The stress hyperglycemia ratio (SHR), a dynamic biomarker of acute glucose dysregulation, has been established as a predictor of adverse acute outcomes. However, its longitudinal associations with chronic disease development, particularly in middle-aged and older populations, remain insufficiently characterized.

This nationwide prospective cohort study analyzed data from 8942 adults aged ≥ 45 years in the China Health and Retirement Longitudinal Study (CHARLS). We established 14 disease-specific cohorts to the relationship between SHR and new-onset chronic conditions. Multivariable-adjusted Cox proportional hazards models with restricted cubic splines were utilized to estimate hazard ratios (HRs) per standard deviation (SD) increase in SHR, supported by comprehensive sensitivity analyses and subgroup stratifications.

Elevated SHR levels were significantly associated with increased risks of incident hypertension (HR = 1.30, 95% CI: 1.06-1.60; P < 0.001), dyslipidemia (HR = 1.43, 95% CI: 1.17-1.74; P < 0.001), diabetes (HR = 2.30, 95% CI: 1.82-2.91; P < 0.001), and liver disease (HR = 1.65, 95% CI: 1.21-2.26; P = 0.002). Conversely, elevated SHR levels correlated with a lower risk of lung disease (HR = 0.67, 95% CI: 0.50-0.89; P = 0.006). Restricted cubic spline analyses revealed a nonlinear relationship between SHR and diabetes risk (P-nonlinear = 0.02), while linear associations were observed for other outcomes. Subgroup analyses demonstrated consistency across demographic strata (P-interaction > 0.05).

SHR demonstrates disease-specific associations with chronic disease development, indicating its potential value as a predictive marker for clinical risk assessment.

Prognostic significance of stress hyperglycemia ratio (SHR) has not been well studied in patients with type 2 diabetes mellitus (T2DM) and acute coronary syndromes (ACS).

We prospectively measured admission fasting blood glucose (AFBG) and glycated hemoglobin A1c (HbA1c), and retrospectively calculated the stress hyperglycemia ratio (SHR, = AFBG/[1.59 × HbA1c (%) - 2.59]) in 791 patients with T2DM and ACS undergoing percutaneous coronary intervention (PCI). The primary endpoint was defined as major adverse cardiovascular and cerebrovascular events (MACCE), including all-cause mortality, non-fatal stroke, non-fatal myocardial infarction, and unplanned repeat coronary revascularization.

The mean age of the study population was 61 ± 10 years, and 72.8% were male. Over a median follow-up of 927 days, 194 patients developed at least one primary endpoint event. The follow-up incidence of MACCE increased in parallel with SHR tertiles (15.6%, 21.9%, and 36.1%, respectively; P for trend < 0.001). The Cox proportional hazards regression analysis adjusted for multiple confounding factors showed hazard ratios for MACCE of 1.525 (95% CI: 1.009-2.305; P = 0.045) for the middle tertile and 2.525 (95% CI: 1.729-3.687; P < 0.001) for the highest tertile of SHR, with the lowest tertile as the reference. The addition of SHR to the baseline reference prediction model improved model predictive performance markedly (C-statistic: increased from 0.704 to 0.721; cNRI: 0.176 [95% CI: 0.063-0.282], P = 0.002; IDI: 0.030 [95% CI: 0.009-0.063], P = 0.002).

SHR was independently and significantly associated with adverse cardiovascular outcomes in T2DM and ACS patients who underwent PCI, and had an incremental effect on the predictive ability of the baseline reference prediction model.

Acute hyperglycemia on admission is frequently observed during the early phase after acute myocardial infarction (MI), even without the history of diabetes mellitus. We previously reported that inhibiting Na+/H+ exchanger 1 (NHE1) activity post-MI may improve outcomes, but not in the setting of MI with acute hyperglycemia. However, the precise role of NHE1 in the pathophysiology of MI with acute hyperglycemia remains to be elucidated, and there are no effective strategies for its prevention or treatment.

We analyzed 85 post-MI patients, identifying acute hyperglycemia (glucose > 7 mM) in non-diabetic individuals, linked to elevated BNP, CK-MB, and reduced plasma Na+. Using retrospective cohort studies and MI with acute hyperglycemia mouse models, we demonstrated that hyperglycemia exacerbates myocardial injury by reducing extracellular Na+, increasing intracellular Na+, and elevating pH, suggesting NHE1 activation as inferred from the observed intracellular pH (pHi) shift. Cardiomyocyte-specific NHE1 ablation or pharmacological inhibition worsened cardiac dysfunction and fibrosis in MI with acute hyperglycemia, while NHE1 overexpression conferred protection. RNA sequencing and drug screening identified accelerated NHE1 activation via 3% NaCl and lithospermic acid (LA) as a novel strategy to mitigate cardiomyocyte necroptosis, alleviating ischemic injury in MI and ischemia reperfusion models. Hypoxia-hyperglycemia and necroptosis induction models in NHE1-knockout, NHE1-overexpressing, and MLKL-overexpressing cardiomyocytes revealed that NHE1 activation, unlike its protective role in oxygen-glucose deprivation, promotes MLKL degradation via autophagosome-lysosomal pathways, reducing cardiomyocyte death. MLKL knockout and MLKL-NHE1 double knockout mice confirmed that MLKL ablation counteracts NHE1 inhibition's detrimental effects.

Activation of myocardial NHE1 promotes MLKL autophagic degradation, mitigating cardiomyocyte necroptosis and acute hyperglycemia-exacerbated MI, highlighting NHE1 as a hyperglycemia-dependent cardioprotective target. Moderate NHE1 activation may represent a novel therapeutic strategy for MI with acute hyperglycemia.

The Stress Hyperglycemia Ratio (SHR) is associated with poor outcomes in coronary artery disease patients, but its link to Acute Myocardial Infarction (AMI) prognosis is unclear. This study explores the relationship between SHR and 1-year outcomes after AMI using a large cohort analysis.

This retrospective study enrolled 4012 AMI patients from General Hospital of Ningxia Medical University(2016-2019). These patients were stratified into three distinct groups according to the tertiles of the SHR: Group T1 (SHR < 0.90, n=1337), Group T2 (0.90 ≤ SHR < 1.11, n=1337), and Group T3 (SHR ≥ 1.11, n=1338). All patients were clinically followed for 1-years to collect major adverse cardiovascular and cerebrovascular events (MACCE). After controlling for different confounding factors, cox regression models and restricted quadratic splines were used to investigate the relationship between SHR and 1-years clinical outcomes.

