Background and purposePrevious studies have described an association between pulse pressure (PP) level and mortality in stroke patients. Evidence of associations between PP level and the risk of mortality remains unknown in non-traumatic subarachnoid hemorrhage (SAH) patients. We aimed to explore the relationship between the baseline PP level and hospital mortality.MethodsThis cohort study of 693 non-traumatic SAH adults used Medical Information Mart for Intensive Care (MIMIC-IV) data from 2008–2019 admissions to Intensive Care Unit (ICU). PP level was calculated as the first value after admission to the ICU. The endpoint of the study was in-hospital mortality. Cox proportional hazards models were utilized to analyze the association between baseline PP level and hospital mortality. Restricted Cubic Splines (RCS) analysis was utilized to determine the relationship curve between hospital mortality and PP level and examine the threshold saturation effect. We further applied Kaplan–Meier survival curve analysis to examine the consistency of these correlations. The interaction test was used to identify subgroups with differences.ResultsThe mean age of the study population was 58.8 ± 14.6 years, and 304 (43.9%) of participants were female. When baseline PP level was assessed in quartiles, compared to the reference group (Q1 ≤ 56 mmHg), the adjusted hazard ratio (HR) in Q2 (57–68 mmHg), Q3(69–82 mmHg), Q4 (≥83 mmHg) were 0.55 (95% CI: 0.33–0.93, p = 0.026), 0.99 (95% CI, 0.62–1.59, p = 0.966), and 0.99 (95% CI: 0.62–1.59, p = 0.954), respectively. In the threshold analysis, for every 5 mmHg increase in PP level, there was an 18.2% decrease in hospital mortality (adjusted HR, 0.818; 95% CI, 0.738–0.907; p = 0.0001) in those with PP level less than 60 mmHg, and a 7.7% increase in hospital mortality (adjusted HR, 1.077; 95% CI, 1.018–1.139; p = 0.0096) in those with PP level was 60 mmHg or higher.ConclusionFor patients with non-traumatic SAH, the association between baseline PP and risk of hospital mortality was non-linear, with an inflection point at 60 mmHg and a minimal risk at 57 to 68 mmHg (Q2) of baseline PP level.

ObjectivePrevious studies linking Triglyceride Glucose (TyG) Index to carotid plaque have yielded inconsistent results. Moreover, related studies on the population of Japan are rare. This study aims to provide further results.DesignA hospital-based cross-sectional study.SettingThe Shin Takeo Hospital.ParticipantsWe assessed 1904 Japanese participants (988 men and 916 women) whose mean age was 57±11.9 years, and those participants underwent health check-ups at Shinbuf Hospital at Shin Takeo Hospital from 1 April 2016 to 31 October 2017.MethodologyCarotid plaque, triglyceride and fasting glucose and other relevant indicators were collected. We used ultrasonography to evaluate carotid plaque. A multivariable logistic regression model and generalised additive model were used to evaluate the association between the TyG Index and carotid plaque. Subgroup and interaction analyses were validated for the consistency of these correlations.ResultsFollowing the adjustment of traditional carotid plaque risk factors, the non-linear relationship between the TyG Index and carotid plaque was investigated. Using a two-piecewise regression model, we calculated the inflection point to be 9.06. The OR and 95% CIs for the inflection points on the left and right sides were 1.70 (1.27 to 2.29) and 0.88 (0.52 to 1.47), respectively. According to the variables tested, the interactions between the TyG Index and all subgroup factors were analysed and significant interactions were not observed.ConclusionIn individuals who underwent a comprehensive check-up in Japan, the relationship between the TyG Index and carotid plaque is non-linear. When the TyG Index is less than 9.06, it is associated with carotid plaque.

BackgroundIn patients with ischemic stroke, low hemoglobin-to-red blood cell distribution width ratio (HRR) was associated with an increased risk of mortality. However, it was unknown in the non-traumatic subarachnoid hemorrhage (SAH) population. The purpose of this study was to examine the association between baseline HRR and in-hospital mortality in patients with non-traumatic SAH.MethodsNon-traumatic SAH patients were screened out of the Medical Information Mart for Intensive IV (MIMIC-IV) database between 2008 and 2019. The Cox proportional hazard regression models were utilized to analyze the association between baseline HRR and in-hospital mortality. Restricted cubic splines (RCS) analysis was utilized to determine the relationship curve between hospital mortality and the HRR level and examine the threshold saturation effect. We further applied Kaplan–Meier survival curve analysis to examine the consistency of these correlations. The interaction test was used to identify subgroups with differences.ResultsA total of 842 patients were included in this retrospective cohort study. Compared with individuals with lower HRR Q1 ( ≤ 7.85), the adjusted HR values in Q2 (7.86–9.15), Q3 (9.16–10.16), and Q4 (≥10.17) were 0.574 (95% CI: 0.368–0.896, p = 0.015), 0.555 (95% CI: 0.346–0.890, p = 0.016), and 0.625 (95% CI: 0.394–0.991, p = 0.045), respectively. The association between the HRR level and in-hospital mortality exhibited a non-linear relationship (p < 0.05). The threshold inflection point value of 9.50 was calculated using RCS analysis. When the HHR level was lower than 9.50, the risk of in-hospital mortality rate decreased with an adjusted HR of 0.79 (95% CI: 0.70–0.90, p = 0.0003). When the HRR level was higher than 9.50, the risk of in-hospital mortality almost hardly increased with the increase in the HRR level (adjusted HR = 1.18, 95% CI: 0.91–1.53, p = 0.2158). K-M analysis showed that patients with low HRR levels had significantly higher in-hospital mortality (p < 0.001).ConclusionThere was a non-linear connection between the baseline HRR level and in-hospital mortality. A low level of HRR could increase the risk of death in participants with non-traumatic SAH.

Background and aims LDL-C/HDL-C ratio predicted atherosclerosis progression better than LDL-C or HDL-C alone. However, the association between LDL-C/HDL-C ratio and Carotid Atherosclerosis(CA) is still controversial. There is a lack of research on this topic in theAsymptomatic Japanese Population. This study aims to provide further results. Methods The study population was a cross-sectional study of 1904 subjects free of cardio-cerebrovascular disease at baseline(mean age 57±11.9 years, 51.9% male). All participant sultrasonography of the carotid artery. The presence of carotid plaque score(PS) aand plaque number (PN) were evaluated by ultrasonography. Multivariate logistic regression models to estimatethe LDL-C/HDL-C ratio and PS relationship. Participants were stratified into three groups based on LDL-C/HDL-C ratio tertiles. Interaction and stratified analyses were conductedaccording to age, sex, smoking status, drinking status, fatty, and histories of diabetes. Results In regression models and after multiple adjustments, the risk of PS was significantly associated with serum LDL-C/HDL-C ratio levels in which LDL-C/HDL-C ratio was included as a categorical variable. It remained significant for the highest vs the first tertile of the LDL-C/HDL-C ratio (OR=1.50, 95% CI 1.04–2.17). Stratified analysis,we found that the association was more significant aged <65 years old, female and non-diabetes subgroups.Interaction analysis showed no interaction between LDL-C/HDL-C ratio and PS in the fatty,smoking, and drinking subgroups. Conclusions In conclusion, LDL-C/HDL-C ratio is an independent risk factor for CA in the Japanese population. A prospective and randomized clinical trial of LDL-C/HDL-C ratio lowering therapy in the Japanese population is needed to assess the causal nature of the relationship.