ObjectiveTo investigate the predictive value of heart rate turbulence(HRT) in patients with diabetes mellitus (DM) after acute myocardial infarction (AMI).MethodsNinety-two AMI patients combined with DM (DM group) and 120 AMI patients without DM (non-DM group) were selected.Turbulence onset (TO) and turbulence slope (TS) were two indexes of HRT.HRT was considered positive when TO was ≥0 and TS was ≤2.5 ms/R-R.The differences in clinical data between HRT-positive and HRT-negative patients were compared.And the related risk factors after AMI were analyzed.ResultsAge,left ventricular ejection fraction (LVEF) level,renal insufficiency,LVEF＜40％,standard deviation of sinus cardiac cycle (R-R interval)(SDNN),heart rate variability (HRV) positiveand HRT indexes (TO,TS) between HRT-positive and HRT-negative patients in DM group had significant differences (P ＜ 0.05 ).Age,LVEF level,SDNN and HRT indexes(TO,TS) between HRT-positive and HRT-negative patients in non-DM group had significant differences(P ＜ 0.05).Multivariate Cox regression analysis showed that renal insufficiency (OR=4.8,95％ CI:1.8 - 10.7,P=0.008) and HRT positive (OR=3.7,95％ CI:1.5 - 8.6,P=0.070) in DM group had statistical significance.And HRT positive in non-DM group had statisticalsignificance(OR=23.0,95％ CI:5.2 ～ 86.0,P ＜ 0.01 ).ConclusionsHRT,an index of dynamic electrocardiogram,can predict the risk in patients with DM or without DM after AMI.

Objective: To explore the diagnostic value of ultrasound imaging for fetal central nervous system(CNS) malformation in early pregnancy. Methods: From January 2017 to January 2018, a total of 190 cases of CNS malformation in early pregnancy, who were diagnosed by ultrasound imaging in Wenzhou Hospital of Integrated Traditional Chinese and Western Medicine were selected to analyze the clinical value of ultrasound imaging in the diagnosis of fetal CNS malformation in early pregnancy. Results: Of the 190 pregnancies, 184 patients had satisfactory median sagittal section of the head and chest, horizontal cross section of the lateral ventricle, long axis of the spine, and cerebellum and posterior fossa pool.In 184 cases, the probability of display from 1 to 11^{+ 6} weeks was 93.33%, the probability of display from 12 to 12^{+ 6} weeks was 97.20%, and the probability of display from 13 to 13^{+ 6} weeks was 97.06%.Compared the display rates of CNS ultrasound examinations at different gestational weeks, the difference was not statistically significant (χ²=0.981, P>0.05). Three cases of 6 cases of CNS malformation diagnosed in early pregnancy were combined with other malformations.One case considered Cantrell's hypothyroidism with CNS malformation, 1 case with left iliac crest and right circumflex, 1 case with median cleft lip and palate, single atrioventricular with pulmonary atresia.The bilateral humerus was missing, in addition, 4 fetuses had an NT value more than 3 mm.The specificity of diagnosis of fetal CNS malformation in early pregnancy was 100.00%, the sensitivity was 85.71%, the specificity was 100.00%, and the positive predictive value was 99.46%. Conclusion Ultrasound imaging in the diagnosis of fetal CNS malformation in early pregnancy can improve the diagnosis rate and has high clinical value.

Objective To investigate the effect and mechanism of Nuanxinkang on plaque formation in obstructive sleep apnea-hypopnea syndrome(OSAHS)comorbid with atherosclerosis(AS)mice by inhibiting endothelial-to-mesenchymal transition(EndMT).Methods Male ApoE-/-mice were randomly divided into six groups:control group,model group,atorvastatin group(2.6 mg·kg-1)and Nuanxinkang low-,medium-and high-dose groups(crude drug 3.5,7.0,14.0 g·kg-1),with eight mice in each group.The mice were exposed to chronic intermittent hypoxia(CIH)environment during sleep for a long time,and fed with high-fat diet to replicate OSAHS comorbid with AS mouse model.Oil red O staining was used to observe the formation of plaque on aortic intima in mice.Masson trichrome staining was used to evaluate the collagen content of atherosclerotic plaques in the aortic root of mice.The expressions of endothelial cell marker CD31 and EndMT marker Vimentin in aortic plaque were detected by immunofluorescence.Blood lipid levels were determined by ELISA;the mRNA expression levels of EndMT markers α-SMA and Cdh2 in aortic tissue were detected by qPCR.Results Compared with the control group,the area of aortic atherosclerotic plaque in the model group was significantly increased(P＜0.01),and the area of collagen deposition in the aortic root plaque was significantly increased(P＜0.01).The number of CD31 positive cells in the plaque were significantly decreased(P＜0.01),and the number of Vimentin positive cells were significantly increased(P＜0.01).Serum TG,T-CHO and LDL-C levels were significantly increased(P＜0.01),and HDL-C level was significantly decreased(P＜0.01).The mRNA expression levels of α-SMA and Cdh2 in aortic tissue were significantly increased(P＜0.01).Compared with the model group,the area of aortic atherosclerotic plaque in Nuanxinkang groups were significantly reduced(P＜0.05,P＜0.01),and the collagen deposition area of aortic root atherosclerotic plaque were significantly reduced(P＜0.05,P＜0.01).The number of CD31 positive expression cells in the plaque of Nuanxinkang high-dose group were significantly increased(P＜0.05),and the number of Vimentin positive expression cells in the plaque of Nuanxinkang medium-and high-dose groups were significantly decreased(P＜0.05,P＜0.01).The serum TG level of mice in the high-dose group of Nuanxinkang was significantly decreased(P＜0.01).The serum T-CHO and LDL-C levels of mice in each Nuanxinkang administration group were significantly decreased(P＜0.05,P＜0.01).The serum HDL-C levels of mice in the medium-and high-dose groups of Nuanxinkang were significantly increased(P＜0.01).The mRNA expression levels of α-SMA and Cdh2 in aortic tissue of mice in each treatment group were significantly decreased(P＜0.01).Conclusion Nuanxinkang can effectively reduce the plaque formation in OSAHS comorbid with atherosclerosis mice,which may be related to its inhibition of EndMT and reduction of collagen fiber formation.