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

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 cm(2)) 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/πD(3), 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; p<0.05 for each). LV hypertrophy was observed (PWT, 1.4±0.1 cm compared with 1.1±0.2 cm; p<0.05) and VFT was lower (3.0±0.9 v 4.3±0.5; p<0.05) in patients with versus without AS. Linear regression analysis showed a significant correlation between VFT and PWT (VFT = -2.57 ×PWT + 6.81; r(2) = 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.