Lin, Grace

Background: Atrial fibrillation (AF) is common in HCM yet the mechanisms are poorly understood but are likely secondary to either the consequences of left atrial structural remodeling (LASR) or myopathy, or triggers arising from pulmonary and other thoracic veins. The presence and severity of LASR as characterized by left atrial strain (LA ϵ), and its relationship to AF in HCM, has not been determined. Therefore, we measured LA ϵ and strain rate (SR) in Pts with HCM both with (AF+) and without (AF−) prior AF and compared these measures to those in age and gender matched controls without HCM or AF. Methods: Two-dimensional speckle-derived LA longitudinal peak ϵ, SR during systole (SR S ), early (SR E ) and late diastole (SR A ) were measured at the basal and mid portions of the lateral, septal, and posterior LA walls using Vector Velocity Imaging during sinus rhythm and were averaged. Results: Mean age of Pts in each of the matched groups was 56 ± 2 years (16 males; 59%). Significant left ventricular outflow tract obstruction was present in all Pts with HCM. Diastolic dysfunction was similar in both HCM groups and worse when compared to controls. Peak LA 3 , SR S , SR E , and SR A for each group is shown (table 1 ). HCM was associated with significantly lower LA ϵ and SR compared to controls. Although LA size was increased in Pts with HCM when compared to controls there was no correlation between LA size and ϵ or SR (p>0.05 for all). No differences in LA ϵ and SR were found between AF+ versus AF− Pts. Conclusion: HCM is associated with LASR as determined by decreased LA ϵ and SR. However, LA ϵ and SR were similar in AF+ versus AF− Pts suggesting that the occurrence of AF in HCM is not due to LASR alone. Table 1. Left Atrial Strain and Strain Rate in Hypertrophic Cardiomyopathy

Background— Whether mechanical dyssynchrony indices predict reverse remodeling (RR) or clinical response to cardiac resynchronization therapy (CRT) remains controversial. This prospective study evaluated whether echocardiographic dyssynchrony indices predict RR or clinical response after CRT. Methods and Results— Of 184 patients with heart failure with anticipated CRT who were prospectively enrolled, 131 with wide QRS and left ventricular ejection fraction <35% had 6-month follow-up after CRT implantation. Fourteen dyssynchrony indices (feasibility) by M-mode (94%), tissue velocity (96%), tissue Doppler strain (92%), 2D speckle strain (65% to 86%), 3D echocardiography (79%), and timing intervals (98%) were evaluated. RR (end-systolic volume reduction ≥15%) occurred in 55% and more frequently in patients without (71%) than in patients with (42%) ischemic cardiomyopathy ( P =0.002). Overall, only M-mode, tissue Doppler strain, and total isovolumic time had a receiver operating characteristic area under the curve (AUC) greater than the line of no information, but none of these were strongly predictive of RR (AUC, 0.63 to 0.71). In nonischemic cardiomyopathy, no dyssynchrony index predicted RR. In ischemic cardiomyopathy, M-mode (AUC, 0.67), tissue Doppler strain (AUC, 0.79), and isovolumic time (AUC, 0.76) -derived indices predicted RR ( P <0.05 for all), although the incremental value was modest. No indices predicted clinical response assessed by Minnesota Living with Heart Failure Questionnaire, 6-minute walk distance, and peak oxygen consumption. Conclusions— These findings are consistent with the Predictors of Response to CRT study and do not support use of these dyssynchrony indices to guide use of CRT.

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.