Abstract 9973: Mitral Regurgitation with Mechanical Dyssynchrony as a Substrate Associated with Long-Term Survival After Cardiac Resynchronization Therapy
Background: Mechanisms for mitral regurgitation (MR) in patients with left ventricular (LV) dysfunction are complex. Cardiac resynchronization therapy (CRT) may improve MR. However, effects are variable and the influence of mechanical dyssynchrony on MR and its association with long-term outcome is unclear.
Methods: We prospectively studied 138 consecutive CRT patients with NYHA class III/IV heart failure, QRS width ≥120ms, and ejection fraction (EF) ≤35%. Quantitative echocardiography was performed before CRT and 1.5±2 months after CRT. Baseline dyssynchrony was assessed as interventricular mechanical delay (IVMD) > 40ms, tissue Doppler opposing wall delay (OWD) > 65ms, Yu Index > 32ms, and speckle tracking radial strain delay >130ms. MR was quantified by vena contracta width and jet area, and severity expressed as a grade from 1 to 4. Long-term outcome events were pre-specified as death, transplant or left ventricular assist device over 4 years.
Results: Of 138 CRT patients aged 66±12 yrs with EF 24±7%, 74 patients (54%) had no significant baseline MR (≤grade 1+), and 64 patients (46%) had significant baseline MR: n=35 grade 2+, n=20 grade 3+, and n=9 grade 4+. At baseline, There are significant differences in EF (p<0.01) and MR severity (<0.0001) between patients with and without significant MR. Dyssynchrony at baseline by all indices were statistically associated with MR reduction (all p<0.03). Among patients with significant MR at baseline, speckle-tracking radial dyssynchrony was significantly associated with long-term event free survival.
Conclusion: The co-existence of baseline dyssynchrony by radial strain in patients with significant MR was associated with a more favorable long term survival after CRT. Patients with significant MR who lacked dyssynchrony had the least favorable outcome. These observations have mechanistic and clinical implications.
- © 2011 by American Heart Association, Inc.