Citations

Background— Various dyssynchrony indexes derived from tissue velocity and strain imaging have been proposed to predict the effectiveness of cardiac resynchronization therapy (CRT). We sought to compare the effect of CRT on dyssynchrony indexes derived by tissue velocity and strain and to determine which baseline intraventricular dyssynchrony parameters correlate with improvement in left ventricular volume after CRT. Methods and Results— Echocardiography with tissue Doppler imaging was performed in 45 patients with systolic heart failure at baseline, 1 day after CRT, and a median of 6 months after CRT. We calculated septal–lateral delay and anteroseptal–posterior delay and standard deviation of time to peak systolic velocity in the 12 basal and mid-left ventricular segments (Tv-SD). The standard deviation for time to peak strain in the 12 basal and mid-left ventricular segments (Tε-SD) was calculated as a strain-derived dyssynchrony index. None of the tissue velocity–derived dyssynchrony indexes improved after CRT (septal–lateral delay, P =0.39; anteroseptal–posterior delay, P =0.46; Tv-SD, P =0.30), whereas Tε-SD decreased significantly after CRT ( P <0.001). Improvement in Tε-SD 1 day after CRT correlated with the reduction in end-systolic volume at follow-up ( r =0.66; P <0.001). Baseline Tε-SD demonstrated significant correlation with the reduction of end-systolic volume at follow-up ( r =0.57; P <0.001); however, baseline tissue velocity–derived dyssynchrony indexes failed to predict the effect of CRT. Conclusions— The strain-derived dyssynchrony index is a better measurement than the tissue velocity dyssynchrony index for monitoring changes in mechanical dyssynchrony after CRT and for predicting reduction in left ventricular volume after CRT.

Background— Several echocardiographic dyssynchrony indexes have been proposed to identify responders to cardiac resynchronization therapy using tissue velocity and strain. The present study aimed to compare tissue velocity–derived and strain-derived dyssynchrony indexes in patients with or without systolic dysfunction and left bundle-branch block. Methods and Results— Tissue Doppler imaging was performed in 120 subjects divided into 4 groups: group 1 (n=40), normal subjects; group 2 (n=20), normal left ventricular ejection fraction and left bundle-branch block; group 3 (n=20), left ventricular ejection fraction <35% and normal conduction; and group 4 (n=40), left ventricular ejection fraction <35% and left bundle-branch block. Dyssynchrony indexes based on time to peak tissue velocity (septal-lateral delay, anteroseptal-posterior delay, and SD in time to peak systolic velocity in the 12 left ventricular segments) and strain (SD of time to peak strain in 12 segments) were measured. The SD in time to peak systolic velocity in the 12 left ventricular segments was greater in group 4 (54 ms; 25th and 75th percentiles, 46 to 64 ms) than group 1 (44 ms; 25th and 75th percentiles, 28 to 53 ms; P =0.006), but there was a considerable overlap of all tissue velocity–derived indexes among 4 groups, with 40% to 68% of group 1 having values proposed for predicting the responders of cardiac resynchronization therapy. The SD of time to peak strain in 12 segments distinguished these groups with much less overlap ( P <0.01 for all pairwise comparisons). Conclusions— A substantial proportion of normal subjects have tissue velocity–derived dyssynchrony indexes higher than the cutoff value proposed for predicting beneficial effect of cardiac resynchronization therapy. Strain-derived timing index appears to be more specific for dyssynchrony in patients with systolic dysfunction and left bundle-branch block. Identifying an optimal tissue velocity– or strain-derived dyssynchrony index requires a large prospective clinical trial.

Objective. To determine whether children with pallid breath-holding spells associated with bradycardia can be treated safely and successfully with permanent pacemaker implantation. Methods. The records of pediatric patients who had apparent breath-holding spells and associated bradycardia and were treated with permanent pacemaker implantation were reviewed. Results. Ten pediatric patients with apparent breath-holding spells associated with bradycardia were treated with a permanent ventricular demand pacemaker at the Mayo Clinic between 1985 and 1995. Patients had onset of symptoms between ages 6 days and 12 months and presented for evaluation between ages 12 months and 5 years. Duration of spells was 15 seconds to 10 minutes. Medications to prevent spells were unsuccessful. Electrocardiograms documented asystolic pauses of 1.7 to 24 seconds (mean: 11.9 seconds). Permanent ventricular demand pacemakers were implanted at 10 months to 5 years of age (median: 14.5 months): 9 endocardial and 1 epicardial. Three patients required pacemaker revision. At follow-up of 38 to 170 months (median: 65.5), 5 patients had complete resolution of spells, 2 had only mild color change without loss of consciousness or seizure activity, and 3 continued to have minor brief spells. Conclusions. Permanent pacemaker therapy for children with pallid breath-holding spells associated with severe bradycardia is safe, efficacious, and warranted.