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Doppler-derived gradients may overestimate total pressure loss in degenerative and prosthetic aortic valve stenosis (AS) due to unaccounted pressure recovery distal to the orifice. However, in congenitally bicuspid valves, jet eccentricity may result in a higher anatomic-to-effective orifice contraction ratio, resulting in an increased pressure loss at the valve and a reduced pressure recovery distal to the orifice leading to greater functional severity. The objective of our study was to determine the impact of local geometry on the total versus Doppler-derived pressure loss and therefore the assessed severity of the stenosis in bicuspid valves. On the basis of clinically obtained measurements, two- and three-dimensional computer simulations were created with various local geometries by altering the diameters of the left ventricular outflow tract (LVOT; 1.8–3.0 cm), orifice diameter (OD; 0.8–1.6 cm), and aortic root diameter (AR; 3.0–5.4 cm). Jet eccentricity was altered in the models from 0 to 25°. Simulations were performed under steady-flow conditions. Axisymmetric simulations indicate that the overall differences in pressure recovery were minor for variations in LVOT diameter (<3%). However, both OD and AR had a significant impact on pressure recovery (6–20%), with greatest recovery being the larger OD and the smaller recovery being the AR. In addition, three-dimensional data illustrate a greater pressure loss for eccentric jets with the same orifice area, thus increasing functional severity. In conclusion, jet eccentricity results in greater pressure loss in bicuspid valve AS due to reduced effective orifice area. Functional severity may also be enhanced by larger aortic roots, commonly occurring in these patients, leading to reduced pressure recovery. Thus, for the same anatomic orifice area, functional severity is greater in bicuspid than in degenerative tricuspid AS.

In early diastole, pressure is lower in the apex than in the base of the left ventricle (LV). This early intraventricular pressure difference (IVPD) facilitates LV filling. We assessed how LV diastolic IVPD and intraventricular pressure gradient (IVPG), defined as IVPD divided by length, scale to the heart size and other physiological variables. We studied 10 mice, 10 rats, 5 rabbits, 12 dogs, and 21 humans by echocardiography. Color Doppler M-mode data were postprocessed to reconstruct IVPD and IVPG. Normalized LV filling time was calculated by dividing filling time by RR interval. The relationship between IVPD, IVPG, normalized LV filling time, and LV end-diastolic volume (or mass) as fit to the general scaling equation Y = kM beta, where M is LV heart size parameter, Y is a dependent variable, k is a constant, and beta is the power of the scaling exponent. LV mass varied from 0.049 to 194 g, whereas end-diastolic volume varied from 0.011 to 149 ml. The beta values relating normalized LV filling time with LV mass and end-diastolic volume were 0.091 (SD 0.011) and 0.083 (SD 0.009), respectively (P < 0.0001 vs. 0 for both). The beta values relating IVPD with LV mass and end-diastolic volume were similarly significant at 0.271 (SD 0.039) and 0.243 (SD 0.0361), respectively (P < 0.0001 vs. 0 for both). Finally, beta values relating IVPG with LV mass and end-diastolic volume were -0.118 (SD 0.013) and -0.104 (SD 0.011), respectively (P < 0.0001 vs. 0 for both). As a result, there was an inverse relationship between IVPG and normalized LV filling time (r = -0.65, P < 0.001). We conclude that IVPD decrease, while IVPG increase with decreasing animal size. High IVPG in small mammals may be an adaptive mechanism to short filling times.

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