BACKGROUND: The potential impact of pre-existing coronary artery stenosis (CAS) on right ventricular (RV) function during acute pulmonary embolism (PE) episodes remains underexplored. This study aimed to investigate the association between pre-existing CAS and RV dysfunction in patients with acute PE. METHODS: In this multicenter, case-control study, 89 cases and 176 controls matched for age were enrolled at three study centers (Peking Union Medical College Hospital, Fuwai Hospital, and the Second Affiliated Hospital of Harbin Medical University) from January 2016 to December 2020. The cases were patients with acute PE with CAS, and the controls were patients with acute PE without CAS. Coronary artery assessment was performed using coronary computed tomographic angiography. CAS was defined as ≥50% stenosis of the lumen diameter in any coronary vessel >2.0 mm in diameter. Conditional logistic regression analysis was used to evaluate the association between CAS and RV dysfunction. RESULTS: The percentages of RV dysfunction (19.1% [17/89] vs. 44.6% [78/176], P <0.001) and elevated systolic pulmonary artery pressure (sPAP) (19.3% [17/89] vs. 39.5% [68/176], P = 0.001) were significantly lower in the case group than those in the control group. In the multivariable logistic regression model, CAS was independently and negatively associated with RV dysfunction (adjusted odds ratio [OR]: 0.367; 95% confidence interval [CI]: 0.185-0.728; P = 0.004), and elevated sPAP (OR: 0.490; 95% CI: 0.252-0.980; P = 0.035), respectively. CONCLUSIONS Pre-existing CAS was significantly and negatively associated with RV dysfunction and elevated sPAP in patients with acute PE. This finding provides new insights into RV dysfunction in patients with acute PE with pre-existing CAS.
Humans ; Pulmonary Embolism/complications* ; Case-Control Studies ; Male ; Ventricular Dysfunction, Right/physiopathology* ; Female ; Middle Aged ; Aged ; Coronary Stenosis/complications* ; Logistic Models ; Adult

Objective To investigate the role of β-arrestin2 in intestinal inflammation and illustrate the mechanisms from the perspective of epithelial barrier function. Methods Dextran sodium sulfate(DSS)is used to induce acute intestinal colitis in mice. The experiment groups are designed as the wild type control(WT),the wild type colitis (WT+DSS) and the β-arrestin2- knockout colitis (KO+DSS). The expression of β-arrestin2 gene by mRNA and protein level is compared between the WT and WT + DSS groups. The difference of weight loss , disease activity index(DAI),spleen weight,colon length,histological score,intestinal permeability and important tight junction proteins (occludin ,claudin1 and ZO-1) were detected in the WT+DSS and KO+DSS groups. Results Compared with the WT group,the expression of β-arrestin2 was significantly higher in the colon of the WT+DSS group. Compared with the WT+DSS group,the KO+DSS group had less weight loss(P < 0.05),lower DAI(P<0.05),smaller spleen,longer colon and lower histological score(P=0.002). The KO+DSS group had a lower intestinal permeability(P = 0.009)and higher protein level of occludin and claudin1.There was no signifi-cant difference of ZO-1 in the two groups. Conclusion β-arrestin2 may promote mouse colitis through impairment of epithelial barrier function.

Objective: To evaluate the efficacy and safety of generic imatinib (Genike, Chiatai Tianqing Pharmaceutical Group Co., Ltd.) and imatinib (Glevic, Novartis, Switzerland) in newly diagnosed patients with chronic myeloid leukemia in chronic phase (CML-CP) . Methods: A retrospective study of 323 CML-CP patients (205 in Glivec treatment group and 118 in Genike group) who were ≥ 18 years old receiving imatinib monotherapy over the period of June 2013 to March 2016 was done to compare the differences of cytogenetics, molecular curative effect, survival, and adverse reactions between the two groups. The beginning dosage of imatinib was 400mg per day. There was no statistically difference between the two groups of patients on baseline. Results: ①The median duration of imatinib treatment was 13 (0.5-36) months in Glevic group and 11 (1-31) months in Genike group. ②The rate of complete hematological remission (CHR) had no statistically difference between Glivec and Genike treatment groups[98% (201/205) vs 97.5% (115/118) , χ²=0.123, P=0.725]. ③Cumulative rates of major cytogenetic responses (MCyR) at 3, 6 and 12 months after imatinib treatment in Gleevec and Genike groups were (59.7±3.5) % vs (79.8±3.1) %, (89.2±2.6) % vs (59.1±4.7) %, (80.3±4.1) % vs (87.1±4.3) %, respectively, the difference was not statistically significant (χ²=0.084, P=0.772) . Cumulative rates of complete cytogenetic response (CCyR) at 3, 6 and 12 months after imatinib treatment in Gleevec and Genike groups were (32.9±3.4) % vs (58.3±3.7) %, (87.4±3.0) % vs (35.2±4.5) %, (64.8±4.8) % vs (87.3±4.7) %, respectively, the difference was not statistically significant (χ²=0.660, P=0.417) . ④Cumulative rates of major molecular responses at 6, 12 months after imatinib treatment in Glevic and Genike groups were (24.9±3.3) % vs (57.0±4.1) %, (16.3±4.0) % vs (55.3±7.7) %, respectively, there was no statistical significance (χ²=1.617, P=0.204) . Cumulative rates of molecular response 4.5 (MR4.5) at 12 months after imatinib treatment in Glevic and Genike groups were (14.9±3.2) % vs (8.1±2.1) % (χ²=3.628, P=0.057) , respectively. ⑤At a median follow-up of 12 months, the difference of progression-free survival (PFS) in Glevic and Genike groups had no statistical significance[ (96.6±1.4) % vs (93.3±2.5) %, χ²=2.293, P=0.130]. The difference of event-free survival (EFS) had no statistical significance, either[ (95.6±1.5) % vs (93.3±2.4) %, χ²=2.124, P=0.145]. ⑥Genike was well tolerated in patients with CML-CP and had no statistically significant difference in adverse events compared with Glevic group. Conclusion There were no statistically significant differences in efficacy and safety between Glevic and Genike treatment in newly diagnosed patients with CML-CP.