During the 1-year follow-up, 229 all-cause deaths were recorded, yielding a mortality rate of 5.71% (n=229). Additionally, 861 MACCE were recorded, yielding a MACCE rate of 21.46%. After adjusting for covariates, SHR was found to be significantly associated with 1-year MACCE [hazard ratio (HR) = 2.18; 95% confidence interval (CI) = 1.64-2.89; P < 0.001] and all-cause mortality (HR = 3.11; 95% CI = 1.77-5.46; P < 0.001) in patients with AMI, and the T3 group exhibited a higher risk of 1-year MACCE (HR = 1.67; 95% CI = 1.34-2.09; P < 0.001) and all-cause mortality (HR = 1.67; 95% CI = 1.02-2.73; P =0.042) compared with T1 group. A J-shaped relationship was observed between SHR and 1-year MACCE as well as all-cause mortality, showing a turning point at 0.87. Beyond this threshold, the hazard ratio for 1-year MACCE was 2.64 (95% CI: 1.91-3.65), and for all-cause mortality was 4.26 (95%: CI 2.30-7.86). The results remained consistent across subgroup.

SHR is significantly and positively associated with one-year clinical outcomes in patients with AMI. Furthermore, there is a specific non-linear association between SHR and MACCE and all-cause mortality (both inflection point 0.87). Interventions aimed at reducing SHR levels below 0.87 through medication management have the potential to significantly improve outcomes.

Blood glucose and serum albumin can be biomarkers at admission since they are easily accessible and demonstrate correlations with cardiovascular diseases. The predictive ability of the admission blood glucose to albumin ratio (AAR) for long-term prognosis in patients with acute coronary syndrome (ACS) and its potential to elevate the predictive value of the Global Registry of Acute Coronary Events (GRACE) risk score in ACS patients post-percutaneous coronary intervention (PCI) remains unknown. Hence, this study aimed to investigate the incremental prognostic value of the AAR in patients with ACS undergoing PCI.

A rigorous development-validation approach was implemented to optimize the GRACE risk score, utilizing the AAR parameter in 1498 patients suffering from ACS after PCI at the Third People's Hospital of Chengdu, Sichuan, China.

Over a median of 31.25 (27.53, 35.10) months, the incidence of major adverse cardiac events (MACEs), defined as a composite outcome encompassing all-cause death, cardiac death, nonfatal myocardial infarction, nonfatal stroke, and unplanned repeat revascularization, was higher in individuals with higher AARs. Thus, the AAR was an independent predictor of long-term prognosis in ACS patients undergoing PCI (HR, 1.145; 95% CI: 1.045-1.255; p = 0.004). The integration of the AAR score with the GRACE risk score increased the C statistic from 0.717 (95% CI: 0.694-0.740) to 0.733 (95% CI: 0.690-0.776) (p < 0.01).

The AAR is an independent predictor of prognosis in ACS patients and significantly increased the predictive value of the GRACE risk score.

Serum osmolality (SOSM) is an indicator of hydration status and is associated with the prognosis of various cardiovascular diseases. This study investigated the association between SOSM and all-cause mortality in critically ill patients with myocardial infarction (MI).

This retrospective cohort study utilized data from the Medical Information for Intensive Care-IV (MIMIC-IV) database, including critically ill patients with a primary diagnosis of MI. Patients were categorized into tertile groups based on the SOSM levels. Kaplan-Meier (K-M) survival analysis, multiple Cox regression models, restricted cubic spline (RCS) analysis, and threshold effect analysis were used to investigate the nonlinear relationship between all-cause mortality in critically ill patients with MI and SOSM.

A total of 5354 patients with MI were included. K-M survival analysis showed that the survival rate of the high SOSM group was significantly lower than that of the other groups, which was consistent with the results after IPTW correction (log-rank P<0.05). Multiple Cox regression confirmed that patients with high SOSM had significantly increased risk of death at 30-day [HR, 1.45 (95% CI 1.21-1.73) P<0.001], 180-day [HR, 1.32 (95% CI 1.15-1.53) P<0.001], and 365-day [HR, 1.31(95% CI1.15-1.49) P<0.001]. RCS analysis and threshold effect analysis showed a J-shaped relationship between SOSM and mortality risk, and the minimum threshold of SOSM was 286.28 mmol/L.

This study revealed a J-shaped relationship between SOSM and all-cause mortality in critically ill MI patients, suggesting its potential as a prognostic marker for risk stratification.

Low blood glucose levels and high urea nitrogen levels affect patient prognosis, but few studies have investigated whether the blood urea nitrogen to glucose (BGR) ratio predicts the risk of death.This retrospective research examined the connection between the BGR and 365-day mortality in patients with chronic kidney disease (CKD) stages 1-4 admitted to an intensive care unit (ICU). The study utilized data from 6,380 patients in the Medical Information Mart for Intensive Care IV version 2.2 (MIMIC-IV v2.2), taking into account confounding factors such as demographics, vital signs, laboratory indicators, and comorbidities. The study employed both univariate and multivariate Cox regression analyses stratified by BGR quartiles. Additionally, restricted cubic spline regression and inflection point analysis were used to explore the linear relationship between BGR and 365-day mortality, while Kaplan-Meier curve analysis was used to observe mortality changes under different BGR stratifications. Subgroup and mediating effect analyses were performed to evaluate the robustness of BGR's effect on 365-day mortality. The study found a cumulative 365-day mortality rate of 34.2% among CKD stages 1-4 patients, with a 2.43-fold increase in the risk of death associated with BGR and at least a 44% increase in the risk of death for each unit increase in BGR (P = 0.022). A significant nonlinear relationship was identified, showing a stepwise change in the risk of death with a marked increase in the slope of the curve for BGR values below 0.52 and above 0.9 (P < 0.001). Subgroup analyses indicated interactions between BGR and factors such as age, sepsis, first-day antibiotic use, and cerebrovascular disease (P < 0.05). In conclusion, this study confirms that BGR is a significant and stable predictor of 1-year mortality risk in patients with CKD stages 1-4. Interventions aimed at timely adjustment, correction of metabolic imbalances, reduction of inflammation, and management of BGR levels are beneficial for reducing mortality in this patient population.

