Objective: To investigate the differences of biochemical markers between the patients with pulmonary hypertension related to left heart disease (PH-LHD) and LHD; to explore the sensitive bio markers which may predict PH in LHD patients. Methods: A total of 355 LHD patients admitted to our hospital from 2014-01 to 2015-05 were enrolled. According to 2009 ESC/ERS guidelines, PH was deifned by pulmonary artery systolic pressure (PASP)>50 mmHg and patients were divided into 2 groups: LHD group,n=224 and PH-LHD group,n=131. The basic information with blood levels of biomarkers was recorded and their accuracy for predicting PH was analyzed. Results: The pathogenesis of LHD included 184 (51.83%) patients of coronary heart disease, 90 (25.35%) of dilated cardiomyopathy and 81 (22.81%) of cardiac valve heart disease. Compared with LHD group, PH-LHD group had increased ratio of NYHA III and IV degree (89.31% vs 45.54%), decreased LVEF [42.0 (33.0, 59.0) % vs 60.0 (42.0, 65.0) %], all P<0.001; PH-LHD group presented elevated blood levels of BNP, bilirubin, red cell distribution width (RDW), uric acid and cystatin C, while reduced lipoprotein (HDL), allP<0.001. PASP was positively related to biomarkers as BNP, bilirubin, RDW, uric acid and cystatin C, while negatively related to HDL. With the combination of BNP, direct bilirubin and RDW, the predictive value for PH-LHD under ROC curve was 0.828 with the sensitivity at 0.813, speciifcity at 0.708. Conclusion: Blood levels of biochemical markers were statistically different between the patients of PH-LHD and LHD; the combination of BNP, direct bilirubin and RDW showed the higher accuracy for predicting PH occurrence in LHD patients.

AIM: To investigate the effect of venous marker chicken ovalbumin upstream promoter-transcription factor Ⅱ (COUP-TFⅡ) expression on vascular endothelial cell senescence and its molecular mechanism.METHODS: The mRNA expression of COUP-TFⅡ in the human coronary artery endothelial cells (HCAEC) and human umbilical vein endothelial cells (HUVEC) was detected by RT-qPCR.After transfection with a COUP-TFⅡ siRNA (siCOUP-TFⅡ) to inhibit COUP-TFⅡ expression in the HUVEC, the senescence and proliferation of endothelial cells were evaluated by β-galactosidase staining, Western blot, CCK-8 assay and cell counting after treatment with 10-5 mol/L angiotensin Ⅱ (AngⅡ).The protein levels of Akt and p-Akt were determined by Western blot.RESULTS: Compared with the HCAEC, COUP-TFⅡ was significantly highly expressed in the HUVEC.Knockdown of COUP-TFⅡ via siCOUP-TFⅡ significantly induced endothelial cell senescence and inhibited endothelial cell proliferation and p-Akt level after treatment with AngⅡ at 10-5 mol/L.Furthermore, an Akt activator SC79 at 4 mg/L partly reversed the effect of siCOUP-TFⅡ on AngⅡ-induced endothelial cell senescence and proliferation.CONCLUSION: Knockdown of COUP-TFⅡ promotes endothelial cell senescence and inhibits endothelial cell proliferation, which might be partly regulated by Akt signaling.