Abstract 16473: Increase in Left Ventricular Mass and Decrease in 3d Global Strain After Right Ventricular Pacing is Determined by the Development of Pacing-Induced Systolic Dyssynchrony - A Study by Novel 3-Dimensional Approach
Aim: The detrimental effect of conventional right ventricular apical (RVA) pacing on reduction of left ventricular (LV) systolic function has been demonstrated in patients with normal ejection fraction (EF). However, little is known whether there is alteration of LV mass, i.e., true LV adverse remodeling, and its relationship with pacing-induced systolic dyssynchrony.
Methods: Eighty-seven patients (71±11 years, 46 males) with high-grade atrioventricular block and preserved EF (mean: 64±7%) were prospectively enrolled at baseline, and 1 year after RVA pacing. Three-dimensional (3D) echocardiography and tissue Doppler imaging (TDI) was performed (GE, Horten, Norway) to assess LV mass, global 3D deformation (area strain) and systolic dyssynchrony [standard deviation of time to peak systolic velocity of 12 LV segments (Ts-SD) ≥33ms].
Results: At 1 year, LV mass increased significantly (133±22 vs. 146±35 g, p=0.028) with decreased area strain (31±6 vs. 24±5%, p<0.001). TDI revealed that pacing-induced systolic dyssynchrony was present in 48 patients (55%). Intriguingly, increase in LV mass, end-systolic volume and decrease in area strain and EF were only observed in those who developed dyssynchrony, but remained unchanged in those without (Table). There was a moderate correlation between change in systolic dyssynchrony and change in LV mass (r=0.41, p=0.008) as well as reduction in 3D area strain (r=0.50, p=0.01). Univariate predictors for increase in LV mass were older age (>55 years) [hazard ratio (HR) =2.83, p=0.05] and presence of systolic dyssynchrony (HR=3.27, p=0.01). In multivariate analysis, only systolic dyssynchrony remained as independent determinant for increase in LV mass (HR=3.19, p=0.01).
Conclusion: In patients who developed RVA pacing-induced systolic dyssynchrony, there was increase in LV mass and impairment of LV systolic strain which underpin the development of true LV adverse remodeling.
Author Disclosures: F. Fang: None. X. Luo: None. L. Ji: None. Q. Zhang: None. Y. Liang: None. C. Ma: None. X. Jiang: None. C. Yu: None.
- © 2014 by American Heart Association, Inc.