Abstract 16606: Compensated Mechanism of Wall Thickening in Patients with Aortic Regurgitation and Preserved Ejection Fraction.
Background: In patients with aortic regurgitation (AR), increased systolic wall stress is known as a cause of left ventricular (LV) systolic dysfunction. We hypothesized that increased wall stress affects LV wall function even in patients with AR and preserved LV ejection fraction (EF). A novel speckle tracking imaging (STI) allows assessing the strain separating the endo (inner)- and the epi (outer)-myocardium. Then, the aim of this study was to assess the mechanism to preserve LVEF against increased wall stress through change in LV wall strain distribution in patients with AR.
Methods: Echocardiographic examinations with STI were performed in 71 patients with AR and 37 normal control subjects. The degree of AR was classified into moderate in 33 patients (LV end-diastolic volume 122±30mm, LVEF 68±8%) and severe in 38patients (LV end-diastolic volume 198±55ml, LVEF 61±6%). On a short-axis B-mode image at the mid-ventricular level, an inner myocardium border and an outer myocardium border were manually traced at end-systole for STI analysis. An inner- and an outer-myocardium were automatically separated, and a total, inner, and outer peak radial strain (RS) were calculated. End-systolic wall stress was calculated from the mean arterial blood pressure, the end-systolic dimension, and the end-systolic wall thickness.
Results:. Although total RS was preserved even in patients with severe AR, inner RS was reduced. In contrast, outer RS was significantly increased in moderate and severe AR compared to control. The end-systolic wall stress in severe AR was higher compared to those in control and moderate AR. LV wall stress was negatively correlated with inner RS (r =- 0.44, P<0.001), but not with outer strain.
Conclusions: The findings suggest that epicardial LV wall compensation for endocardial LV wall dysfunction suffering high LV wall stress is a mechanism to preserve LVEF in patients with AR.
- © 2010 by American Heart Association, Inc.