A 67 year-old Cantonese speaking male was seen at primary care clinic with complaints of dyspnea on exertion and decreased exercise tolerance. His medical history includes rheumatic heart disease, tricuspid regurgitation, tricuspid repair three months ago, mitral regurgitation, mitral valve replacement with a bioprosthetic valve three months ago, atrial fibrillation on anticoagulation therapy, permanent pacemaker implantation, severe pulmonary hypertension, benign prostatic hypertrophy,

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... ophageal reflux disease, and iron deficiency anemia. The patient reports that in the last two weeks, he has been unable to ambulate more than two blocks limited by shortness of breath, which represents an acute change. He also complains of bilateral lower extremity edema. He reports that two weeks after his mitral valve replacement, his exercise tolerance was dramatically improved, and he was able to ambulate more than two blocks without difficulty. He denies associated cough, lightheadedness, dizziness, chest discomfort, abdominal discomfort, nausea or vomiting. He reports occasional palpitations that are not associated with his episodes of dyspnea on exertion. Dyspnea resolves with rest in minutes. He denies recent fevers, sweats, and chills. Medications include metoprolol 25 mg twice a day, warfarin 4 mg daily, furosemide 40 mg daily, enteric-coated aspirin 81 mg daily, sustained-release potassium chloride 20 mEq daily, ferrous sulfate 300 mg three times per day, colace 100 mg twice per day, sennosides 8.6 mg daily and omeprazole 20 mg daily On physical examination, the patient was alert and oriented to person, place, and time and not in acute distress, afebrile, with a heart rate of 76 beats/minute, blood pressure of 90/60 mm Hg, respiratory rate 14 breaths/minute. Pupils were equal and reactive to light, and extraocular muscles were intact. There were no carotid bruits bilaterally, and jugular venous pressure was estimated at 16 cm of water. His lungs were clear to auscultation bilaterally with no wheeze, no crackles, nor rales. Cardiac exam demonstrated a midline sternal surgical scar, an irregularly irregular heart rhythm, no murmurs, gallops, nor rubs. Abdominal exam demonstrated a soft, nontender, nondistended abdomen with normoactive bowel sounds and no organomegaly. His extremities did not demonstrate lower extremity edema, clubbing, or cyanosis, and his pulses were 2+ radial, 2+ femoral, and 2+ dorsalis pedis bilaterally. Neurologic exam did not reveal any focal deficits. Electrocardiogram demonstrated atrial fibrillation with a ventricular response rate of 90 beats per minute, normal axis, peaked T waves, and no acute changes suggestive of ischemia. Routine basic metabolic panel done five days prior to his office visit was remarkable for a potassium of 5.0 mEq/L. The patient also had an appointment with his cardiologist for evaluation of his symptoms. After the evaluation he was admitted directly to hospital for further evaluation of his new symptoms of congestive heart failure. His admission labs were unremarkable with the exception of B-type natriuretic peptide of 1463 pg/mL. His admission chest x-ray was suggestive of a left pleural effusion, cardiomegaly and pulmonary edema. Transthoracic echocardiogram revealed the bioprosthetic valve in the mitral position had its ventricular side tilted toward the interventricular septum. There was no evidence of rocking of the mitral prosthesis. The peak mitral valve gradient was 13 mm of Hg. The mean transmitral valve gradient was 4 mm of Hg. The estimated mitral valve area was 2.6 cm 2 which is described as normal in the setting of a prosthetic valve. There was a moderate paravalvular regurgitant leak between the prosthesis and lateral wall of the left ventricle (LV). The effective regurgitant orifice area of the paravalvular leak is estimated at 0.33 cm 2 . There was evidence of mild aortic regurgitation, mild left atrial enlargement and an overall severely decreased LV systolic function with segmental wall motion abnormalities. The distal half of the LV is akinetic. The proximal walls were severely hypokinetic. LV ejection fraction was estimated to be 20%, and there was right ventricular (RV) enlargement with decreased function. There was no evidence of vegetations on the valves or pacemaker leads. Compared with an echocardiogram done one month following replacement, of his mitral valve, there was interval deterioration of LV function. The paravalvular leak appeared unchanged. Computed tomography of the thorax without contrast demonstrated an irregular consolidation in right upper lobe which was indeterminate, but most likely represented atelectasis and/or pneumonitis, bilateral pleural effusions, a left lower lobe consolidation and an enlarged left heart post mitral and tricuspid valvular repair. Cardiothoracic surgery was consulted. Due to the malpositioning of the prosthetic valve and evidence of worsening ventricular function, it was decided that the patient would need another operation to replace his prosthetic mitral valve.