Stress hyperglycemia is prevalent in critical illnesses and has been associated with adverse short- and long-term outcomes in individuals with acute coronary syndrome (ACS). However, there is limited evidence for the predictive value of stress hyperglycemia and hospitalization mortality in patients with chronic kidney disease (CKD) and ACS. This study aimed to explore the association between hospitalized mortality, stress hyperglycemia ratio (SHR), and admission blood glucose (ABG) in patients with CKD and ACS.

This study included 655 hospitalized patients who were diagnosed with ACS and CKD. Patients with incomplete data were excluded, resulting in the analysis of 550 patients. The primary outcome measured was in-hospital mortality.

The median age of the cohort included in the analysis was 71 years, with a male proportion of 66.2 %, and a mean estimated glomerular filtration rate (eGFR) of 27.8 mL/min/1.73 m2. Patients classified as having stage 3, stage 4, and stage 5 chronic kidney disease (CKD) comprised 46.9 %, 17.1 %, and 36.0 % of the population, respectively. The overall in-hospital mortality rate was 10.7 % (n = 59). Both SHR (OR = 2.67; 95 % CI 1.51-4.74; p < 0.001) and ABG (OR = 1.09; 95 % CI 1.04-1.14; p < 0.001) were significantly associated with in-hospital mortality in CKD and ACS patients. SHR and ABG showed a linear relationship with in-hospital mortality, with SHR demonstrating superior reclassification ability over ABG. The inclusion of SHR or ABG, irrespective of diabetes mellitus status, substantially enhanced the predictive performance of the Global Registry of Acute Coronary Events (GRACE) score model.

In patients with ACS and CKD, a robust correlation was observed between SHR, ABG, and in-hospital mortality. Both SHR and ABG improved the predictive accuracy of the GRACE score in forecasting inpatient mortality in this population.

Background The stress hyperglycemia ratio (SHR) indicates relative hyperglycemia levels. Research on the impact of SHR on mortality in coronary heart disease (CHD) patients in intensive care is limited. This study explores the predictive accuracy of SHR for the prognosis of CHD patients in the ICU. Methods This study included 2,059 CHD patients from the American Medical Information Mart for Intensive Care (MIMIC-IV) database. SHR was determined using the formula: SHR = (admission glucose) (mmol/L) / (1.59 * HbA1c [%] - 2.59). Subjects were stratified into quartiles based on SHR levels to examine the correlation between SHR and in-hospital mortality. The restricted cubic splines and Cox proportional hazards models were employed to assess this association, while Kaplan-Meier survival analysis was executed to ascertain the mortality rates across the SHR quartiles. Results Among the 2059 participants (1358 men), the rates of in-hospital and ICU mortality were 8.5% and 5.25%, respectively. Analysis showed SHR as a significant predictor of increased risk for both in-hospital (HR,1.16, 95% CI: 1.02-1.32, P = 0.022) and ICU mortality (HR, 1.16, 95% CI: 1.01-1.35, P = 0.040) after adjustments. A J-shaped relationship was noted between SHR and mortality risks (p for non-linearity = 0.002, respectively). Kaplan-Meier analysis confirmed substantial differences in in-hospital and ICU mortality across SHR quartiles. Conclusions SHR significantly predicts in-hospital and ICU mortality in critically ill CHD patients, indicating that higher SHR levels correlate with longer ICU stays and increased mortality. This underscores the potential of SHR as a prognostic marker for ICU CHD patients.

There has been a concerning rise in the incidence of major adverse cardiovascular and cerebrovascular events (MACCE) following noncardiac surgeries (NCS), significantly impacting surgical outcomes and patient prognosis. Glucose metabolism abnormalities induced by stress response under acute medical conditions may be a risk factor for postoperative MACCE. This study aims to explore the association between stress hyperglycemia ratio (SHR) and postoperative MACCE in patients undergoing general anesthesia for NCS.

There were 12,899 patients in this perioperative cohort study. The primary outcome was MACCE within 30 days postoperatively, defined as angina, acute myocardial infarction, cardiac arrest, arrhythmia, heart failure, stroke, or in-hospital all-cause mortality. Kaplan-Meier curves visualized the cumulative incidence of MACCE. Cox proportional hazard models were utilized to assess the association between the risk of MACCE and different SHR groups. Restricted cubic spline analyses were conducted to explore potential nonlinear relationships. Additionally, exploratory subgroup analyses and sensitivity analyses were performed.

A total of 592 (4.59%) participants experienced MACCE within 30 days after surgery, and 1,045 (8.10%) within 90 days. After adjusting for confounding factors, compared to the SHR T2 group, the risk of MACCE within 30 days after surgery increased by 1.34 times (95% CI 1.08-1.66) in the T3 group and by 1.35 times (95% CI 1.08-1.68) in the T1 group respectively. In the non-diabetes group, the risk of MACCE within 30 days after surgery increased by 1.60 times (95% CI 1.21-2.12) in the T3 group and by 1.61 times (95% CI 1.21-2.14) in the T1 group respectively, while no statistically significant increase in risk was observed in the diabetes group. Similar results were observed within 90 days after surgery in the non-diabetes group. Additionally, a statistically significant U-shaped nonlinear relationship was observed in the non-diabetes group (30 days: P for nonlinear = 0.010; 90 days: P for nonlinear = 0.008).

In this large perioperative cohort study, we observed that both higher and lower SHR were associated with an increased risk of MACCE within 30 and 90 days after NCS, especially in patients without diabetes. These findings suggest that SHR potentially plays a key role in stratifying cardiovascular and cerebrovascular risk after NCS.

We aimed to determine if hospital admission hyperglycaemia and hypoglycaemia are associated with increased long-term mortality.

A post-hoc analysis of data from a trial of glucose screening in the emergency department was conducted. Data were linked with a death registry up to 5 years after admission. The relationship between admission glucose and mortality was examined by cox regression. Further analyses of people who survived the admission and subsequent 28 days was performed.

There were 131,322 patients, of whom 38,712 (29.5 %) died. Mean follow-up was 3·3 ± 1·5 years. Compared to the reference glucose band of 6·1-8·0 mmol/L, there was increased mortality in higher bands, reaching a hazard ratio (HR) of 1·44 (95 %CI 1·34-1·55, p < 0·001) for people with glucose > 20·0 mmol/L. The HR was 1·56 (95 %CI 1·46-1·68, p < 0·001) for people with glucose ≤ 4·0 mmol/L. Similar relationships were observed among 28-day survivors. The relationships were attenuated among people with known diabetes. Among 4867 subjects with glucose ≥ 14·0 mmol/L, those diagnosed with diabetes during the admission had lower mortality compared to subjects where the diagnosis was not made (HR 0·53, 95 %CI 0·40-0·72, p < 0·001). This was attenuated among 28-day survivors.

