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 61-year-old woman arrived at our emergency department because of the appearance of intense palpitations for 3 days. She denied cardiovascular risk factors or a previous cardiac disease, did not assume pharmacological therapy, and reported only a recent domestic accidental fall without apparent complications. The heart rhythm appeared tachycardic and irregular, and the remaining vital parameters were normal with a good hemodynamic compensation (systemic blood pressure 135/75 mmHg, SaO2 98%). Electrocardiogram reported atrial fibrillation with high ventricular response (136 bpm). The blood tests were all normal, except for a mild and nonspecific increase in the high-sensitivity troponin T.\nThe patient underwent a cardiology consult in order to plan the following therapy procedure. Subsequent transthoracic echocardiogram revealed a dilated LA with an interior septum which extended across the longitudinal length of the atrial chamber, by causing the obstruction to the left ventricular (LV) filling, in the absence of additional pathologic findings. By considering that the atrial fibrillation had begun more than 48 h before and the need of investigating the above findings, we have decided to perform a transesophageal echocardiogram (TEE) the following day.\nThe TEE documented the presence of atrial thrombosis in the appendage, a spherical image with clear margins and fibrin branches inside, and a seamless cleavage with the posterolateral wall of the LA, which determined an obstacle to the ventricular filling [].\nWe decided to perform an urgent contrast-enhanced cardiac computed tomography (CT) which confirmed a capsulated lesion within the posterolateral left atrial wall with sharp margins and a basal density of + 30 HU, without any significant contrast enhancement in the arterial and late phases, features resembling those of a chronic hematoma [].\nAfter a consultation with our cardiac surgeon, and suspecting an atrial dissection, we planned to perform a cardiac magnetic resonance (CMR). CMR was performed with a 1.5T scanner with cine B-TFE, black-blood turbo spin echo, phase-sensitive inversion recovery, and THRIVE sequences before and after a standard 0.2 mmol/kg gadolinium contrast agent dose. CMR confirmed the intramural formation, within the inferolateral wall of the LA, with diameters of 4.3 cm × 6.2 cm × 4.4 cm, characterized by marked hyperintensity in T2-weighted sequences and high signal in both unsuppressed and fat-suppressed T1-weighted images, as well as the absence of signs of local invasiveness; a thin hypointense rim demarcated the lesion in the steady-state cine sequences. In contrast-enhanced images, a thin rim of peripheral enhancement is appreciated, mostly evident on the posterior side. These findings were deemed compatible with the original hypothesis of an intramural hematoma of the wall of the atrium, probably subacute/chronic [].\nIn consideration of the extension of the intramural hematoma and the LV inflow tract obstruction, the patient underwent a surgery to empty the hematoma and reattach the atrial wall.\nHistological examination confirmed the presence of histiocytes, crenated red blood cells, and crystals, hence a chronic hematoma [].