Preservation of subvalvular mitral apparatus and maintenance of continuity between structures and annulus is recognized, and widely accepted as a significant factor for avoiding impairment to ventricular function and preventing left ventricular rupture during mitral valve replacement. However, we encountered a patient who developed posteromedial papillary muscle rupture following chordal sparing mitral valve replacement. The patient was a 67-year-old man who underwent mitral valve replacement with a porcine bioprosthesis 29M for acute mitral valve insufficiency due to several spontaneous chordal ruptures. The subvalvular apparatus of both leaflets was retained, the center of the anterior leaflet was excised elliptically, and the entire posterior leaflet was preserved. Although his postoperative course was uneventful, the transthoracic echocardiogram showed a floating structure prolapsing through the aortic valve in the left ventricle synchronizing with the cardiac cycle. The severed papillary muscle was removed successfully via an aortotomy through the native aortic valve on the 57th day after the first surgery. The patient recovered with no events. Surgeons should consider avoiding an excessive tension on the preserved chordae and delivering a cardioplegia sufficiently and uniformly during mitral valve replacement.

A 61-year-old man underwent an emergency operation for a ruptured infrarenal abdominal aortic aneurysm. Operations included bifurcated graft replacement of the abdominal aorta, oversewing of five lumbar arteries between L3 and L5, and ligation of the occluded inferior mesenteric artery. Because of the severe adhesions and arteriosclerotic changes over the bifurcation of the abdominal aorta and both common iliac arteries, prolonged aortic cross-clamp time was needed. In spite of stable his postoperative general condition, he suffered paresthesia and complete sensory loss on the left lower leg and the right sole. Moreover he was found to have paresis on the left leg and the right thigh. Knee and ankle deep-tendon reflexes were absent on the left. Lasègue's sign was positive bilaterally, which was more brisk on the left. There was no incontinence of urine and feces. EMG showed neurogenic polyphasic potentials on the lower extremities. MRI of the thoracolumbar spine and sacrum showed no evidence responsible for this neurological deficit, but IV-DSA revealed complete occlusion of the left common and internal iliac arteries. Following the active rehabilitation, he was able to walk unaided, but remained to have residual paresthesia on the left lower leg at his discharge. It was concluded that ischemic injuries to the cauda equina resulted in this rare complication, which seemed to be secondary to oversewing of critical lumbar arteries, prolonged aortic cross-clamp time, and the acute occlusion of the left common and internal iliac arteries.