Obiective To observe the value of speckle tracking imaging(STI)in assessing left atrial(LA) function in patients with chronic heart failure(CHF).Methods Twenty-two patients with CHF[LVEF(37.1± 10.5)%]and twenty normal controls[LVEF(61.94±10.68)%]were studied.CHF group was subdevided into patients with normal or abnormal LV filling pressure.Velocity vector imaging(Siemens Medical Solutions)was used to acquire 2-D images at parasternallong axis and apical 4-chamber views.The LA dimension and volume,LV volume and ejection fraction,ratio of mitral valve E wave and mitral annulus velocity e'E/e')were measured. LA tangential and radial velocity(Vt-As,Vr-As)and time to peak velocity(TVt-As,TVr-As)were analysed on Syngo Workplace offline.Results Vt-As and Vr-As of the CHF group were significantly smaller than those of the controls(P＜0.05),and Vr-As was even decreased in patient with elevated LV filling pressure(P＜0.05), however,TVt-AS and TVr-AS didn't show evident impairment in the CHF group(P＞0.05).Vt-As and Vr-AS were closely correlated with LVEF,EDV and ESV(P＜0.05).Vt-As was negtively correlated with LA volume (P＜0.05).Conclusions STI can quickly and accurately assess LA function,and help to recognize patients with elevated LV filling pressure,which is useful in the risk stratification,treatment evaluation and prognosis prediction of CHF patients.

Myoclonus dystonia syndrome (MDS) is an inherited movement disorder, and most MDS-related mutations have so far been found in the ε-sarcoglycan (SGCE) coding gene. By generating SGCE-knockout (KO) and human 237 C > T mutation knock-in (KI) mice, we showed here that both KO and KI mice exerted typical movement defects similar to those of MDS patients. SGCE promoted filopodia development in vitro and inhibited excitatory synapse formation both in vivo and in vitro. Loss of function of SGCE leading to excessive excitatory synapses that may ultimately contribute to MDS pathology. Indeed, using a zebrafish MDS model, we found that among 1700 screened chemical compounds, Vigabatrin was the most potent in readily reversing MDS symptoms of mouse disease models. Our study strengthens the notion that mutations of SGCE lead to MDS and most likely, SGCE functions to brake synaptogenesis in the CNS.