Hyperglycaemia and hypoglycaemia on hospital admission are associated with increased long-term mortality.

Although blood glucose changes have been suggested to be a potential better target for clinical control than baseline blood glucose levels, the association of blood glucose changes with the prognosis in acute myocardial infarction (AMI) patients with diabetes mellitus (DM) is unclear. Herein, this study aimed to investigate association of short-term longitudinal trajectory of blood glucose with 30-day mortality in this population.

Data of AMI patients with DM were extracted from the Medical Information Mart for Intensive Care (MIMIC) database in 2003-2019 in this retrospective cohort study. The latent growth mixture modeling (LGMM) model was utilized to classify the 24-hour longitudinal trajectory of blood glucose of the patients. Kaplan-Meier (KM) curve was drawn to show 30-day mortality risk in patients with different trajectory classes. Univariate and multivariate Cox regression analyses were employed to explore the association of longitudinal trajectory of blood glucose within 24 hours after the ICU admission with 30-day mortality. Also, subgroups analysis of age, gender, and AMI types was performed. The evaluation indexes were hazard ratios (HRs) and 95% confidence intervals (CIs).

Among 1,523 eligible patients, 227 (14.9%) died within 30 days. We identified 4 longitudinal trajectories of blood glucose, including class 1 (a low initial average blood glucose level with steady trend within 24 hours), class 2 (a high initial average blood glucose with gently decreased trend), class 3 (the highest initial average blood glucose with rapidly decreased trend) and class 4 (a high initial average blood glucose level with the trend that increased at first and then decreased). After adjusting for covariates, an average blood glucose level of ≥200 mg/dL was linked to higher risk of 30-day mortality, comparing to that of <140 mg/dL (HR = 1.80, 95%CI: 1.23-2.63). Comparing to patients whose longitudinal trajectory of blood glucose conformed to class 1, those with class 2 (HR = 2.52, 95%CI: 1.79-3.53) or class 4 (HR = 3.53, 95%CI: 2.07-6.03) seemed to have higher risk of 30-day mortality. Additionally, these associations were also significant in aged ≥60 years old, female, male, NSTEMI, and STEMI subgroups (all P<0.05).

A low level of average blood glucose at the ICU admission or reducing blood glucose to a normal level quickly with adequate measures in 24 hours after ICU admission may be beneficial for AMI patients with DM to reduce the risk of 30-day mortality. These findings may provide some information for further exploration on appropriate range of blood glucose changes in clinical practice.

Acute hyperglycemia (HG) enhances inflammatory and oxidative stress and exacerbates myocardial infarct size during ischemia-reperfusion injury by activating splenic leukocytes. Formyl peptide receptor 1 (FPR1) on leukocytes is activated by and mediates myocardial ischemia-reperfusion injury. We hypothesize that selective FPR1 antagonist cinnamoyl-F-(D)L-F-(D)L-F (CF) or potent reducing agent tris (2-carboxyethyl) phosphine hydrochloride (TCEP) could abrogate hyperglycemic infarct exacerbation, both alone and synergistically via a novel CF-TCEP compound that would target leukocytes for antioxidative effect.

Acute HG was induced in wild type mice with an intraperitoneal dextrose injection followed by left coronary artery occlusion (30 min) and reperfusion (60 min). In treatment groups, CF (0.1 mg/kg or 1 mg/kg), TCEP (1 mg/kg or 20 mg/kg), or the CF-TCEP conjugate (0.1 mg/kg) was administered intravenously before reperfusion. The hearts were harvested to measure infarct size (IF).

HG resulted in >50% increase in IF compared to euglycemic mice (52.1 ± 3.0 versus 34.0 ± 3.2%, P < 0.05). Neither CF nor TCEP independently exerted an infarct-sparing effect at lower doses (46.2 ± 2.1% or 50.9 ± 4.1%, P > 0.05 versus HG control) but at high doses, significantly attenuated IF exacerbation (23.2 ± 5.2% or 33.9 ± 3.6%, P < 0.05 versus HG control). However, the low-dose CF-TCEP conjugate significantly reduced IF (39.1 ± 1.7%, P < 0.05 versus HG control). IF was decreased to near euglycemic control levels (P > 0.05).

The CF-TECP conjugate synergistically attenuated HG infarct exacerbation at significantly lower respective doses of CF and TCEP. In addition to the intrinsic anti-inflammatory effect of blocking FPR1, CF is also a feasible tool for leukocyte-targeted therapy to treat IRI.

Acute hyperglycemia is a transient increase in plasma glucose level (PGL) frequently observed in patients with ST-elevation myocardial infarction (STEMI). The aim of this review is to clarify the molecular mechanisms whereby acute hyperglycemia impacts coronary flow and myocardial perfusion in patients with acute myocardial infarction (AMI) and to discuss the consequent clinical and prognostic implications. We conducted a comprehensive literature review on the molecular causes of myocardial damage driven by acute hyperglycemia in the context of AMI. The negative impact of high PGL on admission recognizes a multifactorial etiology involving endothelial function, oxidative stress, production of leukocyte adhesion molecules, platelet aggregation, and activation of the coagulation cascade. The current evidence suggests that all these pathophysiological mechanisms compromise myocardial perfusion as a whole and not only in the culprit coronary artery. Acute hyperglycemia on admission, regardless of whether or not in the context of a diabetes mellitus history, could be, thus, identified as a predictor of worse myocardial reperfusion and poorer prognosis in patients with AMI. In order to reduce hyperglycemia-related complications, it seems rational to pursue in these patients an adequate and quick control of PGL, despite the best pharmacological treatment for acute hyperglycemia still remaining a matter of debate.

