This project aims to investigate the performance of edge-to-edge mitral valve repair (MVR) within reanimated swine hearts. Direct imaging and hemodynamic data of the mitral valve during normal cardiac function (Normal), after an induced prolapse (Prolapse), and post surgical repair (E2E) was obtained. Isolated swine hearts (n=6) were reanimated using a clear Krebs–Henseleit buffer. Mitral prolapse, and regurgitation, in the P2 region was induced by cutting chordae tendinae of the posterior leaflet. An edge-to-edge MVR procedure was performed, suturing the prolapsed P2 region to the A2 region of the anterior leaflet. The mitral valve was imaged using endoscopic cameras in the left atrium and ventricle allowing verification of stitch placement and leaflet coaptation. Analysis of the endoscopic images provided measures of annulus area, orifice area, and regurgitant area. Echocardiography, the standard clinical imaging modality, was used to determine the hemodynamic performance of the valve. Additionally, ECG and left chamber pressures were recorded at a sample rate of 5 kHz. Prolapse of the P2 region was consistently created, and edge-to-edge repair of the mitral leaflet showed full leaflet coaptation. The annulus area of the valve was tracked throughout the procedure and did not show significant variation. The orifice area, defined as the area of the annulus that does not contain leaflets, normalized to the corresponding annulus area for Normal, Prolapse and E2E were: 41±13%, 44±14% and 21±13%, p=0.02. The regurgitant area, normalized to the corresponding annulus area, increased from 2±2% for Normal to 8±3% for the Prolapse and then decreased to 1±1% for the E2E group. The regurgitant fraction, normalized against the maximum observed, for Normal, Prolapse and E2E was 10±6%, 57±26% and 13±13%, p<0.01. Over the course of the experiment the left ventricular (LV) systolic pressure and negative dP/dt reduced from 95 to 54 mm Hg and 743 to 402 mm Hg/s, respectively. Our results show that orifice area was significantly smaller after MVR when compared to Normal and Prolapse periods. There was no significant change in regurgitant area and regurgitant fraction from the Normal to repaired valve as compared to a significant increase in regurgitant area and regurgitant fraction during Prolapse. Low gradients were observed for all three groups, with no indications for symptomatic stenosis. The reduction of LV function was caused by global ischemia and the progressive onset of edema. In this acute assessment of edge-to-edge repair of P2 prolapse, repair does not affect annulus area, decreases orifice area, and successfully eliminates regurgitant area with no evidence of mitral stenosis.