Validation of methods for effective orifice area measurement of prosthetic valves by two-dimensional and Doppler echocardiography following transcatheter self-expanding aortic valve implantation

Background The effective orifice area(EOA)is utilized to characterize the hemodynamic performance of the transcatheter heart valve(THV).However,there is no consensus on EOA measurement of self-expanding THV.We aimed to compare two echocardiographic methods for EOA measurement following transcatheter self-expanding aortic valve implantation.Methods EOA was calculated according to the continuity equation.Two methods were constructed.In Method 1 and Method 2,the left ventricular outflow tract diameter(LVOTd)was measured at the entry of the prosthesis(from trailing-to-leading edge)and proximal to the prosthetic valve leaflets(from trailing-toleading edge),respectively.The velocity-time integral(VTI)of the LVOT(VTILVOT)was recorded by pulsed-wave Doppler(PW)from apical windows.The region of the PW sampling should match that of the LVOTd measurement with precise localization.The mean transvalvular pressure gradient(MG)and VTI of THV was measured by Continuous wave Doppler.Results A total of 113 consecutive patients were recruited.The mean age was 77.2±5.5 years,and 72 patients(63.7%)were male.EOA1 with the use of Method 1 was larger than EOA2(1.56±0.39 cm2 vs.1.48±0.41 cm2,P=0.001).MG correlated better with the indexed EOA1(EOAI1)(r=-0.701,P<0.001)than EOAI2(r=-0.645,P<0.001).According to EOAI(EOAI≤0.65 cm2/m2,respectively),the proportion of sever prosthesis-patient mismatch with the use of EOA1 was lower than EOA2(12.4%vs.21.2%,P<0.05).Compared with EOA2,EOA1 had lower interobserver and intra-observer variability(intra:0.5%±17%vs.3.8%±22%,P<0.001;inter:1.0%±9%vs.3.5%±11%,P<0.001).Conclusions For transcatheter self-expanding valve EOA measurement,LVOTd should be measured in the entry of the prosthesis stent(from trailing-to-leading edge),and VTILVOT should match that of the LVOTd measurement with precise localization.

Effect of tanshinone combined with valsartan therapy on the renal injury and endothelial injury in patients with hypertensive nephropathy

Objective:To study the effect of tanshinone combined with valsartan therapy on the renal injury and endothelial injury in patients with hypertensive nephropathy.Methods: A total of 72 patients with hypertensive nephropathy who were treated in our hospital between January 2013 and April 2016 were selected and randomly divided into the control group (n=36) who received conventional treatment + valsartan therapy and the observation group (n=36) who received conventional treatment + tanshinone combined with valsartan therapy, and both therapies lasted for 2 weeks. Before treatment and after 2 weeks of treatment, automatic biochemical analyzer was used to determine the renal function indexes in peripheral blood, enzyme-linked immunosorbent assay (ELISA) was used to determine the levels of endothelial injury markers and inflammatory cytokines in peripheral blood, and RIA method was used to determine the serum levels of oxidative stress indexes.Results:Before treatment, the differences in the peripheral blood renal function indexes and endothelial injury markers as well as the serum inflammatory factors and oxidative stress indexes were not statistically significant between two groups of patients. After 2 weeks of treatment, peripheral blood renal function indexes Scr and BUN levels as well as urine mAlb level of observation group were lower than those of control group, and endothelial injury indexes E-selectin and ET levels were lower than those of control group while NOS and CGRP levels were higher than those of control group;serum inflammatory cytokines IL-1, IL-6, CRP and TNF-α levels of observation group were lower than those of control group, and oxidative stress index GSH-Px level was higher than that of control group while MDA and AOPP levels were lower than those of control group. Conclusion: Tanshinone combined with valsartan can reduce the renal injury and endothelial injury in patients with hypertensive nephropathy, and the specific mechanism may be related to controlling the systemic inflammatory response and oxidative stress reaction.