Lactate and glucose are widely used biochemical parameters in current predictive risk scores for cardiogenic shock. Data regarding the relationship between lactate and glucose levels in cardiogenic shock are limited. Thus, we aimed to analyze glucose and lactate as early markers for in-hospital mortality in cardiogenic shock. In this retrospective cohort study, 312 patients presenting with cardiogenic shock to a tertiary-care hospital between 2016 and 2018 were included. Apparent cardiogenic shock was defined as hypoperfusion with hemodynamic compromise and biochemical marker increase due to diminished tissue perfusion, corresponding to SCAI shock stages. In-hospital mortality was assessed as the primary endpoint. The median age of the study population was 71 (60-79) years and the etiology of cardiogenic shock was acute myocardial infarction in 45.8%. Overall in-hospital mortality was 67.6%. In the receiver operating curve analysis, the area under the receiver-operating curve (AUC) for prediction of in-hospital mortality was higher for lactate (AUC: 0.757) than for glucose (AUC: 0.652). Both values were significantly associated with outcome (groups created with best cutoff values obtained from the Youden index). Correlation analysis showed a significant non-linear association of both values. In a multivariable stepwise Cox regression analysis, lactate remained an independent predictor for in-hospital mortality, whilst glucose, despite being implicated in energy metabolism, was not independently predictive for mortality. Together, these data suggest that lactate at admission is superior for mortality prediction in patients with apparent cardiogenic shock. Glucose was not independently predictive for mortality.

Coronary three-vessel disease (CTVD) accounts for one-third of the overall incidence of coronary artery disease, with heightened mortality rates compared to single-vessel lesions, including common trunk lesions. Dysregulated glucose metabolism exacerbates atherosclerosis and increases cardiovascular risk. The stress hyperglycemia ratio (SHR) is proposed as an indicator of glucose metabolism status but its association with cardiovascular outcomes in CTVD patients undergoing percutaneous coronary intervention (PCI) remains unclear.

10,532 CTVD patients undergoing PCI were consecutively enrolled. SHR was calculated using the formula: admission blood glucose (mmol/L)/[1.59×HbA1c (%)-2.59]. Patients were divided into two groups (SHR Low and SHR High) according to the optimal cutoff value of SHR. Multivariable Cox regression models were used to assess the relationship between SHR and long-term prognosis. The primary endpoint was cardiovascular (CV) events, composing of cardiac death and non-fatal myocardial infarction (MI).

During the median follow-up time of 3 years, a total of 279 cases (2.6%) of CV events were recorded. Multivariable Cox analyses showed that high SHR was associated with a significantly higher risk of CV events [Hazard Ratio (HR) 1.99, 95% Confidence interval (CI) 1.58-2.52, P < 0.001). This association remained consistent in patients with (HR 1.50, 95% CI 1.08-2.10, P = 0.016) and without diabetes (HR 1.97, 95% CI 1.42-2.72, P < 0.001). Additionally, adding SHR to the base model of traditional risk factors led to a significant improvement in the C-index, net reclassification and integrated discrimination.

SHR was a significant predictor for adverse CV outcomes in CTVD patients with or without diabetes, which suggested that it could aid in the risk stratification in this particular population regardless of glucose metabolism status.

Stress hyperglycemia, which is associated with poor prognosis in patients with acute myocardial infarction (AMI), can be determined using the stress hyperglycemia ratio (SHR). Impaired left ventricular function and microvascular obstruction (MVO) diagnosed using cardiac magnetic resonance (CMR) have also been proven to be linked to poor prognosis in patients with AMI and aid in risk stratification. However, there have been no studies on the correlation between fasting SHR and left ventricular function and MVO in patients with acute ST-segment elevation myocardial infarction (ASTEMI). Therefore, this study aimed to investigate the additive effect of fasting SHR on left ventricular function and global deformation in patients with ASTEMI and to explore the association between fasting SHR and MVO.

Consecutive patients who underwent CMR at index admission (3-7 days) after primary percutaneous coronary intervention (PPCI) were enrolled in this study. Basic clinical, biochemical, and CMR data were obtained and compared among all patients grouped by fasting SHR tertiles: SHR1: SHR < 0.85; SHR2: 0.85 ≤ SHR < 1.01; and SHR3: SHR ≥ 1.01. Spearman's rho (r) was used to assess the relationship between fasting SHR and left ventricular function, myocardial strain, and the extent of MVO. Multivariable linear regression analysis was performed to evaluate the determinants of left ventricular function and myocardial strain impairment in all patients with AMI. Univariable and multivariable regression analyses were performed to investigate the correlation between fasting SHR and the presence and extent of MVO in patients with AMI and those with AMI and diabetes mellitus (DM).

A total of 357 patients with ASTEMI were enrolled in this study. Left ventricular ejection fraction (LVEF) and left ventricular global function index (LVGFI) were significantly lower in SHR2 and SHR3 than in SHR1. Compared with SHR1 and SHR2 groups, left ventricular strain was lower in SHR3, as evidenced by global radial (GRS), global circumferential (GCS), and global longitudinal (GLS) strains. Fasting SHR were negatively correlated with LVEF, LVGFI, and GRS (r = - 0.252; r = - 0.261; and r = - 0.245; all P<0.001) and positively correlated with GCS (r = 0.221) and GLS (r = 0.249; all P <0.001). Multivariable linear regression analysis showed that fasting SHR was an independent determinant of impaired LVEF, LVGFI, GRS, and GLS. Furthermore, multivariable regression analysis after adjusting for covariates signified that fasting SHR was associated with the presence and extent of MVO in patients with AMI and those with AMI and DM.

Fasting SHR in patients with ASTEMI successfully treated using PPCI is independently associated with impaired cardiac function and MVO. In patients with AMI and DM, fasting SHR is an independent determinant of the presence and extent of MVO.

Background Acute decompensated heart failure (ADHF) significantly contributes to global morbidity. Stress hyperglycemia (SHGL), although commonly observed in non-diabetic ADHF patients, remains underexplored. This study investigates the predictive value of SHGL for major adverse cardiac events (MACEs) and its impact on coronary intervention outcomes. Methods In this prospective observational study at a tertiary care center, 650 non-diabetic ADHF patients admitted for coronary intervention between April 2021 and April 2022 were assessed. SHGL was defined by random blood sugar levels >140 mg/dl. We monitored the incidence of MACEs, including cardiac death, non-fatal myocardial infarction, and heart failure rehospitalization, alongside the success rates of coronary revascularizations over 12 months. Results SHGL was present in 54% of patients (n=352) and was significantly associated with increased MACEs (p<0.001), higher rehospitalization rates (p<0.01), and lower success in revascularization (p<0.05). Using logistic regression, SHGL, age >65, and prior heart failure hospitalization were identified as independent predictors of MACEs. Statistical analyses were performed using two-tailed Mann-Whitney U tests, with significance levels set at p<0.05 for noteworthy findings and p<0.01 or p<0.001 for highly significant findings. Conclusions SHGL significantly impacts coronary intervention outcomes and the future prognosis of heart failure in non-diabetic ADHF patients, identifying it as a critical, modifiable risk factor. These findings advocate integrating SHGL management into ADHF care, emphasizing the need for further research to develop standardized treatment protocols. Proper management of SHGL could potentially improve patient outcomes, highlighting the importance of metabolic control in heart failure management.

