Bruce, Charles J.

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.

Background— In this study we evaluate the diastolic deformation of ischemic/reperfused myocardium and relate this deformation to tissue elastic properties. Methods and Results— Farm pigs were subjected to left anterior descending coronary artery occlusion followed by reperfusion to create either stunning (n=12) or transmural myocardial infarction (n=12). Ultrasound-derived radial strain rates (SR) and strain were measured in the ischemic and remote walls. Myocardial stiffness was estimated from diastolic pressure–wall thickness relationship obtained from preload alterations. At reperfusion, end-systolic strain (ε sys ) was significantly reduced in both stunned and infarcted walls compared with their remote walls (3±3% versus 26±2% and 1±0% versus 33±5%, respectively; P <0.0001) or baseline values. Diastolic passive deformation (ε A ) and rates of deformation during early (E SR ) and late (A SR ) diastole were comparable between stunned and remote walls (ε A : 7.3±1.6% versus 7.9±1.9%; E SR : −2.7±0.4 s −1 versus −2.6±0.5 s −1 ; A SR : −1.8±0.2 s −1 versus −1.9±0.3 s −1 ; P =NS for all) but were of significantly lower magnitude in infarcted walls versus remote walls (ε A : 1.1±0.2% versus 11.4±1.9%; E SR : −0.3±0.1 s −1 versus −2.4±0.4 s −1 ; A SR : −0.3±0.1 s −1 versus −2.5±0.4 s −1 ; P <0.0001 for all). Stiffness coefficient of exponential diastolic pressure–wall thickness relation was higher for infarcted ( P <0.05) but not for stunned walls ( P =NS) compared with their remote walls. Conclusions— Early after postischemic reperfusion and in the presence of severely reduced systolic deformation, diastolic passive deformation (and rates of deformation) can distinguish stiff, noncompliant, transmurally infarcted myocardial walls from those more compliant walls containing viable but stunned myocardium.