The patient is an 84 year old man with a history of flail posterior mitral leaflet and severe mitral regurgitation. During serial follow-up, he remained asymptomatic with normal left ventricular (LV) size and function. Due to his advanced age and lack of symptoms, the patient was managed medically until March 2004 when he developed exertional dyspnea. He was referred for a cardiac surgical evaluation and left heart catheterization in preparation for possible mitral valve surgery. On March 31, 2004, the patient underwent coronary artery bypass grafting and mitral valve replacement with a bovine bioprosthesis. His operative and immediate post-operative course was uneventful. A post-operative transthoracic echocardiogram (TTE) revealed a dilated LV with severely reduced function. The tissue valve appeared to function normally. An echodensity of unclear etiology was noted superior to the left atrium (LA). He felt well and was observed clinically. A follow-up TTE on 8/16/2004 showed improvement in LV size and function, normal tissue valve function, and the previously noted echodensity superior to the LA. The differential diagnosis of this echodensity included vegetation, thrombus, mitral chordae, or reverberation artifact. In the interim, the patient developed a significant decrease in his hematocrit (27.0%). Evaluation in consultation with a hematologist revealed a hemolytic anemia, possibly secondary to the prosthetic valve. He subsequently underwent transesophageal echocardiography (TEE). Antibiotic therapy for presumed endocarditis was initiated but a one-week course did not change the size of the mass as documented by repeat TEE. The patient also had no physical or laboratory evidence (including multiple blood cultures with no growth) of endocarditis. On September 14, 2004, the patient underwent repeat cardiac surgery. The intraoperative findings included 1) a potential space between the sewing ring and the annulus; 2) the suspected prosthetic mitral valve mass was identified as a previously preserved primary chord to the anterior leaflet, which had a small portion of papillary muscle attached to it. This was prolapsing into the left ventricular outflow tract through the aortic valve. The surgeon performed a primary repair of the paravalvular leak and excision of the residual anterior leaflet chordae with attached papillary muscle. The papillary muscle presumably ruptured and resulted in its prolapse into the left ventricular outflow tract through the aortic valve. Pathology demonstrated infarcted papillary muscle tissue attached to chordae consistent with the contention of a ruptured papillary muscle.