407 AN INCIDENTAL FINDING OF A CHALLENGING MITRAL MASS


 A 53-year-old woman, with no previous cardiologic history, presented to our emergency department reporting a pleomorphic symptomatology that had been affecting her in the last few months. She complained weakness, dyspnea for severe exertion and intermittent atypical chest pain worsening with the supine position. The patient had a history of migraine with aura. On admission she was asymptomatic and apyretic. Her blood pressure was 120/80 mmHg. Clinical examination revealed rhythmic heart sounds without murmurs, normal lung sounds, no jugular venous distention and no peripheral edema, no signs nor symptoms of infection. Her laboratory tests showed normal cardiac high-sensitivity troponin I (4.1 ng/L), BNP levels (4 ng/L) and C-reactive protein 0.3 mg/dL. The electrocardiogram showed a sinus rhythm with a rate of 86 beats/min, AV conduction and ventricular repolarization were within normal limits. Transthoracic echocardiogram revealed a normal sized (end-diastolic diameter 40 mm), slightly hypertrophic left ventricle (interventricular septum thickness 12 mm) with normal ejection fraction (55%), inferior-lateral wall curling and grade I diastolic dysfunction. Left atrium size was normal. A 15×14 mm globe-shaped echogenic structure was seen protruding in the left atrium throughout the whole cardiac cycle, which apparently originated from the P2 scallop (Figure 1A). There were no signs of mitral regurgitation or stenosis. Aortic valve was normal. Inferior vena cava was not dilated and collapsing.
 During the hospitalization she was always apyretic and asymptomatic, laboratory tests and blood culture negative. Transesophageal echocardiography showed a saccular cavitary structure, 14 mm in diameter bulging from the posterior mitral leaflet toward the left atrium throughout systole and diastole (Figure 1B). Differential diagnosis included cardiac tumor (e.g., fibroelastoma), and mitral valve aneurysm and/or excessive P2 prolapse. The absence of history of endocarditis, mitral regurgitation and the involvement of the posterior leaflet favored the first hypothesis, whilst morphology the latter. Libman-Sacks endocarditis was excluded thanks to lesions morphology and the absence of history of cancer or autoimmune disease.
 We performed a cardiac MRI investigation which confirmed the presence of bi-leaflet mitral prolapse with a thickened, dysmorphic and abnormal posterior mitral leaflet without any evidence of cardiac tumors (Figure 2). No regurgitation was found. Adiposus intramyocardial tissue was also reported in the inferior-lateral wall, supporting the diagnosis of atypical mitral valve prolapse with aneurysmatic posterior leaflet. Finally, a brain MRI excluded prior cerebral embolism. We therefore decided to follow-up the patient, who at 6 months remained asymptomatic without any medical therapy. Figure 1.A: transthoracic echocardiography (apical four-chamber view) showing the mitral mass. B: transesophageal echocardiography (three-chamber view with X-plane section) showing the mitral mass as an aneurysmatic posterior mitral leaflet at P2 level. C: 3D transesophageal echocardiography showing the aneurysmatic posterior mitral leaflet.Figure 2.Cardiac MRI (three-chamber view) showing the mitral posterior leaflet prolapse with aneurysm.