Machine learning-based models for predicting mortality and acute kidney injury in critical pulmonary embolism.

OBJECTIVES: We aimed to use machine learning (ML) algorithms to risk stratify the prognosis of critical pulmonary embolism (PE). MATERIAL AND METHODS: In total, 1229 patients were obtained from MIMIC-IV database. Main outcomes were set as all-cause mortality within 30 days. Logistic regression (LR) and simplified eXtreme gradient boosting (XGBoost) were applied for model constructions. We chose the final models based on their matching degree with data. To simplify the model and increase its usefulness, finally simplified models were built based on the most important 8 variables. Discrimination and calibration were exploited to evaluate the prediction ability. We stratified the risk groups based on risk estimate deciles. RESULTS: The simplified XGB model performed better in model discrimination, which AUC were 0.82 (95% CI: 0.78-0.87) in the validation cohort, compared with the AUC of simplified LR model (0.75 [95% CI: 0.69-0.80]). And XGB performed better than sPESI in the validation cohort. A new risk-classification based on XGB could accurately predict low-risk of mortality, and had high consistency with acknowledged risk scores. CONCLUSIONS: ML models can accurately predict the 30-day mortality of critical PE patients, which could further be used to reduce the burden of ICU stay, decrease the mortality and improve the quality of life for critical PE patients.

Critical appraisal of international guidelines for the screening and treatment of asymptomatic peripheral artery disease: a systematic review.

BACKGROUND: Peripheral artery disease (PAD) is often asymptomatic but increases the risk of developing cardiovascular events. Due to the uncertainties regarding the quality of related guidelines and a lack of clear-cut evidence, we performed a systematic review and critical appraisal of these guidelines to evaluate their consistency of the recommendations in asymptomatic PAD population. METHODS: Guidelines in English between January 1st, 2000 to December 31th, 2017 were screened in databases including Medline via PubMed, EMBASE, the G-I-N International Guideline Library, the National Guidelines Clearinghouse, the Canadian Medication Association Infobase and the National Library for Health. Those guidelines containing recommendations on screening and treatment for asymptomatic PAD were included, and three reviewers evaluated the quality of the guidelines using Appraisal of Guidelines Research and Evaluation (AGREE) II instrument. Related recommendations were then fully extracted and compared by two reviewers. RESULTS: Fourteen guidelines were included finally and the AGREE scores ranged from 39 to 73%. Most of included guidelines scored low in Rigor of development and Editorial independence, and only two guidelines (ACCF/AHA, AHA/ACC) reached the standard on Conflict of Interest from Institute of Medicine (IOM). Eight guidelines recommended screening at different strength while the others found insufficient evidence or were against screening. Conflicting recommendations on treatment were found in the target value of the lipid lowering and antiplatelet therapy. The treatment policies in three guidelines (BWG, CEVF, ESC) appeared more aggressive, but they had low transparency between guideline developer and industry or did not reach the standard of IOM. CONCLUSIONS: Current guidelines on asymptomatic PAD varied in the methodological quality and fell short of the standard in the rigor of development and editorial independence. Conflicting recommendations were found both on the screening and treatment. More effort is needed to provide clear-cut evidences with high quality and transparency among guideline developer and industry.

Serum anion gap on admission predicts intensive care unit mortality in patients with aortic aneurysm.

It has been widely reported that the serum anion gap is significantly associated with mortality in intensive care unit (ICU); however, it remains unknown whether the association is present in aortic aneurysm (AA) patients. The present study aimed to investigate the association between the admission serum anion gap and ICU mortality in AA patients. Data extracted from a publicly accessible clinical database using a modifiable data mining technique were analyzed retrospectively, mainly by employing multivariable logistic regression analysis. The primary study outcome was ICU mortality. A total of 273 patient records were analyzed. The ICU mortality was 8.79% (24/273). The median serum anion gap was significantly higher in non-survivors [17.50 mEq/l, interquartile range (IQR) 15.75-22.50 mEq/l] compared with survivors [13.00 mEq/l, IQR 11.00-15.00 mEq/l, P<0.001]. Multivariate analysis resulted in identification of a clear association between admission serum anion gap and ICU mortality in AA patients [odds ratio (OR) 1.38 per 1 mEq/l increase, 95% confidence interval (CI) 1.08-1.76]. The area under the receiver operating characteristic curve showed an outstanding discrimination ability in predicting ICU mortality (area under curve 0.8513, 95% CI 0.7698-0.9328). In conclusion, admission serum anion gap may serve as a strong predictor of ICU mortality for AA patients.

Serum uric acid on admission cannot predict long-term outcome of critically ill patients: a retrospective cohort study.

PURPOSE: We aimed to evaluate the association of serum uric acid on admission with long-term outcome of critically ill patients. MATERIALS AND METHODS: We conducted a retrospective cohort study using data extracted from the Medical Information Mart for Intensive Care III database. The primary endpoint was 90-day mortality. Propensity score matching (PSM) was performed, and multivariate Cox regression analysis was used to adjust for potential confounders. Receiver operating characteristic (ROC) curves were also used to assess the mortality predictions. RESULTS: A total of 2,123 patients were included finally with a PSM cohort consisting of 556 90-day non-survivors matched 1:1 with 556 90-day survivors. No statistically significant difference of median admission uric acid was observed between the two groups (survivors 5.50 mg/dL vs non-survivors 5.60 mg/dL, p=0.536). ROC area under the curve was 0.511 (95% confidence interval [CI] 0.477-0.545), suggesting that uric acid had poor discriminative powers for predicting 90-day mortality. No significant association between uric acid and 90-day mortality was found (hazard ratio 1.00, 95% CI 0.98-1.03, p=0.6835). CONCLUSION: Serum uric acid on intensive care unit admission failed to predict 90-day mortality of critically ill patients.

Berberine Attenuates NLRP3 Inflammasome Activation in Macrophages to Reduce the Secretion of Interleukin-1ß.

OBJECTIVES: The purpose of this study is to evaluate whether Berberine can suppress the inflammatory response in atherosclerosis lesions and its potential associated signaling pathways and mechanism of action. METHODS: We isolated human peripheral blood mononuclear cells. After co-culturing them with ox-LDL stimulated cells, ROS was measured by its fluorescence intensity and NADPH oxidase activity was detected by the OD value from the spectrophotometer. Human peripheral blood mononuclear cells were then pretreated with different concentrations of berberine after treatment with NLRP3 activator ATP. Western blot was used to measure the releas of IL-1ß. We also used confocal microscopy to detect the nuclear import of NF-kB in macrophages. RESULTS: In this study we observed that berberine suppressed IL-1ß secretion that was induced by the activation of the NLRP3 inflammasome in macrophages. In addition, we demonstrated that berberine may possibly reduce reactive oxygen species (ROS)-dependent NLRP3 inflammasome activation. Moreover, Berberine inhibited the expression of pro-IL-1ß through inhibition of the nuclear factor κb (NF-κB) pathway, which prevented the priming IL-1ß secretion. CONCLUSION: Our results suggest that berberine alleviates NLRP3 inflammation activation by reducing IL-1ß secretion from macrophages, which could be an important therapeutic target in atherosclerosis.