DK2985_C000 1..28 - AlSharqia Echo Club

336 Transesophageal Echocardiography(A)(B)NCCLCCRCC(C)RCCANCCLCCFigure 15.9 Quadricuspid aortic valve. (A, B) Note the lack of coaptation in the center of the valve which results in a diamond-shapedregurgitant orifice. (C) Corresponding intraoperative finding of a quadricuspid aortic valve of a different patient is shown below (LCC,left coronary cusp; NCC, non-coronary cusp; RCC, right coronary cusp). (Photo C courtesy of Dr. Raymond Cartier.)patients with degenerative calcification tends to be fasterthan in rheumatic heart disease, it is difficult to predictthe rate of progression in individual patients. Survivalsignificantly decreases when left ventricular ejectionfraction (LVEF) decreases to ,45–50% or when theleft ventricular end-systolic dimension (LVESD)exceeds 55 mm (3).Two-dimensional echocardiographic evaluation shouldidentify the number, morphology (thickening, calcification),and mobility (restriction) of the aortic cusps. Systolicdoming occurs when the AoV does not fully open, andis most commonly associated with bicuspid AoVs butmay also be observed with commissural fusion in rheumaticheart disease (Fig. 15.15). Senile calcification orAoV sclerosis may occur without stenosis. Indirectsigns of significant AS include the presence of leftventricular hypertrophy (usually concentric) and poststenoticaortic root dilatation. The latter in some patients,particularly those with bicuspid valves, represents aninherent aortopathy rather than a consequence of thealtered hemodynamics from the AS (Fig. 15.16) (5,6).An association between bicuspid AoV disease andcoarctation of the descending thoracic Ao has also beenreported.2. Supra- and Subaortic StenosisPatients with a significant systolic gradient across the AoVshould always be evaluated for evidence of supra-(Fig. 15.17) or subvalvular disease. While native supravalvularstenosis is uncommon, subvalvular stenosis(proximal to the AoV) may originate from dynamicobstruction or fixed structural abnormalities. Congenitalcauses of fixed obstruction include the presence of a subaorticmembrane (Fig. 15.18) or diaphragm and, tunnelsubvalvular stenosis. Dynamic LVOT obstruction canoccur with hypertrophic obstructive cardiomyopathy(HOCM), basal septal hypertrophy, and following MVrepair (Fig. 15.19). In these conditions, the systolic gradientacross the LVOT will increase with tachycardia,increased contractility, and decreased ventricular filling.The dynamic LVOT obstruction is associated with systolicanterior motion (SAM) of the MV which is thought toresult from either “venturi” effect and/or drag forces.Significant septal contact of the anterior mitral leaflet