Chronic pressure-overload hypertrophy attenuates vortex formation time in patients with severe aortic stenosis and preserved left ventricular systolic function undergoing aortic valve replacement

摘要

Objective: Transmitral blood flow produces a vortex ring that enhances the hydraulic efficiency of early left ventricular (LV) filling. The effect of pressure-overload hypertrophy on the duration of LV vortex ring formation (vortex formation time [VFT]) is unknown. The current investigation tested the hypothesis that chronic LV pressure-overload hypertrophy produced by severe aortic stenosis (AS) reduces VFT in patients with preserved LV systolic function undergoing aortic valve replacement. Design: Observational study. Setting: Veterans Affairs Medical Center. Participants: After the Institutional Review Board's approval, 8 patients (7 men and 1 woman; age, 62±5 y; and ejection fraction, 59%±5%) with AS (peak pressure gradient, 81±22 mmHg; aortic valve area, 0.78±0.25 cm2) scheduled for aortic valve replacement were compared with 8 patients (all men; age, 63±3 y; and ejection fraction, 60%±7%) without AS undergoing coronary artery bypass graft surgery. Interventions: None. Measurements and Main Results: 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 echocardiography to determine E/A and atrial filling fraction (β). Mitral valve diameter (D) was calculated as the average of minor and major axis lengths obtained in the midesophageal bicommissural and long-axis transesophageal echocardiography imaging planes, respectively. Posterior wall thickness (PWT) was measured at end-diastole using M-mode echocardiography. VFT was calculated as 4×(1-β)×SV/πD3, where SV = stroke volume measured using thermodilution. Systemic and pulmonary hemodynamics, LV diastolic function, PWT, and VFT were determined during steady-state conditions 30 minutes before cardiopulmonary bypass. Early LV filling was attenuated in patients with AS (eg, E/A, 0.77±0.11 compared with 1.23±0.13; β, 0.43±0.09 compared with 0.35±0.02; p0.05 for each). LV hypertrophy was observed (PWT, 1.4±0.1 cm compared with 1.1±0.2 cm; p0.05) and VFT was lower (3.0±0.9 v 4.3±0.5; p0.05) in patients with versus without AS. Linear regression analysis showed a significant correlation between VFT and PWT (VFT = -2.57 ×PWT + 6.81; r2 = 0.345; p = 0.017). Conclusion: The results indicated that pressure-overload hypertrophy produced by AS reduced VFT in patients with normal LV systolic function undergoing aortic valve replacement.