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Background— Cardiac resynchronization therapy (CRT) improves LV structure, function, and clinical outcomes in New York Heart Association class III/IV heart failure with prolonged QRS. It is not known whether patients with New York Heart Association class I/II systolic heart failure exhibit left ventricular (LV) reverse remodeling with CRT or whether reverse remodeling is modified by the cause of heart failure. Methods and Results— Six hundred ten patients with New York Heart Association class I/II heart failure, QRS duration ≥120 ms, LV end-diastolic dimension ≥55 mm, and LV ejection fraction ≤40% were randomized to active therapy (CRT on; n=419) or control (CRT off; n=191) for 12 months. Doppler echocardiograms were recorded at baseline, before hospital discharge, and at 6 and 12 months. When CRT was turned on initially, immediate changes occurred in LV volumes and ejection fraction; however, these changes did not correlate with the long-term changes (12 months) in LV end-systolic ( r =0.11, P =0.31) or end-diastolic ( r =0.10, P =0.38) volume indexes or LV ejection fraction ( r =0.07, P =0.72). LV end-diastolic and end-systolic volume indexes decreased in patients with CRT turned on (both P P Conclusions— CRT in patients with New York Heart Association I/II resulted in major structural and functional reverse remodeling at 1 year, with the greatest changes occurring in patients with a nonischemic cause of heart failure. CRT may interrupt the natural disease progression in these patients. Clinical Trial Registration— Clinicaltrials.gov Identifier: NCT00271154.

International audience; Cardiac resynchronization therapy (CRT) has been shown to induce a spectacular effect on left ventricular (LV) function in certain patients. Our aim was to analyze and characterize the super-responders (SRs) to CRT using echocardiography in 186 patients with a conventional indication according to the European Society Cardiology guidelines. The investigation took place before and 6 months after implantation. CRT-SRs were defined by an improvement of the New York Heart Association functional class and LV ejection fraction to > or = 50% in absolute values associated with a relative LV end-systolic volume reduction of > or = 15%. Of the 186 patients, 18 (9.7%) were identified as CRT-SRs and had a significantly lower prevalence of ischemic etiology (11%), lower LV dimensions, lower left atrial volume, and greater global longitudinal strain at baseline. Receiver operating characteristics curves identified global longitudinal strain as the strongest parameter for predicting CRT-SRs, with a cutoff value of -12% (area under the curve 0.87, sensitivity 71%, and specificity 85%, p

International audience; AIM: To date, most published echocardiographic methods have assessed left ventricular (LV) dyssynchrony (DYS) alone as a predictor for response to cardiac resynchronization therapy (CRT). We hypothesized that the response is instead dictated by multiple correctable factors. METHODS AND RESULTS: A total of 161 patients (66 +/- 10 years, EF 24 +/- 6%, QRS > 120 ms) were investigated pre- and post-CRT (median of 6 months). Reduction in NYHA Class >/=1 or LV reverse remodelling (end-systolic volume reduction >/= 10%) defined response. Four different pathological mechanisms were identified. Group1: LVDYS characterized by a pre-ejection septal flash (SF) (87 patients, 54%). Elimination of SF (77 of 87 patients) resulted in reverse remodelling in 100%. Group 2: short-AV delay (21 patients, 13%) resolution (19 of 21 patients) resulted in reverse remodelling in 16 of 19. Group 3: long-AV delay (16 patients, 10%) resolution (14 of 16 patients) resulted in NYHA Class reduction >/=1 in 11 with reverse remodelling in five patients. Group 4: exaggerated LV-RV interaction (15 patients, 9%) reduced post-CRT. All responded clinically with fall in pulmonary artery pressure (P = 0.003) but did not volume respond. Group 5: patients with none of the above correctable mechanisms (22 patients, 14%). None responded to CRT. CONCLUSION: CRT response is dictated by correction of multiple independent mechanisms of which LVDYS is only one. Long-axis DYS measurements alone failed to detect 40% of responders.