“…6 There are several mechanisms of MVA formation: in the presence of aortic valve IE, the jet lesion may result in secondary destruction of the mitral valve due to: A) the jet damaging the endothelial surface of the mitral valve, B) retrograde dissemination of bacteria, or C) the presence of neovessels (prominent in AMVL) which results in localized inflammation, valvulitis, protrusion of weakened MV into the left atrium cavity, and subsequently aneurysmal formation. 3,5,10 Respect retrograde dissemination might result from 1) direct contact between the aortic vegetation and the AMVL during diastole, known as «mitral kissing vegetations» when they exceed 6 mm in length, 2) secondary infection of the damaged endothelium by bacteria from regurgitation blood flow, or 3) local spread of the infection through the mitral-aortic intervalvular fibrosa. 5 Approximately two-thirds of MVAs rupture or perforate; the size of the aneurysm does not correlate with the risk of perforation; the AMVL is much more commonly involved than the posterior leaflet for unknown reasons.…”