ObjectiveSystemic immune-inflammation index (SII) is a novel biomarker that can predict poor outcomes in tumours, nervous system diseases and chronic heart failure. Here, we investigated the predictive value of SII on the poor postoperative outcomes and short-term prognosis of heart valve diseases (HVDs).Design, setting and participantsThis retrospective cohort study enrolled all consecutive patients with HVDs (aortic stenosis, aortic regurgitation, mitral stenosis and mitral regurgitation) who underwent surgery (valve replacement or valve repair) at the Affiliated Hospital of North Sichuan Medical College between 2017 and 2020.Main outcomes and measuresMajor complications in the perioperative period, all-cause mortality within 30 days and readmission within 30 days.ResultsA total of 431 patients with HVDs were enrolled in this study, including 202 males and 229 females, aged 58.9±27.3 years. SII levels of patients in the poor outcomes group were significantly higher than those of patients in the favourable outcomes group (658.40±436.29 vs 335.72±174.76, respectively; p<0.001). Multivariate logistic regression analysis showed that age (OR 1.064, 95% CI 1.026 to 1.104, p=0.025), SII (OR 1.034, 95% CI 1.012 to 1.631, p=0.008) and aortic cross-clamping time (OR 1.013, 95% CI 1.004 to 1.023, p=0.006) were independent risk factors for poor outcomes and short-term prognosis in patients with HVD. The area under the curve of poor outcomes predicted by SII in patients with HVD was 0.806 (95% CI 0.763 to 0.848) and the optimised cut-off value 423.8×109 /L, with a sensitivity of 70.3% and specificity of 81.1%. The incidence of poor outcomes (p<0.001), 30-day mortality (p<0.001) and 30-day readmission rate (p=0.026) in the high SII group was significantly higher than that in the low SII group.ConclusionsSII is closely related to poor postoperative outcomes and short-term prognosis of HVD and can serve as an independent predictive factor.

Background This study aimed to investigate whether CXCL1/CXCR2 mediates intestinal injury or white matter injury by delivering inflammatory mediators through the gut–brain regulation axis. Methods Neonatal SD rats, regardless of sex, were administered 3% dextran sulfate sodium via intragastric administration at different time points to construct necrotizing enterocolitis (NEC) models. Meanwhile, hypoxia and ischemia were induced in 3 day-old SD rats to construct hypoxic–ischemic brain injury (HIBI) and NEC + HIBI models, without gender discrimination. Hematoxylin–eosin staining was used to observe pathological changes in neonatal rat intestinal and brain tissues. Western blotting detected CXCL1 and CXCR2 expression in NEC, HIBI, and NEC + HIBI rat intestinal and brain tissues. Results Compared with normal rats, pathological damage to periventricular white matter was observed in the NEC group. In addition to the increased mortality, the histopathological scores also indicated significant increases in brain and intestinal tissue damage in both HIBI and NEC + HIBI rats. Western blotting results suggested that CXCL1 and CXCR2 expression levels were upregulated to varying degrees in the intestinal and brain tissues of NEC, HIBI, and NEC + HIBI neonatal rats compared to that in the normal group. Compared with the HIBI group, the expression of CXCL1 and CXCR2 continued to increase in NEC + HIBI rats at different time points. Conclusions CXCL1/CXCR2 may be involved in white matter injury in neonatal rats by delivering intestinal inflammatory mediators through the gut–brain axis.

Acute aortic dissection (AAD) is a serious disease characterized by high mortality. However, there are no accurate indicators to predict in-hospital mortality. The objective of this study was to identify the potential value of ischemia modified albumin (IMA) in prediction of in-hospital mortality of AAD patients. This was a single-center, prospective study involved 314 patients undergoing AAD, including 197 males and 117 females, aged 26–87 (57.14 ± 21.71) years old, 116 cases of TAAD and 198 cases of TBAD (37 cases of complicated, 114 cases of high risk, and 47 cases of uncomplicated), 228 cases were underwent surgery/intervention treatment (77 cases of TAAD,151 cases of TBAD) and 86 cases were underwent conservative therapy (39 cases of TAAD, 47 cases of TBAD). The basic data, on-admission IMA level, and the all-cause in-hospital mortality was recorded. IMA in the non-survivor group and TAAD group was found to be significantly higher than that in the survivor group and TBAD group (P < 0.001). Multivariate logistic regression analysis results revealed that age (OR = 1.923, 95%CI: 1.102–4.481, P = 0.020), conservative therapy (OR = 17.892, 95%CI: 7.641–24.748, P < 0.001), D-dimer level (OR = 3.517, 95%CI: 1.874–7.667, P = 0.011) and IMA level (OR = 5.406, 95%CI: 2.951–10.395, P = 0.004) served as independent risk factors for in-hospital mortality of TAAD patients. And D-dimer level (OR = 2.241, 95%CI: 1.475–5.663, P = 0.018), IMA level (OR = 3.115, 95%CI: 1.792–6.925, P = 0.009) also served as independent risk factors for in-hospital mortality of TBAD patients, whereas surgery (OR = 0.110, 95%CI: 0.075–0.269, P < 0.001) was the protective factor of in-hospital mortality of TAAD patients. After IMA prediction, the AUC, optimal cut-off value, sensitivity, and the specificity of in-hospital mortality of AAD patients were observed to be 0.801 (95%CI: 0.744–0.858), 86.55 U/mL, 79.1%, and 73.2%, respectively. In addition, it was found that AUC was 0.799 (95%CI: 0.719–0.880) in TAAD and 0.753 (95% CI: 0.641–0.866) in TBAD. Overall, it was concluded that on-admission IMA level acted as an independent prediction index for in-hospital mortality of AAD patients.

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