Risk assessment for triple-vessel disease (TVD) remain challenging. Stress hyperglycemia represents the regulation of glucose metabolism in response to stress, and stress hyperglycemia ratio (SHR) is recently found to reflect true acute hyperglycemic status. This study aimed to evaluate the prognostic value of SHR and its role in risk stratification in TVD patients with acute coronary syndrome (ACS).

A total of 3812 TVD patients with ACS with available baseline SHR measurement were enrolled from two independent centers. The endpoint was cardiovascular mortality. Cox regression was used to evaluate the association between SHR and cardiovascular mortality. The SYNTAX (Synergy Between Percutaneous Coronary Intervention With Taxus and Cardiac Surgery) II (SSII) was used as the reference model in the model improvement analysis.

During a median follow-up of 5.1 years, 219 (5.8%) TVD patients with ACS suffered cardiovascular mortality. TVD patients with ACS with high SHR had an increased risk of cardiovascular mortality after robust adjustment for confounding (high vs. median SHR: adjusted hazard ratio 1.809, 95% confidence interval 1.160-2.822, P = 0.009), which was fitted as a J-shaped pattern. The prognostic value of the SHR was found exclusively among patients with diabetes instead of those without diabetes. Moreover, addition of SHR improved the reclassification abilities of the SSII model for predicting cardiovascular mortality in TVD patients with ACS.

The high level of SHR is associated with the long-term risk of cardiovascular mortality in TVD patients with ACS, and is confirmed to have incremental prediction value beyond standard SSII. Assessment of SHR may help to improve the risk stratification strategy in TVD patients who are under acute stress.

Hyperglycemia increases the heart sensitivity to ischemia-reperfusion (IR), but the underlying cellular mechanisms remain unclear. Mitochondrial dynamics (the processes that govern mitochondrial morphology and their interactions with other organelles, such as the reticulum), has emerged as a key factor in the heart vulnerability to IR. However, it is unknown whether mitochondrial dynamics contributes to hyperglycemia deleterious effect during IR. We hypothesized that (i) the higher heart vulnerability to IR in hyperglycemic conditions could be explained by hyperglycemia effect on the complex interplay between mitochondrial dynamics, Ca2+ homeostasis, and reactive oxygen species (ROS) production; and (ii) the activation of DRP1, a key regulator of mitochondrial dynamics, could play a central role. Using transmission electron microscopy and proteomic analysis, we showed that the interactions between sarcoplasmic reticulum and mitochondria and mitochondrial fission were increased during IR in isolated rat hearts perfused with a hyperglycemic buffer compared with hearts perfused with a normoglycemic buffer. In isolated mitochondria and cardiomyocytes, hyperglycemia increased mitochondrial ROS production and Ca2+ uptake. This was associated with higher RyR2 instability. These results could contribute to explain the early mPTP activation in mitochondria from isolated hearts perfused with a hyperglycemic buffer and in hearts from streptozotocin-treated rats (to increase the blood glucose). DRP1 inhibition by Mdivi-1 during the hyperglycemic phase and before IR induction, normalized Ca2+ homeostasis, ROS production, mPTP activation, and reduced the heart sensitivity to IR in streptozotocin-treated rats. In conclusion, hyperglycemia-dependent DRP1 activation results in higher reticulum-mitochondria calcium exchange that contribute to the higher heart vulnerability to IR.

Stress-related glycemic indicators, including admission blood glucose (ABG), stress-hyperglycemia ratio (SHR), and glycemic gap (GG), have been associated with worse outcomes after acute myocardial infarction (AMI). However, data regarding their prognostic value in the oldest old with AMI are unavailable. Therefore, this study aimed to investigate the association of stress-related glycemic indicators with short- and long-term cardiovascular mortality (CVM) in the oldest old (≥ 80 years) with AMI.

In this prospective study, a total of 933 consecutive old patients with AMI admitted to FuWai hospital (Beijing, China) were enrolled. On admission, ABG, SHR, and GG were assessed and all participants were classified according to their quartiles. Kaplan-Meier, restricted cubic splines (RCS), and multivariate Cox regression analyses were performed to evaluate the association between these glycemic indicators and CVM within 30 days and long-term follow-up.

During an average of 1954 patient-years of follow-up, a total of 250 cardiovascular deaths were recorded. Kaplan-Meier analyses showed the lowest CVM in quartile 1 of ABG and in quartile 2 of SHR and GG. After adjusting for potential covariates, patients in quartile 4 of ABG, SHR, and GG had a respective 1.67-fold (95% CI: 1.03-2.69; P = 0.036), 1.80-fold (95% CI: 1.16-2.79; P = 0.009), and 1.78-fold (95% CI: 1.14-2.79; P = 0.011) higher risk of long-term CVM risk compared to those in the reference groups (quartile 1 of ABG and quartile 2 of SHR and GG). Furthermore, RCS suggested a J-shaped relationship of ABG and a U-shaped association of SHR and GG with long-term CVM. Additionally, we observed similar associations of these acute glycemic parameters with 30-day CVM.

Our data first indicated that SHR and GG consistently had a U-shaped association with both 30-day and long-term CVM among the oldest old with AMI, suggesting that they may be useful for risk stratification in this special population.

Stress hyperglycemia ratio (SHR) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) are independently associated with increased mortality risk in diabetic patients with coronary artery disease (CAD). However, the role of these biomarkers in patients with diabetes and multivessel disease (MVD) remains unknown. The present study aimed to assess the relative and combined abilities of these biomarkers to predict all-cause mortality in patients with diabetes and MVD.

This study included 1148 diabetic patients with MVD who underwent coronary angiography at Tianjin Chest Hospital between January 2016 and December 2016. The patients were divided into four groups according to their SHR (SHR-L and SHR-H) and NT-proBNP (NT-proBNP-L and NT-proBNP-H) levels. The primary outcome was all-cause mortality. Multivariate Cox regression analyses were performed to evaluate the association of SHR and NT-proBNP levels with all-cause mortality.

