Article ID: CJ-22-0497
A 25-year-old man, who had undergone Rastelli-type operation and pulmonary valve replacement (PVR) at the ages of 3 and 19 years, respectively, for pulmonary atresia with ventricular septal defect (VSD), presented with a fever. Transthoracic echocardiography and computed tomography showed vegetations around the VSD patch and Rastelli-conduit (Figure A,B). No residual VSD shunt was observed. Four separate blood cultures were positive for Staphylococcus aureus, leading to the diagnosis of infective endocarditis (IE). 18F-fluorodeoxyglucose positron emission tomography showed infection only in the right-sided heart (Figure C). However, after 1 week of antibiotic treatment, transesophageal echocardiography revealed a mitral valve aneurysm (MVA) with perforation, causing severe mitral regurgitation (MR) (Figure D,E). After 6 weeks of antibiotic treatment, he underwent debridement, VSD closure, re-PVR and MV repair, which successfully controlled the infection and MR. Histology of the MV indicated chronic active inflammation with fibrinous material.
(A) Vegetation (arrow) detected by transthoracic echocardiography. (B) Vegetation (arrow) and (C) abnormal 18F-fluorodeoxyglucose uptake (arrow) around ventricular septal defect patch. (D,E) Mitral valve aneurysm (arrowheads) inducing severe mitral regurgitation through a perforation (*) on transesophageal echocardiography. LA, left atrium; LV, left ventricle; PA, pulmonary artery.
The mechanism of MVA is mycotic destruction of the anterior mitral leaflet, mostly enhanced by physical damage from the aortic regurgitation (AR) jet.1 However, significant AR or MR was not seen at the time he was diagnosed with IE. Therefore, the MVA may have been caused by expansion of the right-sided endocarditis. To our knowledge, this is the first report to clearly demonstrate progression of MVA.
This study was supported by JSPS KAKENHI grant no. JP22K08208.
H.T. is a member of Circulation Journal’s Editorial Team.
Not applicable.
