Background: Defecation delay is a common symptom in patients after tricuspid valve replacement (TVR). Previous studies have demonstrated that defecation delay was associated with worse clinical outcomes of critically ill patients. Our study aimed to investigate the incidence and risk factors of defecation delay in patients after TVR and its adverse clinical outcomes. Methods: A retrospective study was conducted in 206 patients undergoing TVR under cardiopulmonary bypass from May 2005 to July 2021. According to the first postoperative defecation time after surgery, patients were divided into the delayed group (>3 days) and control group (≤3 days). Baseline characteristics and preoperative, intraoperative, and postoperative data were collected to investigate the clinical outcomes of defecation delay. Results: Among the 206 patients, 51.9% (107/206) cases were classified into the defecation delay group. Univariate analysis showed that age (P = 0.043), preoperative platelets (PLT) (P < 0.001), cardiopulmonary bypass (CPB) time (P = 0.013), minimum rectal temperature (P = 0.042), and the use of prokinetic drugs (P = 0.015) were significantly different in the two groups. In addition, the perioperative adverse events in the defecation delay group were significantly higher than that of the control group. Logistic regression analysis indicated that the mortality of patients was associated with postoperative renal dysfunction (P = 0.047) and postoperative respiratory failure (P = 0.004) but was not associated with defecation delay (P > 0.05). Conclusion: Patients with defecation delay after TVR were more likely to appear adverse events, however, defecation delay was not associated with mortality after TVR.

Calcific aortic valve disease (CAVD) is the most common valvular heart disease, with an increasing prevalence due to an aging population. The pathobiology of CAVD is a multifaceted and actively regulated process, but the detailed mechanisms have not been elucidated. The present study aims to identify the differentially expressed genes (DEGs) in calcified aortic valve tissues, and to analyze the correlation between DEGs and clinical features in CAVD patients. The DEGs were screened by microarray in normal and CAVD groups (n = 2 for each group), and confirmed by quantitative real‐time polymerase chain reaction in normal (n = 12) and calcified aortic valve tissues (n = 34). A total of 1048 DEGs were identified in calcified aortic valve tissues, including 227 upregulated mRNAs and 821 downregulated mRNAs. Based on multiple bioinformatic analyses, three 60S ribosomal subunit components (RPL15, RPL18, and RPL18A), and two 40S ribosomal subunit components (RPS15 and RPS21) were identified as the top 5 hub genes in the protein–protein interaction network of DEGs. The expression of RPL15 and RPL18 was also found significantly decreased in calcified aortic valve tissues (both p < .01), and negatively correlated with the osteogenic differentiation marker OPN in CAVD patients (both p < .01). Moreover, inhibition of RPL15 or RPL18 exacerbated the calcification of valve interstitial cells under osteogenic induction conditions. The present study proved that decreased expression of RPL15 and RPL18 was closely associated with aortic valve calcification, which provided valuable clues to find therapeutic targets for CAVD.

BackgroundCAVD is a common cardiovascular disease, but currently there is no drug treatment. Therefore, it is urgent to find new and effective drug therapeutic targets. Recent evidence has shown that the infiltration of M1 macrophages increased in the calcified aortic valve tissues, but the mechanism has not been fully elucidated. The purpose of this study was to explore the shared gene characteristics and molecular mechanisms of macrophages M1 polarization in CAVD, in order to provide a theoretical basis for new drugs of CAVD.MethodsThe mRNA datasets of CAVD and M1 polarization were downloaded from Gene Expression Omnibus (GEO) database. R language, String, and Cytoscape were used to analyze the functions and pathways of DEGs and feature genes. Immunohistochemical staining and Western Blot were performed to verify the selected hub genes.ResultsCCR7 and GZMB were two genes appeared together in hub genes of M1-polarized and CAVD datasets that might be involved in the process of CAVD and macrophages M1 polarization. CCR7 and CD86 were significantly increased, while CD163 was significantly decreased in the calcified aortic valve tissues. The infiltration of M1 macrophages was increased, on the contrary, the infiltration of M2 macrophages was decreased in the calcified aortic valve tissues.ConclusionThis study reveals the shared gene characteristics and molecular mechanisms of CAVD and macrophages M1 polarization. The hub genes and pathways we found may provide new ideas for the mechanisms underlying the occurrence of M1 polarization during CAVD process.

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