Abstract 3376: Can Cardiac Resynchronization Therapy Reverse Segmental Perfusion Defects in Patients with Left Bundle Branch Block?
Background: Septal defects in MP are observed in patients with right ventricular (RV) apical pacing or Left Bundle Branch Block (LBBB). It is unclear whether segmental MP defects are related to ischemia or left ventricular (LV) contractile dyssynchrony caused by LBBB or RV pacing. We sought to determine whether Bi-Ventricular (BiV) pacing can acutely and chronically improve segmental myocardial perfusion (MP) by correcting dyssynchrony.
Methods: Patients (N=18) with ischemic cardiomyopathy, LBBB and congestive heart failure indicated for BiV pacing were prospectively enrolled. Patients were aged 73 ± 7 years with left ventricular ejection fraction of 24 ± 6 %. MP with sestamibi was evaluated at rest and with adenosine stress test at baseline, after 24 hours of RV pacing, after 1 week of BiV pacing and 4 months of BiV pacing. MP of individual segments was determined based on 20-segment model and 0 – 4 MP scale (0-normal MP, 4-no MP). MP scores were calculated for individual segments, stress minus rest (i.e. reversible ischemia) and total summed perfusion scores (SPS), and then compared between each study phase (ANOVA).
Results: Baseline rest and stress SPS were 22±12 and 26±11, respectively. There was no difference in total MP rest, stress or stress minus rest between baseline, RV, BiV one week and BiV 4 month (table⇓; *=p<0.01). Segmental analysis showed that baseline and RV pacing septal MP scores at rest and stress were almost 33% higher than BiV pacing at 1 week and 4 months. MP scores at rest and stress for anterior, inferior, posterior and apical segments were similar between baseline and pacing phases.
Conclusions: BiV pacing reverses septal segmental myocardial perfusion defects in patients with left bundle branch block. However, BiV pacing had no acute or chronic effect on global myocardial perfusion These data suggest that improved septal wall MP may be due to correction of LV contractile dysfunction which leads to less septal wall stress and improved coronary perfusion.