Moderate Aortic Valvular Insufficiency Invalidates Vortex Formation Time as an Index of Left Ventricular Filling Efficiency in Patients With Severe Degenerative Calcific Aortic Stenosis Undergoing Aortic Valve Replacement.

Abstract

Transmitral blood flow produces a vortex ring (quantified using vortex formation time [VFT]) that enhances the efficiency of left ventricular (LV) filling. VFT is attenuated in LV hypertrophy resulting from aortic valve stenosis (AS) versus normal LV geometry. Many patients with AS also have aortic insufficiency (AI). The authors tested the hypothesis that moderate AI falsely elevates VFT by partially inhibiting mitral leaflet opening in patients with AS. Observational study. Veterans Affairs medical center. Patients with AS in the presence or absence of moderate AI (n = 8 per group) undergoing aortic valve replacement (AVR) were studied after institutional review board approval. None. Under general anesthesia, peak early LV filling (E) and atrial systole (A) blood flow velocities and their corresponding velocity-time integrals were obtained using pulse-wave Doppler transesophageal echocardiography (TEE) to determine E/A and atrial filling fraction (beta). Mitral valve diameter (D) was calculated as the average of major and minor axis lengths obtained in the midesophageal bicommissural (transcommissural anterior-lateral-posterior medial) and LV long-axis (anterior-posterior) TEE imaging planes, respectively. VFT was calculated as 4·(1-beta)·SV/πD(3), where SV = stroke volume measured using thermodilution. Hemodynamics, diastolic function, and VFT were determined during steady-state conditions before cardiopulmonary bypass. The severity of AS (mean and peak pressure gradients, peak transvalvular jet velocity, aortic valve area) and diastolic function (E/A, beta) were similar between groups. Moderate centrally directed AI was present in 8 patients with AS (ratio of regurgitant jet width to LV outflow tract diameter of 36±6%). Pulse pressure and mean pulmonary artery pressure were elevated in patients with versus without AI, but no other differences in hemodynamics were observed. Mitral valve minor and major axis lengths, diameter, and area were reduced in the presence versus the absence of AI. VFT was increased significantly (5.7±1.7 v 3.2±0.6; p = 0.00108) in patients with AS and AI compared with AS alone. Moderate AI falsely elevates VFT in patients with severe AS undergoing AVR by partially inhibiting mitral valve opening. VFT may be an unreliable index of LV filling efficiency with competitive diastolic flow into the LV.