A 68-year-old woman presented to our hospital complaining of dyspnea at rest for approximately 2 months and was classified as New York Heart Association functional class III. She had previously been treated for breast and colon cancers and had not suffered from cardiovascular disease. Her height, weight, and body mass index were 150.0 cm, 91.0 kg, and 40.4 kg/m2, respectively. A grade IV/VI pan-systolic murmur was heard at the apex on cardiac auscultation. Her pulse rate was 105 beats/min and she was diagnosed with an irregularly rapid heartbeat (tachycardia). Her blood pressure was 124/76 mmHg. A chest radiograph revealed severe cardiomegaly with a cardiothoracic ratio of 80%, while an electrocardiogram showed persistent atrial fibrillation with a low-voltage F-wave. Computed tomography demonstrated the retention of pleural fluid or abdominal dropsy and hepatosplenomegaly. No significant coronary stenosis was observed by coronary angiography. Transthoracic echocardiography revealed severe mitral regurgitation with annular enlargement and severe tricuspid regurgitation. The cause of mitral regurgitation was severe tethering due to extreme annular enlargement, and the prolapse of the anterior leaflet. The left ventricular ejection fraction was 49%, the left ventricular diastolic diameter was 63 mm, and the left atrial diameter was 71 mm. Laboratory evaluations did not show any abnormalities, apart from an N-terminal-proB-type natriuretic peptide level of 7439 pg/ml. Because of the medication-refractory heart failure, we decided to perform surgery after a written informed consent was obtained.\nA median sternotomy was performed and standard cardio-pulmonary bypass was initiated with ascending aortic and bicaval cannulation. A left atrial vent was introduced from the right upper pulmonary vein. Myocardial protection was achieved in an antegrade and retrograde fashion. The retrograde cardioplegia cannula was inserted smoothly under direct vision. After aortic cross-clamping, the left atrium was opened through a longitudinal left atriotomy, revealing the tethering mechanism secondary to the prolapse of the anterior leaflet of the mitral valve. The clear zone of the anterior leaflet was excised and the rough zone with its attached chord were divided equally. Each divided structure was transferred to the anterolateral and the posteromedial commissures separately. The posterior leaflet, including the subvalvular apparatus, was wholly preserved. The mitral valve was replaced with a 29-mm St. Jude mechanical valve (St. Jude Medical Inc., St. Paul, MN) in an intra-annular position using everting mattress sutures. Subsequently, tricuspid annuloplasty was performed with a 32-mm Carpentier-Edwards PhysioTricuspid ring (Edwards LifeSciences, Irvine, CA) for annular enlargement. Weaning from the cardio-pulmonary bypass was successful. After closing the thorax, to our surprise, an atrial mass of 3 cm × 2 cm was detected by TEE, which showed an oval hypoechoic appearance extending from the posterior annulus of the mitral valve to the posterior wall of the left atrium (Fig. a). Although it occupied one-third of the left atrium, there was no significant obstruction of the pulmonary venous return and left ventricular filling. The prosthetic valve movement was unobstructed and there were no paravalvular leaks or pericardial effusion. No communication between the mass and the atrial true lumen was detected using color Doppler echocardiogram. We diagnosed the mass as LAD. Because hemodynamic conditions were stable after a consulting with the anesthesiologist, the patient was deemed unsuitable for surgery. She was transferred to the intensive care unit and remained under close observation. On postoperative day 2, TEE showed that the atrial mass had vanished and the broken piece of the endocardium merely remained fluttering in the atrium (Fig. b). On postoperative day 6, the appearance of the left atrium had normalized completely, leaving no traces of LAD (Fig. c). The patient had an uneventful postoperative course, except for prolonged respiratory failure. She was discharged from the hospital on postoperative day 47 and is currently being followed up once a month.
A 69-year-old man was admitted in our hospital due to fever, chill, orthopnea and paroxysmal nocturnal dyspnea. In physical examination, respiratory sounds were reduced in both his lower half of lung fields.\nHe had undergone a major cardiac surgery including CABG, MVR, aortic valve replacement (AVR) and ascending aorta replacement due to severe coronary artery disease, significant valvular heart disease (rheumatic) and aneurysmally dilated ascending aorta, 75 days prior to his recent admission.\nAn electrocardiogram revealed atrial fibrillation rhythm, normal axis and non-specific ST-T changes in inferior and lateral leads (). The posteroanterior view of the chest radiography showed massive bilateral pleural effusion. Transthoracic echocardiography followed by TEE showed normal LV size with preserved systolic function, bioprosthetic MV with acceptable hemodynamic and mobility and no paravalvular regurgitation. Bioprosthetic AV had acceptable hemodynamic and mobility without paravalvular regurgitation. There was normal functioning ascending aorta Dacron tube graft without leakage from proximal and distal part of prosthesis.\nThe LA was enlarged and dissection was found on the posterior wall. Two homogenous particles (1.18 × 0.4 cm and 0.9 × 0.58 cm) were attached to the dissecting flaps which were highly suggestive for vegetations and IE (, , and , , , and ).\nLaboratory tests showed severe coagulopathy, high levels of fibrin degradation products, leukocytosis (white blood cells count: 26700/cm3, predominantly poly morphonucleated), severe anemia, thrombocytopenia, elevated liver enzymes and serum creatinine levels. These data were suggestive for DIC. The blood culture revealed enterococci septicemia.\nHis general condition deteriorated rapidly. He suffered from tonic-clonic seizures, diminished consciousness, widespread mucosal bleeding and oliguria. Bilateral chest tubes were inserted for massive pleural effusion. The patient was treated with intravenous vancomycin, cefepim, gentamycin and oral rifampin. He received infusion of fresh frozen plasma, packed cells, valproic acid, diazepam and phenytoin.\nBased on his poor general condition, cardiac surgery was not performed and finally he expired from multi organ failure. Autopsy findings were consistent with clinical, laboratory and echocardiographic findings.