Abstract 8613: Load-Independency of the 2D Speckle Tracking-Derived Left Ventricular Twist and Apex-to-Base Rotation Delay in Longstanding, Non-Ischemic Dilated Cardiomyopathy
Background: Although Left ventricular(LV) twist is known to be load-dependent in healthy volunteers, this has not been examined in patients with dilated cardiomyopathy(DCMP), in whom alterations in myofiber architecture and its arrangement could perturb the intrinsic dependence of LV twist on loading conditions. This study tried to examine whether LV twist remains load-dependent in DCMP.
Methods: 34 DCMP patients with a baseline LV ejection fraction of <40% were enrolled. After baseline measurements, pneumatic compression of the lower extremities(Pcom) was employed to increase LV afterload. Subsequently, sublingual nitroglycerin(SL-NG) was administered to modify preload. Conventional echocardiographic parameters, LV end-systolic wall stress(LV-ESWS), LV twist, and apex-to-base-rotation delay were assessed under each condition.
Results: Although LV-ESWS significantly increased under Pcom(196.9±64.9 at baseline vs. 231.8±78.9g/m2 under Pcom, P<0.017) and decreased after SL-NG(231.8±78.9 under Pcom vs. 197.4±67.4g/m2 after SL-NG, P<0.017), LV twist and apex-to-base rotation delay showed no significant changes with modification of LV loading condition(for LV twist, 7.78±4.63° at baseline vs. 7.19±4.34° under Pcom vs. 7.41±4.46 after SL-NG, P=0.65; for apex-to-base rotation delay, 16.56±13.81 at baseline vs. 17.19±14.81 under Pcom vs. 15.95±13.27 after SL-NG, P=0.53). Careful examination of individual patient data revealed that LV twist was load-independent when patients had a LV twist <12°. Apex-to-base rotation delay was also found to be load-independent, but only in patients with a LV ejection fraction <34%.
Conclusion: LV twist and its component, apex-to-base rotation delay, had relatively load-insensitive properties in patients with longstanding DCMP, and can be used in future clinical trial as load-independent LV dyssynchrony indexes.
- © 2011 by American Heart Association, Inc.