.0 cm length, along the posterior mitral leaflet, was found responsible for the insufficiency. This defect had features of a potential congenital origin and it was successfully repaired with direct suture. Whether it is an atypical mitral cleft, a variation of Barlow's morphology spectrum or a new congenital heart defect remains unclear.

A 77-year-old woman had undergone dual-chamber pacemaker implantation in 2011 due to symptomatic sinus node dysfunction. An electrocardiogram taken at that time showed indications of being prone to low voltages in limb leads (Figure 1). The patient was admitted in 2012 for heart failure, with an electrocardiogram showing dual chamber pacemaker pacing and an echocardiogram showed normal systolic function and left ventricular thickness (Figures 2A and B). The pacemaker was checked, revealing an increase (> 99%) in the percentage of atrioventricular pacing. The patient was admitted again in 2013 for heart failure with refractory bilateral pleural effusion with diuretic therapy, requiring thoracentesis (with negative pleural fluid cytology for malignancy) (Figure 2C). During this stay, we decided to reprogram the pacemaker (Figure 3A) to avoid pacing from the right ventricle, in case this was the cause of the heart failure; then, we obtained pacing readouts consistent with infiltrative disease, ie, low voltage in limb leads and poor precordial lead R-wave progression (Figure 3B). Given the heart failure with preserved ejection fraction and the above-mentioned electrocardiogram, the patient was examined to rule out cardiac amyloidosis; finally, she was diagnosed with IgGl multiple myeloma with amyloid-positive subcutaneous fat staining. Chemotherapy was initiated but was ineffective, and the patient died 2 months later. We would like to highlight the electrocardiographic masking caused by these devices in this patient, hiding data consistent with storage disease, resulting in delayed diagnosis and worse prognosis. I