Background: The Peguero-Lo Presti criteria are novel electrocardiographic (ECG) diagnostic criteria for the detection of left ventricular hypertrophy (LVH) and represent the sum of the amplitude of the deepest S wave in any lead with the S wave in lead V₄(S_D+SV₄). The diagnostic efficacy of the Peguero-Lo Presti criteria in LVH is still debatable. We aimed to test the sensitivity and specificity of the Peguero-Lo Presti criteria and compared them with those of the Cornell voltage index to assess their overall performance in LVH diagnosis.Methods: Electronic databases (e.g., Medline, Web of Knowledge, Embase, and the Cochrane Library) were searched from their inception until May 18, 2020. Trials written in English that investigated the Peguero-Lo Presti criteria for detecting LVH were included. Data were independently extracted and analyzed by two investigators.Results: A total of 51 records were screened, and 6 trials comprising 13,564 patients were finally included. A bivariate analysis showed that the sensitivity of the Peguero-Lo Presti criteria (0.52, 95% confidence interval (CI) 0.46–0.58) was higher than that of the Cornell voltage index (0.29, 95% CI 0.23–0.36) and Sokolow-Lyon criteria (0.24, 95% CI 0.21–0.27); the diagnostic accuracy of the Peguero-Lo Presti criteria (0.69, 95% CI 0.65–0.73) was also higher than that of the Cornell voltage index (0.67, 95% CI 0.62–0.71) and Sokolow-Lyon criteria (0.28, 95% CI 0.25–0.32); and the specificity of the Peguero-Lo Presti criteria (0.85, 95% CI 0.79–0.90) was similar to that of the Cornell voltage index (0.92, 95% CI 0.89–0.95) and Sokolow-Lyon criteria (0.94, 95%CI 0.88–0.97). Two trials (including 12,748 patients) were discharged because they included partly healthy subjects and accounted for substantial heterogeneity. Pooled analysis of the remaining 4 trials (including 816 patients) showed that the sensitivity of the Peguero-Lo Presti criteria (0.56, 95% CI 0.51–0.61) was also higher than that of the Cornell voltage index (0.36, 95% CI 0.31–0.42) and Sokolow-Lyon criteria (0.24, 95% CI 0.18–0.31); the diagnostic accuracy of the Peguero-Lo Presti criteria (0.84, 95% CI 0.80–0.87) was also higher than that of the Cornell voltage index (0.54, 95% CI 0.50–0.58) and Sokolow-Lyon criteria (0.38, 95% CI 0.34–0.42); and the specificity of the Peguero-Lo Presti criteria (0.90, 95% CI 0.87–0.92) was similar to that of the Cornell voltage index (0.93, 95% CI 0.88–0.96) and Sokolow-Lyon criteria (0.97, 95% CI 0.90–0.99). Both the likelihood ratio and posttest probability of the Peguero-Lo Presti criteria and Cornell voltage index were moderate.Conclusion: Based on this systematic review and meta-analysis, the Peguero-Lo Presti criteria-based ECG diagnostic method for LVH has high sensitivity, specificity and diagnostic accuracy and should be applied in clinical practice settings.

Excessive neutrophil extracellular trap (NET) formation is an important contributor to sepsis-induced acute lung injury (ALI). Recent reports indicate that platelets can induce neutrophil extracellular trap formation. However, the specific mechanism remains unclear. Tph1 gene, which encodes the rate-limiting enzyme for peripheral 5-hydroxytryptophan (5-HT) synthesis, was knocked out in mice to simulate peripheral 5-HT deficiency. Cecal ligation and puncture (CLP) surgery was performed to induce sepsis. We found that peripheral 5-HT deficiency reduced NET formation in lung tissues, alleviated sepsis-induced lung inflammatory injury, and reduced the mortality rate of CLP mice. In addition, peripheral 5-HT deficiency was shown to reduce the accumulation of platelets and NETs in the lung of septic mice. We found that platelets from wild-type (WT), but not Tph1 knockout (Tph1^−/−), mice promote lipopolysaccharide (LPS)-induced NET formation. Exogenous 5-HT intervention increased LPS-induced NET formation when Tph1^−/− platelets were co-cultured with WT neutrophils. Therefore, our study uncovers a mechanism by which peripheral 5-HT aggravated sepsis-induced ALI by promoting NET formation in the lung of septic mice.