During a mean 4.2 year follow-up, 138 patients died. Multivariate analysis showed that SHR and NT-proBNP were strong independent predictors of all-cause mortality in diabetic patients with MVD (SHR: HR hazard ratio [2.171; 95%CI 1.566-3.008; P < 0.001; NT-proBNP: HR: 1.005; 95%CI 1.001-1.009; P = 0.009). Compared to patients in the first (SHR-L and NT-proBNP-L) group, patients in the fourth (SHR-H and NT-proBNP-H) group had the highest mortality risk (HR: 12.244; 95%CI 5.828-25.721; P < 0.001). The areas under the curve were 0.615(SHR) and 0.699(NT-proBNP) for all-cause mortality. Adding either marker to the original models significantly improved the C-statistic and integrated discrimination improvement values (all P < 0.05). Moreover, combining SHR and NT-proBNP levels into the original model provided maximal prognostic information.

SHR and NT-proBNP independently and jointly predicted all-cause mortality in diabetic patients with MVD, suggesting that strategies to improve risk stratification in these patients should incorporate SHR and NT-porBNP into risk algorithms.

Acute kidney injury (AKI) represents a significant challenge to global public health problem and is associated with poor outcomes. There is still considerable debate about the effect of mean blood glucose (MBG) and coefficient of variation (CV) of blood glucose on the short-term mortality of AKI patients. This retrospective cohort study aimed to explore the association between glycemic variability and short-term mortality in patients with AKI. Data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database were analyzed, including 6,777 adult AKI patients. MBG and CV on the first day of ICU admission were calculated to represent the overall glycemic status and variability during the ICU stay in AKI patients. The primary outcome indicator was ICU 30-day mortality of AKI patients. Multivariate Cox regression analysis and smoothed curve fitting were used to assess the relationship between blood glucose levels and mortality. Eventually, the ICU 30-day mortality rate of AKI patients was 23.5%. The increased MBG and CV were significantly correlated with ICU 30-day mortality (hazards ratio (HR) = 1.20, 95% confidence interval (CI) 1.14-1.27; HR = 1.08, 95% CI 1.03-1.13). The smoothed curve fitting showed a U-shaped relationship between MBG on the first day of ICU admission and ICU 30-day mortality (inflection point = 111.3 mg/dl), while CV had a linear relationship with 30-day ICU mortality. Thus, we conclude that MBG and CV were significantly associated with short-term mortality in intensive care patients with AKI. Tighter glycemic control may be an effective measure to improve the prognosis of patients with AKI.

The stress hyperglycaemic ratio (SHR), a new marker that reflects the true hyperglycaemic state of patients with acute coronary syndrome (ACS), is strongly associated with adverse clinical outcomes in these patients. Studies on the relationship between the SHR and in-hospital cardiac arrest (IHCA) incidence are limited. This study elucidated the relationship between the SHR and incidence of IHCA in patients with ACS.

In total, 1,939 patients with ACS who underwent percutaneous coronary intervention (PCI) at the Affiliated Hospital of Zunyi Medical University were included. They were divided into three groups according to the SHR: group T1 (SHR ≤ 0.838, N = 646), group T2 (0.838< SHR ≤ 1.140, N = 646), and group T3 (SHR3 > 1.140, N = 647). The primary endpoint was IHCA incidence.

The overall IHCA incidence was 4.1% (N = 80). After adjusting for covariates, SHR was significantly associated with IHCA incidence in patients with ACS who underwent PCI (odds ratio [OR] =  2.6800; 95% confidence interval [CI] =  1.6200-4.4300; p<0.001), and compared with the T1 group, the T3 group had an increased IHCA risk (OR =  2.1800; 95% CI =  1.2100-3.9300; p =  0.0090). In subgroup analyses, after adjusting for covariates, patients with ST-segment elevation myocardial infarction (STEMI) (OR =  3.0700; 95% CI =  1.4100-6.6600; p =  0.0050) and non-STEMI (NSTEMI) (OR =  2.9900; 95% CI =  1.1000-8.1100; p =  0.0310) were at an increased IHCA risk. After adjusting for covariates, IHCA risk was higher in patients with diabetes mellitus (DM) (OR =  2.5900; 95% CI =  1.4200-4.7300; p =  0.0020) and those without DM (non-DM) (OR =  3.3000; 95% CI =  1.2700-8.5800; p =  0.0140); patients with DM in the T3 group had an increased IHCA risk compared with those in the T1 group (OR =  2.4200; 95% CI =  1.0800-5.4300; p =  0.0320). The restriction cubic spline (RCS) analyses revealed a dose-response relationship between IHCA incidence and SHR, with an increased IHCA risk when SHR was higher than 1.773. Adding SHR to the baseline risk model improved the predictive value of IHCA in patients with ACS treated with PCI (net reclassification improvement [NRI]: 0.0734 [0.0058-0.1409], p =  0.0332; integrated discrimination improvement [IDI]: 0.0218 [0.0063-0.0374], p =  0.0060).

In patients with ACS treated with PCI, the SHR was significantly associated with the incidence of IHCA. The SHR may be a useful predictor of the incidence of IHCA in patients with ACS. The addition of the SHR to the baseline risk model had an incremental effect on the predictive value of IHCA in patients with ACS treated with PCI.

Stress hyperglycemia and glycemic variability (GV) can reflect dramatic increases and acute fluctuations in blood glucose, which are associated with adverse cardiovascular events. This study aimed to explore whether the combined assessment of the stress hyperglycemia ratio (SHR) and GV provides additional information for prognostic prediction in patients with coronary artery disease (CAD) hospitalized in the intensive care unit (ICU).

Patients diagnosed with CAD from the Medical Information Mart for Intensive Care-IV database (version 2.2) between 2008 and 2019 were retrospectively included in the analysis. The primary endpoint was 1-year mortality, and the secondary endpoint was in-hospital mortality. Levels of SHR and GV were stratified into tertiles, with the highest tertile classified as high and the lower two tertiles classified as low. The associations of SHR, GV, and their combination with mortality were determined by logistic and Cox regression analyses.

