Abstract 16908: Effect of Variable Degrees of Tricuspid Regurgitation, Right Ventricular Enlargement and Dysfunction on Left Ventricular Deformation in Ebstein’s Anomaly
Background: We have previously demonstrated that left ventricular (LV) radial strain is decreased in Ebstein’s anomaly (EA) compared to normal controls and this improves after cardiac surgery. We postulated the degree of tricuspid regurgitation (TR), right ventricular (RV) enlargement and RV dysfunction would adversely effect ventricular-ventricular interactions in EA.
Methods: Retrospective evaluation of 83 unrepaired EA patients (age 34 ±13 years; 64% women) with LV ejection fraction >50% and without LV myocardial disease were graded for TR severity, RV size and RV function. Classifications of moderate or less were combined together as a non-severe group whereas the remainder were defined as the severe group. Velocity vector imaging was used to measure myocardial strain and strain rate (SR) of the LV and RV free walls. Unpaired t-tests and Wilcoxon’s rank sum tests were used for statistical analyses.
Results: No LV or RV strain or SR difference was found between different TR severity groups. Compared to the non-severe RV enlargement group, patients with severe enlargement showed a significant increase in LV global circumferential strain and SR as well as circumferential strain and SR, radial strain and SR and longitudinal SR specifically in the LV lateral wall. Significantly lower lateral wall radial strain and SR were found in the non-severe RV dysfunction group compared to severe RV dysfunction group. Similar results were found when compared in subgroup analysis with only severe TR and with combined severe TR and severe RV enlargement.
Conclusions: The effect of EA on LV function as demonstrated by LV strain assessment varies with the severity of RV size and dysfunction but not TR severity. This likely reflects altered RV and LV chamber geometry and myocardial fiber orientation. LV contractility is adversely influenced by increasing RV dilatation and dysfunction with the loss of the ability to augment these myocardial fibers as RV size and function worsens.
- © 2013 by American Heart Association, Inc.