Abstract
Infective endocarditis (IE) is the infection of inner endothelial layer of the heart including the heart valves and it may present as rapidly progressive or manifest itself as subacute or chronic disease. The epidemiology of infective endocarditis has been changed over the past few decades and the incidence of IE in children in United States and Canada is 1 in 1250 pediatric hospital admissions in the early 1980s. At least 70% of infective endocarditis in children occurs with congenital heart disease whereas rheumatic heart disease in southern states of India and the degenerative mitral valve disease (myxomatous, mitral valve prolapse) in the western countries are the most underlying predisposing conditions to infective endocarditis in adolescents. The characteristic lesion of infective endocarditis is “vegetation” and a “large” vegetation >10 mm in size has been reported with an incidence of 15.9% - 62.5% in patients. The significance of vegetation size has been a subject of discussion for many years to predict the embolic episodes. Background of this case study illustrated the varying size and shape of giant vegetation attached to the anterior leaflet of mitral valve in an underlying rheumatic mitral valvulitis and its consequence of valve damage such as chordal rupture, flail leaflet and mitral regurgitation with a description of anatomic features and echocardiographic manifestations in a 10-year-old female child.
Highlights
The mitral valve apparatus consists of leaflets, subvalvular apparatus, annulus and the left ventricle
Intrinsic valvular involvements by degenerative, rheumatic and infective endocarditis produce organic mitral regurgitation whereas abnormal function of normal leaflets due to impaired ventricular function caused by ischemic heart disease and dilated cardiomyopathy [11], produce functional mitral regurgitation as a result of an imbalance between tethering forces (annular dilatation, LV dilatation, papillary muscle displacement, LV sphericity) and closing forces
Rheumatic valvulitis is characterized by variable thickening of the leaflets at their free edges, chordal fibrosis, rigidity and reduced motion of posterior leaflet in diastole and in some patients, the posterior leaflet remains in a semi-open position throughout the cardiac cycle and the friction of anterior leaflet in systole produce a false aspect of prolapse
Summary
The mitral valve apparatus consists of leaflets, subvalvular apparatus (chordae tendineae and papillary muscle), annulus and the left ventricle. The fibrosa is composed of dense collagen (type I—74%, type III—24%, type V—2%) [3] and it is providing the strength and stiffness to the leaflets It is the major load bearing layer that faces the greatest pressure during valve closure, extends from the annulus into two-thirds of the leaflets and it is absent at the free edge. The cause of pure mitral regurgitation are multiple and include floppy mitral valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and ruptured chordae tendineae. In a study by Olson and associates [9], the reported leading causes to be floppy (38%), rheumatic (31%), and papillary muscle dysfunction (11%), but Wallen and colleagues [10] found rheumatic disease accounted for only 3% of purely regurgitant mitral valves. It is uncommon in the western world (22 cases per million), but more prevalent in developing countries and a giant vegetation blocking the mitral valve orifice is uncommon and so this case had been reported
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