The aim of this study was to estimate the association between blood urea nitrogen (BUN) and clinical prognosis in patients with COVID-19. A multicenter, retrospective study was conducted in adult patients with COVID-19 in 3 hospitals in Zhenjiang from January 2023 to May 2023. Patients were divided into survival and death group based on whether they survived at day 28. The demographic, comorbidities, and laboratory data were independently collected and analyzed, as well as clinical outcomes. Total 141 patients were enrolled and 23 (16.3%) died within 28 days. Patients who died within 28 days had a higher level of BUN compared with survivors. Bivariate logistic regression analysis showed that BUN was a risk factor for 28-day mortality in patients with COVID-19. ROC curve showed that BUN could predict 28-day mortality of COVID-19 patients (AUC = 0.796, 95%CI: 0.654–0.938, P < .001). When the cutoff value of BUN was 7.37 mmol/L, the sensitivity and specificity were 84.62% and 70.31%. Subgroup analysis demonstrated that hyper-BUN (≥7.37 mmol/L) was associated with increased 28-day mortality among COVID-19 patients. Patients with COVID-19 who died within 28 days had a higher level of BUN, and hyper-BUN (≥7.37 mmol/L) was associated with increased 28-day mortality.

Background: Sepsis is characterized by upregulated lipolysis in adipose tissue and a high blood triglyceride (TG) level. It is still debated whether serum TG level is related to mortality in septic patients. The aim of this study is to investigate the association between serum TG level and mortality in septic patients admitted to the intensive care unit (ICU). Methods: Data from adult septic patients (≥18 years) admitted to the ICU for the first time were obtained from the Multiparameter Intelligent Monitoring in Intensive Care IV (MIMIC-IV) database. The patients’ serum TG levels that were measured within the first week after ICU admission were extracted for statistical analysis. The endpoints were 28-day, ICU and in-hospital mortality. Results: A total of 2,782 septic patients were included. Univariate analysis indicated that the relationship between serum TG levels and the risk of mortality was significantly nonlinear. Both the Lowess smoothing technique and restricted cubic spline analyses revealed a U-shaped association between serum TG levels and mortality among septic patients. The lowest mortality rate was associated with a serum TG level of 300–500 mg/dL. Using 300∼500 mg/dL as the reference range, we found that both hypo-TG (<300 mg/dL) and hyper-TG (≥500 mg/dL) were associated with increased mortality. The result was further adjusted by Cox regression with and without the inclusion of some differential covariates. Conclusions: There was a U-shaped association between serum TG and mortality in septic ICU patients. The optimal concentration of serum TG levels in septic ICU patients is 300–500 mg/dL.

Uncontrolled formation of neutrophil extracellular traps (NETs) is one of the main mechanisms leading to death in septic patients. PFKFB3, a notable enzyme of glycolysis metabolism, is involved in the inflammatory activation of granulocytes. Our previous studies demonstrated that PFKFB3-involved glycolytic metabolism supports CXCR4^hi neutrophil inflammatory activation, which is a key mechanism for the inflammatory injury of the lungs induced by sepsis. However, the specific mechanism by which PFKFB3 supports NET formation in sepsis remains unclear. Here, we found that high expression of neutrophil PFKFB3 is essential for sepsis-induced NET formation. Further mechanistic studies revealed that PFKFB3 promoted sepsis-related NET formation via glycolytic reprogramming and peptidylarginine deiminase 4 (PAD4)-dependent chromatin decondensation. However, inhibiting glycolytic metabolism supported by PFKFB3 can significantly reduce PAD4-dependent NET formation and alleviate sepsis-related lung inflammatory damage. In summary, our results revealed that PFKFB3-supported glycolytic metabolism promotes sepsis-induced NET formation via PAD4-mediated chromatin decondensation. Targeting PFKFB3-supported glycolysis represents a potential strategy to alleviate sepsis-induced hyperinflammation and tissue damage.