A 45-year-old woman with a history of rheumatic mitral disease underwent valve replacement. After surgery, the patient became hemodynamically unstable. A transesophageal echocardiogram showed an underfilled left ventricle with a clot impinging on the lateral aspect of the left ventricle and a malfunctioning mitral valve prosthesis. After evacuation of the clot in the operating room, the mitral valve prosthesis began functioning normally. The prosthesis malfunction resulted from external cardiac compression. This dynamic device malfunction was replicated when the surgeon compressed the lateral aspect of the heart. To our knowledge, this dynamic form of leaflet dysfunction from external compression has not been described. This case highlights the importance of closely evaluating prosthetic valve function in the setting of hemodynamic deterioration.
A 45-year-old woman with a history of lupus anticoagulant syndrome, pulmonary embolism, hypertension, and rheumatic mitral valve disease was admitted with a chief symptom of shortness of breath. Physical examination showed a 5/6 systolic murmur best heard at the cardiac apex and diffuse bilateral rales and wheezes. A chest x-ray demonstrated increased interstitial markings with bibasilar patchy opacities consistent with pulmonary edema. A transthoracic echocardiogram showed severe mitral regurgitation secondary to Carpentier type IIIa restrictive leaflet motion, and the patient was scheduled for mitral valve surgery. Her medications included Coumadin for treatment of lupus anticoagulant syndrome and pulmonary embolism prevention.
Case Report
In the operating room, general anesthesia was induced and transesophageal echocardiography (TEE) was performed. TEE confirmed severe mitral regurgitation secondary to restrictive leaflet motion. Given the extensive calcification of the valve annulus and valve apparatus, valve repair was deemed unfeasible. Given the patient’s age and chronic Coumadin use, a mechanical valve (27-mm MCRI On-X bileaflet mechanical prosthesis; Medical Carbon Research Institute, LLC, Austin, TX) was implanted. Of note, much of the mitral valve subvalvular apparatus was preserved, including most of the posterior leaflet.
The patient was weaned from bypass uneventfully, and the mechanical valve was functioning normally ( Video 1 ). The patient had normal pulmonary artery pressures and was transported to the intensive care unit on minimal vasopressor support. Overnight the patient developed systemic hypotension, pulmonary hypertension, excessive chest tube output, and respiratory variation of the arterial line tracing. TEE showed a clot in the pericardial space impinging on the dilated left atrium. The left ventricle was severely underfilled and hyperdynamic, and there was restricted leaflet opening of the mitral prosthesis, with sluggish opening of one of the prosthesis leaflets. The patient was urgently taken to the operating room, where a large pericardial clot was removed from the chest. After evacuation of the clot, the valve began to function normally. The surgeon was able to replicate the condition caused by the clot by pressing on the outside of the heart with his finger. External compression with his finger impaired the prosthesis valve leaflet opening, whereas release of external compression restored normal prosthesis valve leaflet opening. This illustrates the dynamic nature of prosthesis dysfunction ( Video 2 ; Figures 1 and 2 ) . After surgery, the patient was readmitted to the intensive care unit and ultimately made a good recovery.
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