Background. Heart failure (HF) is a common cardiovascular disease, which is related to systemic inflammation for decades. Fibrinogen (FIB) is a sign of thrombosis and inflammation, which is associated with the prognosis of many diseases. Nevertheless, the role of fibrinogen level in the prognosis of critically ill patients with acute exacerbation of chronic heart failure is unclear. Methods. The data are from the Medical Information Mart for Intensive Care III (MIMIC III) database, which is a freely accessible critical care database. The primary outcome in our study was 90-day mortality. The prognostic value of fibrinogen was analyzed with receiver operating characteristic (ROC) curve analysis, Kaplan-Meier curve, and Cox model. Results. A total of 554 patients were included. Patients were divided into two groups, low fibrinogen level (<284 mg/dl) and high fibrinogen level (≥284 mg/dl), through the cut-off value of the ROC curve. The area under the ROC curve of fibrinogen for predicting 90-day mortality was 0.65 (95% CI: 0.59–0.70). In the unadjusted Cox model, compared with the low fibrinogen level (<284 mg/dl), the 90-day mortality of the hazard ratio (HR) with 95% confidence intervals (CI) of the high fibrinogen level is 3.33 (95% CI 2.15-5.15). In different multivariable Cox models, compared with the low fibrinogen level (<284 mg/dl), the 90-day mortality of the hazard ratio of the high fibrinogen level is from 2.83 to 3.13. In subgroup analyses, significant interactions were observed only in age, chronic kidney disease (CKD), and APS III scores. Conclusion. Our data suggest that high fibrinogen levels (≥284 mg/dl) independently predict mortality in critically ill patients with acute exacerbation of chronic heart failure. Our findings need to be further validated by large prospective studies and longer follow-up time.

Background Previous studies have shown that inflammation plays an important role in atherosclerosis and cardiovascular disease. Platelet to lymphocyte ratio (PLR) has been reported as a novel inflammatory marker. However, it is not clear whether PLR is associated with short‐term all‐cause mortality in critically ill patients with non‐ST‐segment elevation myocardial infarction (NSTEMI). Methods The data for the study is from the Medical Information Mart for Intensive Care III database. The primary outcome in our study was 28‐day mortality. Kapan‐Meier curve, lowess smoother curve, and multivariate Cox regression models were used to determine whether the association between PLR and 28‐day mortality of critically ill patients with NSTEMI. Results A total of 1273 critically ill patients with NSTEMI were included in this analysis. Kapan‐Meier curve and lowess smoother curve show that high PLR is associated with an increased risk of 28‐day all‐cause mortality. The study population is divided into two groups according to the cut‐off value of PLR level. In the Cox model, high PLR levels (PLR≥195.8) were significantly associated with increased 28‐day mortality (HR 1.54; 95%CI 1.09–2.18, p = .013). In quartile analyses, the HR (95% CI) for the third (183 ≤ PLR < 306) and fourth quartile (PLR≥306) was 1.55 (1.05–2.29) and 1.61 (1.03–2.52), respectively, compared to the reference group(111 ≤ PLR < 183). In subgroup analyses, there is no interaction effect in most of the subgroups except for respiratory failure and vasopressor use. Conclusion High PLR is associated with an increased risk of short‐term mortality in critically ill patients with NSTEMI.

Acute myocardial infarction (AMI) in patients with acute kidney injury (AKI) is associated with poor long-term outcome. However, the short-term prognosis of AKI in patients with ST-elevation AMI (STEMI) needs to be explored further. We assessed this relationship between these patients and short-term mortality in relation to AKI and chronic kidney disease (CKD). All data were extracted from the Medical Information Mart for Intensive Care III database. The primary outcome was 28-day mortality. Kaplan-Meier curves, logistic regression models, and propensity score matching analysis were used to evaluate the associations between AKI in patients with STEMI and outcomes. A total of 1031 patients with STEMI met the inclusion criteria. For 28-day mortality, in the multivariable logistic regression models, the odds ratio (95% CI) of group 2 (AKI but no CKD) and group 3 (AKI in the presence of CKD) were 3.24 (1.46-7.18) and 4.57 (1.83-11.37), respectively, compared with group 1 (no AKI and no CKD). Comorbid AKI increased the risk of short-term mortality among patients with STEMI, especially for those with AKI in the presence of CKD.