DK2985_C000 1..28 - AlSharqia Echo Club

428 Transesophageal Echocardiography(A)(B)(C)LA(D) Max Vel: 282cm/secMn Vel: 21.3cm/secVTI: 61.7cmMax PG: 31.8mmHgMn PG: 19.0mmHgAoLVFigure 18.17 (A–C) Mid-esophageal long-axis view of a dysfunctional mitral bioprosthesis with thickened and calcified leaflets withreduced mobility. An ecccentric regurgitation jet is present. (D) The continuous-wave Doppler demonstrates a very high mean (Mn) diastolicpressure gradient (PG) of 19 mmHg with regurgitation through the dysfunctional mitral tissue prosthesis (Ao, aorta; LA, left atrium;LV, left ventricle; Max, maximum; VTI, velocity–time integral; Vel, velocity).rupture of a suture due to degenerescence could be thecause, endocarditis and abscess should be ruled out.The leaflets of a normal bioprosthesis should be thinand pliable. Thickening and calcification of the leafletsor the annulus can be demonstrated by 2D imaging.These degenerative changes decrease the mobility of theleaflets or may lead to fracture and tears of the cusps,with resulting stenosis and/or regurgitation detectable bycolor-flow imaging and CW Doppler (Fig. 18.17).Degenerative changes can also be seen in the clothcoveredmodel of the Starr–Edwards prosthesis (Figs.18.18–18.20).The presence of thrombus on bioprosthesis is much lesscommon than with mechanical valves but can sometimesbe seen (Fig. 18.21). Valve degenerescence or endocarditismay cause ring dehiscence and rocking with periprostheticregurgitation. Endocarditis can also cause leaflet destructionand perforation with significant regurgitation.B. Transvalvular Prosthetic RegurgitationDuring TEE imaging, one must resist the urge to turn onthe color flow imaging mode too soon without havingproperly performed a thorough 2D examination of allparts of the prosthesis. Similarly, during color flowimaging, the operator should not hesitate to turn off thecolor when a flow abnormality is found in order to understandits underlying anatomical basis.Thrombus, vegetation, abnormal tissue growth(pannus), interfering residual subvalvular apparatus andintrinsic prosthetic valve failure (Fig. 18.22) could all beresponsible for dysfunctional mitral prosthetic regurgitation.This type of regurgitation will usually be transvalvularor intraprosthetic, meaning that the regurgitationoriginates from within the prosthetic sewing ring, due toincomplete closure of one of the mobile components(Figs. 18.17 and 18.22). Intraprosthetic dysfunctionalregurgitation is uncommon in the immediate postoperativeperiod. When present with a mechanical prosthesis, it isgenerally associated with abnormal disk closure due tointerfering residual subvalvular tissue or apparatus. Thiscan often be immediately corrected by rotating the valvewithin the sewing ring. Early postoperative bioprostheticvalve regurgitation could arise from suture misplacementor improper sizing. In rare cases, an intrinsic bioprostheticmanufacturing problem could be responsible.As mentioned previously, normal prosthetic valves maypresent a mild degree of intraprosthetic functionalregurgitation characteristic of their valve design. On theother hand, pathologic intraprosthetic regurgitation will