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Differential effects of afterload on left ventricular long- and short-axis function: Insights from a clinical model of patients with aortic valve stenosis undergoing aortic valve replacement

2009; Elsevier BV; Volume: 158; Issue: 4 Linguagem: Inglês

10.1016/j.ahj.2009.07.008

1097-6744

Shemy Carasso, Oved Cohen, Diab Mutlak, Zvi Adler, Jonathan Lessick, Shimon A. Reisner, Harry Rakowski, Gil Bolotin, Yoram Agmon,

Cardiac Structural Anomalies and Repair

The effects of left ventricular (LV) afterload on longitudinal versus circumferential ventricular mechanics are largely unknown. Our objective was to examine changes in LV deformation before and early after aortic valve replacement (AVR) in patients with severe aortic valve stenosis (AS). Paired echocardiographic studies before and early (7 ± 3 days) after AVR were analyzed in 45 patients (age 67 ± 12 years, 49% men) with severe AS and normal LV ejection fraction without segmental wall motion abnormalities. Longitudinal myocardial function was assessed from 3 apical views (average of 18 segments). Circumferential function was assessed at mid and apical levels (averaging 6 segments per view). Strain, strain rate (SR), and LV twist (relative rotation of the mid and apex) were measured using 2-dimensional strain software. Early post-AVR, (1) LV size and LV ejection fraction did not change; (2) longitudinal systolic strain, which was lower than normal before AVR, increased (−12.8 ± 1.7 to −15.9 ± 2.2, P < .05), whereas mid-LV circumferential strain, which was higher than normal, decreased (−27.0 ± 5.1 to −22.3 ± 4.9, P < .05); (3) longitudinal early diastolic SR increased (0.6 ± 0.1 to 0.7 ± 0.2, P < .05), whereas mid-LV circumferential diastolic SR decreased (1.2 ± 0.5 to 1.0 ± 0.3, P < .05); and (4) LV twist increased (3.7° ± 2.1° to 6.1° ± 2.9°, P < .05). Aortic valve stenosis causes differential changes in longitudinal and circumferential mechanics that partially normalize after AVR. These findings provide new insights into the mechanical adaptation of the LV to chronic afterload elevation and its response to unloading.