ABSTRACT
Objective To investigate the influence of interventional treatment of ventricular septal defect (VSD) on QT dispersion (QTd), corrected QT dispersion (QTcd) and the left ventricular voltage. Methods Fifty patients with VSD, admitted from May 2010 to October 2011 for interventional occlusion therapy, were included in the present study. The electrocardiograms and echocardiography of the patients were analyzed before and 1 day and 6 months after interventional treatment, including QTd, QTcd, RV5, SV1, RaVL, SV3, left ventricular ejection fraction (EF) and fractional shortening (FS). The changes in QTd, QTcd and the left ventricular voltage (RV5+SV1, RaVL+SV3) were observed after interventional occlusion therapy. Results Compared with preoperative electrocardiogram, the QTd and QTcd were obviously shortened (P<0.05), and the left ventricular voltage (RV5+SV1, RaVL+SV3) declined significantly after interventional occlusion therapy (P<0.05). Conclusions The QTd and QTcd are shortened and left ventricular voltage lowered significantly after interventional occlusion treatment in VSD patients. Transcatheter interventional occlusion therapy can obviously improve electrical remodeling.
ABSTRACT
PURPOSE:To evaluate the changes of QT dispersion (QTd) in CAPD patients serially from the period before the initiation of CAPD until several years after CAPD, and to find any associated factors. METHODS:We performed a retrospective cohort study with a total of 101 patients who initiated CAPD between 1990 and 1996. All data were recruited from the patients' medical records before CAPD initiation, within one year after CAPD, and between one and three years after CAPD. RESULTS:QTd and Corrected QTd (QTdc) values after CAPD did not show differences in the paired t-test of those before CAPD and within one year after CAPD. There was a definite correlation between the QTds before CAPD and that within one year after CAPD (r=0.530, p<0.001). In addition, the QTds from within one year after CAPD showed a correlation with those taken from one to three years after CAPD (r=0.487, p=0.019). Upon analysis of all-cause mortality, the change rate of QTd after CAPD initiation was revealed as a predicting factor along with the QTd, QTc max, and QTdc within one year after CAPD (RR=1.055, p=0.005). The change rate also remained a predictor of cardiovascular mortality (RR= 1.088, p=0.007). In a multivariate Cox regression, cardiomegaly and previous cardiovascular disease were revealed to be independent factors for the change rate of QTd. CONCLUSION:QTd in CAPD patients did not change after initiation of CAPD, and the change rate of QTd after CAPD initiation was revealed as a risk factor for both all-cause mortality and cardiovascular mortality.