title: Echocardiographic volume flow and stenosis severity measures with changing flow rate in aortic stenosis.
abstract: The anatomy of degenerative valvular aortic stenosis has been poorly represented in animal models, limiting the evaluation of noninvasive echo-Doppler measures of transvalvular volume flow rate and stenosis severity during progressive disease evolution or under conditions of changing volume flow rates. To study these issues, chronic valvular aortic stenosis, characterized by stiff leaflets without commissural fusion, was created in nine adult mongrel dogs by suturing pericardial covered Teflon-felt pads into the sinuses of Valsalva below the coronary ostia during hypothermic cardiac arrest. In the eight surviving dogs, echo-Doppler examinations were performed weekly for up to 8 wk postoperatively. Simultaneous invasive micromanometer pressure data were collected at 2-wk intervals in all subjects, with simultaneous ascending aortic transit time-volume flow measurement in four subjects. Volume flow rates were altered with saline and dobutamine infusions during invasive studies for comparison of echo-Doppler and invasive pressure gradients, volume flow, and valve areas. Serial echo-Doppler follow-up (39 +/- 11 days) demonstrated that, from baseline to final study, mean transvalvular pressure gradient increased (4 +/- 1 to 38 +/- 7 mmHg, P = 0.001), continuity equation aortic valve area decreased (2.06 +/- 0.18 to 0.54 +/- 0.04 cm2, P < 0.0001), and progressive left ventricular hypertrophy developed (62 +/- 6 to 114 +/- 9 g, P = 0.0003). Echo-Doppler and invasive data correlated well for measures of transvalvular pressure gradients (n = 98, maximum instantaneous gradient r = 0.95, mean gradient r = 0.91), volume flow (n = 75, stroke volume r = 0.86, cardiac output r = 0.86), and valve area (n = 73, r = 0.73) despite acute alterations in volume flow and progressive disease evolution. This chronic canine model, with anatomy and hemodynamics similar to clinical degenerative valvular aortic stenosis, should provide a valuable tool for investigating clinically relevant new measures of stenosis severity with use of invasive or noninvasive techniques.
authors.affiliation: Department of Medicine, University of Washington, Seattle 98195.
authors.forename: I G
authors.initials: IG
authors.lastname: Burwash
authors.forename: A D
authors.initials: AD
authors.lastname: Forbes
authors.forename: M
authors.initials: M
authors.lastname: Sadahiro
authors.forename: E D
authors.initials: ED
authors.lastname: Verrier
authors.forename: A S
authors.initials: AS
authors.lastname: Pearlman
authors.forename: R
authors.initials: R
authors.lastname: Thomas
authors.forename: C
authors.initials: C
authors.lastname: Kraft
authors.forename: C M
authors.initials: CM
authors.lastname: Otto
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001020:Aortic Stenosis, Subvalvular / Q000175:diagnosis / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D001024:Aortic Valve Stenosis / Q000175:diagnosis / Q000000981:diagnostic imaging* / Q000503:physiopathology; D001783:Blood Flow Velocity; D001794:Blood Pressure; D002302:Cardiac Output; D004195:Disease Models, Animal; D004285:Dogs; D004452:Echocardiography / Q000379:methods*; D006439:Hemodynamics; D006801:Humans; D008365:Manometry / Q000379:methods; D013318:Stroke Volume