Abstract 11057: Reverse Ventricular and Myocardial Remodeling Following Restrictive Mitral Annuloplasty in Ischemic Dilated Cardiomyopathy: Longitudinal MDCT Analysis
Background. To evaluate the longitudinal data on left ventricular (LV) and myocardial reverse remodeling after restrictive mitral annuloplasty (RMA).
Methods. A 64-row multi-detector computed tomography (MDCT) study was performed on 15 patients (age, 64±6 years) with functional mitral regurgitation (MR) associated with ischemic dilated cardiomyopathy (ejection fraction: EF ≤35%) before RMA (baseline), soon after RMA (2 months), and >1 year after RMA (16 months). The longitudinal data on LV end-diastolic and end-systolic volume indices (EDVI and ESVI), LVEF, LV mass index (LVMI), and end-systolic wall stress (ESS) were obtained. The analysis included data on these outcomes from 3 time points and was performed using linear mixed-effects models with random intercepts (to account for the within-subject correlation over time) and with time as a fixed effect and subjects as random effects; the models were adjusted for baseline variables.
Results. At the follow-up following RMA, the LVEDVI, LVESVI and LVMI significantly decreased over time (p<.01 for all), and the LVEF significantly increased over time (p<.01). In the period soon after RMA, there was a significant reverse LV remodeling, with a decrease in LVEDVI and LVESVI and an increase in LVEF, with further reverse remodeling changes later after the surgery. In the early postoperative period, LVMI did not significantly change, while it had significantly decreased in the later period. ESS was significantly decreased in the early period and was well sustained later after the surgery (Table). Furthermore, the increase in LVEF observed in the late postoperative period was significantly associated with the magnitude of ESS reduction (p =.01).
Conclusions. Our findings indicate that ventricular reverse remodeling occurs soon after surgery, whereas myocardial remodeling is a process that occurs over time, suggesting that the late improvement in the LV systolic ejection may be attributable to a decrease in the LV afterload.
- © 2011 by American Heart Association, Inc.