The Clinical And Basic Research On The Expression Of Inflammatory Factors In Pte Secondary To CTEPH

Objectives: 1.To observe the incidence of chronic thromboembolic pulmonary hypertension(CTEPH)in patients with acute pulmonary thromboembolism(PTE)3months after regular anticoagulant therapy;expression in patients with inflammatory factor PTE;analysis of risk factors and prognosis.2.To observe the expression changes of inflammatory factors in two PTE models of Japanese white rabbits.Study contents and methods: 1.We enrolled 112 patients with acute PTE,according to clinical manifestations,Wells score and improved Geneva score;blood samples,blood biochemistry,blood gas analysis,CRP,TNF-α were measured in patients admitted;calculated according to ECG Electrocardiogram score: ECG was detected,pulmonary artery diameter,ventricular septum and right ventricular wall motion were observed by echocardiography.The inferior vena cava,right atrium,right ventricle,right ventricular outflow tract,pulmonary artery trunk and left and right pulmonary artery bifurcation were observed.Pulmonary systolic pressure(PASP)was calculated by tricuspid regurgitation pressure difference;pulmonary artery and pulmonary artery branches were evaluated according to CTPA results,and the Qanadli embolization index and Mastora embolization index were calculated;the treatment was given according to the patient’s condition,and cardiac ultrasound was reviewed regularly.CTPA.2.Using the Japanese white rabbit as the experimental object,two PTE models were made by the jugular vein technique,and the pulmonary artery pressure was measured by 4F pigtail catheter;HE staining was used to understand the changes of pulmonary artery;enzyme-linked immunosorbent assay(ELISA)was used.Detecting TNF-α in plasma;Western Bloting was used to detect TNF-α in lung;real-time quantitative fluorescent PCR was used to detect TNF-α in lung.Results: 1.According to the inclusion and exclusion criteria,112 patients with acute PTE who met the inclusion criteria for acute PTE were excluded from the study.Among the 12 patients,5 were patients with chronic obstructive pulmonary disease,2were for lung cancer,and 3 were cardiac.In patients with valvular disease,1 patient had pulmonary fibrosis and 1 patient had congenital heart disease.2.Follow-up: 13 of112 patients fell off,3 of whom died during hospitalization,9 were lost to follow-up,1 patient died of heart failure after discharge,and a total of 99 patients reached the3-month follow-up.All 99 patients underwent long-term follow-up.The shortest follow-up time was 5 months,the longest follow-up time was 60 months,and the average follow-up time was 27.8 ± 14.2 months.3.The age of the two groups of patients was significantly different between CTEPH patients and non-CTEPH patients.The gender of the patients in the two groups was higher in men with CTEPH.4.Right atrial diameter,right ventricular diameter and CK-MB were significantly different between CTEPH patients and non-CTEPH patients.5.Alveolar arterial oxygen pressure difference was statistically significant in patients with CTEPH and non-CTEPH patients.6.There was a statistically significant difference between PPE and recurrent PTE in patients with CTEPH and non-CTEPH.7.Detection of plasma inflammatory factors in patients,the results showed that CRP,TNF-α in the CTEPH patients and non-CTEPH patients were significantly different.8.Analysis of the influencing factors of CTEPH for three months showed that PASP,CK-MB,CRP and TNF-α in the acute phase were the influencing factors of CTEPH(P<0.05),among which the acute phase PASP increased by 20 mm Hg.The incidence of CTEPH is increased by about 4.5 times;re-opening of PTE can increase CTEPH by about 35times;the increase of inflammatory factors can increase the incidence of CTEPH by about 2 times.9.Two PTE models were made through the jugular vein.The experimental group showed respiratory and purpura,heart rate acceleration,urgency and agitation,and angiography confirmed local pulmonary filling defect,truncated or completely lost.10.Pulmonary arterial pressure was measured with a 4F pigtail catheter.The results showed that the pulmonary artery pressure increased after the first interventional injection of the embolus,which was statistically significant compared with that before the model was established.After the second intervention,the pulmonary artery pressure continued.The increase was statistically significant compared with that before the model was established.11.HE staining showed that the experimental group could see a large amount of inflammatory cell infiltration around the alveoli,and thrombus was also seen in the pulmonary artery,which appeared to be thickened.12.Enzyme-linked immunosorbent assay(ELISA)was used to detect TNF-α in plasma.After the first interventional injection of embolus in theexperimental group,TNF-αincreased,which was statistically significant compared with that before modeling.The second intervention After injection of the embolus,TNF-αcontinued to increase,which was statistically significant compared with that before modeling.13.Western Bloting detected TNF-αin the left heart,right heart and lung.The expression of TNF-αin the heart tissue of the experimental group was significantly increased(P < 0.05).Real-time quantitative fluorescent PCR was used to detect TNF-αin the left and right hearts.The results showed that the expression of TNF-αin the heart tissue of the experimental group was significantly increased(P <0.05).Conclusions: 1.The study enrolled 112 patients with acute PTE,99 of whom achieved a 3-month endpoint follow-up period,with an incidence of CTEPH of13.1%(13/99).Acute PASP,recurrent PTE,CK-MB,CRP,and TNF-α are risk factors for CTEPH.Patients with these risk factors should be followed closely and active measures should be taken to prevent the recurrence of CTEPH.2.In this experiment,the Japanese large ear white was used as the research object.The jugular vein was used as the approach,and the 4F pigtail catheter was sent to the pulmonary artery opening.Two PTE models were made and the pulmonary artery pressure changes were accurately determined.The expression of TNF-α and its m RNA was determined by ELISA,immunohistochemistry and molecular biology methods.It was found that the expression of TNF-α in blood and heart was enhanced in the two PTE models.Combined with the previous research results of this subject,the fibrinolytic activity after embolization is enhanced,TNF-α is involved in the inflammatory-coagulationthrombus cycle,and the study of inflammatory response may provide a new solution for the treatment of pulmonary hypertension.