Cardiac electrical and mechanical synchrony of super-responders to cardiac resynchronization therapy / 中华医学杂志(英文版)

BACKGROUND@#Super-responders (SRs) to cardiac resynchronization therapy (CRT) regain near-normal or normal cardiac function. The extent of cardiac synchrony of SRs and whether continuous biventricular (BIV) pacing is needed remain unknown. The aim of this study was to evaluate the cardiac electrical and mechanical synchrony of SRs.@*METHODS@#We retrospectively analyzed CRT recipients between 2008 and 2016 in 2 centers to identify SRs, whose left ventricular (LV) ejection fraction was increased to ≥50% at follow-up. Cardiac synchrony was evaluated in intrinsic and BIV-paced rhythms. Electrical synchrony was estimated by QRS duration and LV mechanical synchrony by single-photon emission computed tomography myocardial perfusion imaging.@*RESULTS@#Seventeen SRs were included with LV ejection fraction increased from 33.0 ± 4.6% to 59.3 ± 6.3%. The intrinsic QRS duration after super-response was 148.8 ± 30.0 ms, significantly shorter than baseline (174.8 ± 11.9 ms, P = 0.004, t = -3.379) but longer than BIV-paced level (135.5 ± 16.7 ms, P = 0.042, t = 2.211). Intrinsic LV mechanical synchrony significantly improved after super-response (phase standard deviation [PSD], 51.1 ± 16.5° vs. 19.8 ± 8.1°, P < 0.001, t = 5.726; phase histogram bandwidth (PHB), 171.7 ± 64.2° vs. 60.5 ± 22.9°, P < 0.001, t = 5.376) but was inferior to BIV-paced synchrony (PSD, 19.8 ± 8.1° vs. 15.2 ± 6.4°, P = 0.005, t = 3.414; PHB, 60.5 ± 22.9° vs. 46.0 ± 16.3°, P = 0.009, t = 3.136).@*CONCLUSIONS@#SRs had significant improvements in cardiac electrical and LV mechanical synchrony. Since intrinsic synchrony of SRs was still inferior to BIV-paced rhythm, continued BIV pacing is needed to maintain longstanding and synchronized contraction.

The roles of Epac in ventricularar rhythmogenesis and chronic heart failure / 医学研究生学报

Epac acts as a guanine nucleotide exchange factor for the Raslike small G-proteins Rap1 and Rap2,which activates independently classical effector of cAMP,protein kinase A. Many studies have demonstrated that Epac modulates various cAMP-de-pendent cardiovascular functions,such as calcium handling and ion channel remodeling,which are involved in the development of ar-rhythmias and heart failure. The novel cAMP sensor may represent an attractive therapeutic target for the treatment of several cardiovas-cular disorders,including cardiac arrhythmias and heart failure,because themodulation of Epac function is expected to enable morespe-cific regulation of particular cAMP-mediated signals than therapies targeting β-AR and Acs.