Objective To explore the impact of COVID-19 infection on the early clinical efficacy of valve replacement patients. MethodsThe perioperative data of patients who underwent single valve replacement in our center from January to February 2023 were collected continuously. According to the COVID-19 infection situation, the patients were divided into a COVID-19 infected group and a non-infected group. The relevant data of the two groups were compared, including general situation, comorbidities, operation time, aortic occlusion time, postoperative ventilator use time, intensive care unit (ICU) stay time, myocardial enzyme profile and respiratory related complications were statistically analyzed. The primary end point of the study was the incidence of postoperative respiratory and circulatory system complications, and the secondary end point was postoperative myocardial enzyme profiles in both groups. ResultsA total of 136 patients were included, including 53 males and 83 females, with an average age of 53.4±10.2 years. Thirty-two patients underwent aortic valve replacement, 102 mitral valve replacement, and 2 tricuspid valve replacement.There was no significant difference in the incidence of postoperative disease between the two groups (9.09% vs. 11.43%, P=0.654), and the duration of postoperative mechanical ventilation in the novel coronavirus infection group [913.50 (465.50, 1 251.00) min vs. 1 201.00 (1 003.75,1 347.75) min, P=0.001], ICU stay time [2 (2, 3) d vs. 3 (2, 3) d, P＜0.001) was a new champions league group, the myocardial enzyme spectrum [TnI-I: 2.66(1.19, 5.65) ng/mL vs. 4.76 (2.55, 7.93) ng/mL, P=0.001; BNP: 192.00 (100.93, 314.75) pg/mL vs. 608.5 (249.75, 1150) pg/mL, P＜0.001], and the difference was statistically significant. Conclusion For single valvular disease patients undergoing elective surgery, the short-term efficacy of surgical treatment after recovery from COVID-19 infection was relatively good, and the incidence of in-hospital mortality and postoperative complications was not significantly increased.
Objective To explore the causal relationship between DNA copy number and the risk of Alzheimer disease (AD) using Mendelian randomization (MR) methods, as well as to investigate the potential mediating effects of immune cells. Methods The data related to 731 immune cell types, DNA copy number and AD from the Genome-Wide Association Study database were collected. A bidirectional MR analysis was conducted to explore the causal relationship between DNA copy number and AD, primarily using the inverse-variance weighted method and MR-Egger method. Additionally, a two-step mediation analysis was performed to identify potential mediating immune cells. Results A total of 134 single-nucleotide polymorphisms were included for bidirectional MR analysis. The MR methods results showed a negative causal relationship between DNA copy number and the risk of AD (P<0.05), while the reverse analysis showed no statistical significance. Sensitivity analysis confirmed the robustness of these results. The mediation analysis indicated that the immune cell phenotype (HVEM on CD45RA-CD4+) partially mediated the causal relationship between DNA copy numbers and the risk of AD, with a mediation effect proportion of 4.6%. Conclusion An increase in DNA copy numbers may reduce the risk of AD, and immune cells partially mediate this causal relationship.