A total of 2789 patients were included, with a mean age of 69.6 years, and 30.1% were female. Overall, 138 (4.9%) patients died in the hospital, and 404 (14.5%) patients died at 1 year. The combination of SHR and GV was superior to SHR (in-hospital mortality: 0.710 vs. 0.689, p = 0.012; 1-year mortality: 0.644 vs. 0.615, p = 0.007) and GV (in-hospital mortality: 0.710 vs. 0.632, p = 0.004; 1-year mortality: 0.644 vs. 0.603, p < 0.001) alone for predicting mortality in the receiver operating characteristic analysis. In addition, nondiabetic patients with high SHR levels and high GV were associated with the greatest risk of both in-hospital mortality (odds ratio [OR] = 10.831, 95% confidence interval [CI] 4.494-26.105) and 1-year mortality (hazard ratio [HR] = 5.830, 95% CI 3.175-10.702). However, in the diabetic population, the highest risk of in-hospital mortality (OR = 4.221, 95% CI 1.542-11.558) and 1-year mortality (HR = 2.013, 95% CI 1.224-3.311) was observed in patients with high SHR levels but low GV.

The simultaneous evaluation of SHR and GV provides more information for risk stratification and prognostic prediction than SHR and GV alone, contributing to developing individualized strategies for glucose management in patients with CAD admitted to the ICU.

Critical illness is often accompanied by elevated blood glucose, which generally correlates with increased morbidity and mortality. Prehospital blood glucose (PBG) level might be a useful and easy-to-perform tool for risk assessment in emergency medicine. This retrospective single-center cohort study was designed to analyze the association of prehospital glucose measurements with hospitalization rate and in-hospital mortality.

Records of 970 patients admitted to a university hospital by an emergency physician were analyzed. Patients with a PBG ≥140 mg/dL (G1, n = 394, equal to 7.8 mmol/L) were compared with patients with a PBG <140 mg/dL (G2, n = 576). Multivariable logistic regression models were used to correct for age, prediagnosed diabetes, and sex.

Five hundred thirty-four patients (55%) were hospitalized. In comparison to normoglycemic patients, hyperglycemic patients were more likely to be hospitalized with an adjusted odds ratio (OR) of 1.48 (95% confidence interval [CI] 1.11-1.97), more likely to be admitted to the intensive care unit (ICU) with an adjusted OR of 1.74 (95% CI 1.31-2.31) and more likely to die in the hospital with an adjusted OR of 1.84 (95% CI 0.96-3.53). Hospitalized hyperglycemic patients had a median length of stay of 6.0 days (interquartile range [IQR] 8.0) compared to 3.0 days (IQR 6.0) in the normoglycemic group (P < 0.001). In the subgroup analysis of cases without known diabetes, patients with PBG ≥140 mg/dL were more likely to be hospitalized with an adjusted OR of 1.49 (95% CI 1.10-2.03) and more likely to be admitted to ICU/intermediate care with an adjusted OR of 1.80 (95% CI 1.32-2.45), compared to normoglycemic patients.

Elevated PBG ≥140 mg/dL was associated with a higher hospitalization risk, a longer length of stay, and a higher mortality risk and may therefore be included in risk assessment scores.

The stress hyperglycemia ratio (SHR) is significantly associated with short-term adverse cardiovascular events. However, the association between SHR and mortality after the acute phase of acute coronary syndrome (ACS) remains controversial.

This study used data from the Medical Information Mart for Intensive Care-IV database. Patients with ACS hospitalized in the intensive care unit (ICU) were retrospectively enrolled.

A total of 2668 ACS patients were enrolled. The incidence of in-hospital and 1-year mortality was 4.7 % and 13.2 %, respectively. The maximum SHR had a higher prognostic value for predicting both in-hospital and 1-year mortality than the first SHR. Adding the maximum SHR to the SOFA score could significantly improve the prognostic prediction. In the landmark analysis at 30 days, the maximum SHR was a risk factor for mortality within 30 days regardless of whether patients had diabetes. However, it was no longer associated with mortality after 30 days in patients with diabetes after adjustment (HR = 1.237 per 1-point increment, 95 % CI 0.854-1.790).

The maximum SHR was significantly associated with mortality in patients with ACS hospitalized in the ICU. However, caution is warranted if it is used for predicting mortality after 30 days in patients with diabetes.

The stress hyperglycemia ratio (SHR) has been demonstrated as an independent risk factor for acute kidney injury (AKI) in certain populations. However, this relationship in patients with congestive heart failure (CHF) remains unclear. Our study sought to elucidate the relationship between SHR and AKI in patients with CHF.

A total of 8268 patients with CHF were included in this study. We categorized SHR into distinct groups and evaluated its association with mortality through logistic or Cox regression analyses. Additionally, we applied the restricted cubic spline (RCS) analysis to explore the relationship between SHR as a continuous variable and the occurrence of AKI. The primary outcome of interest in this investigation was the incidence of AKI during hospitalization.

Within this patient cohort, a total of 5,221 (63.1%) patients experienced AKI during their hospital stay. Upon adjusting for potential confounding variables, we identified a U-shaped correlation between SHR and the occurrence of AKI, with an inflection point at 0.98. When the SHR exceeded 0.98, for each standard deviation (SD) increase, the risk of AKI was augmented by 1.32-fold (odds ratio [OR]: 1.32, 95% CI: 1.22 to 1.46). Conversely, when SHR was below 0.98, each SD decrease was associated with a pronounced increase in the risk of AKI.

Our study reveals a U-shaped relationship between SHR and AKI in patients with CHF. Notably, we identified an inflection point at an SHR value of 0.98, signifying a critical threshold for evaluating AKI in this population.

The role of stress hyperglycemia in acute myocardial infarction (AMI) has long been emphasized. Recently, the stress hyperglycemia ratio (SHR), a novel index reflecting an acute glycemia rise, has shown a good predictive value in AMI. However, its prognostic power in myocardial infarction with nonobstructive coronary arteries (MINOCA) remains unclear.

In a prospective cohort of 1179 patients with MINOCA, relationships between SHR levels and outcomes were analyzed. SHR was defined as acute-to-chronic glycemic ratio using admission blood glucose (ABG) and glycated hemoglobin. The primary endpoint was defined as major adverse cardiovascular events (MACE), including all-cause death, nonfatal MI, stroke, revascularization, and hospitalization for unstable angina or heart failure. Survival analyses and receiver-operating characteristic (ROC) curve analyses were performed.

Over the median follow-up of 3.5 years, the incidence of MACE markedly increased with higher SHR tertile levels (8.1%, 14.0%, 20.5%; p < 0.001). At multivariable Cox analysis, elevated SHR was independently associated with an increased risk of MACE (HR 2.30, 95% CI: 1.21-4.38, p = 0.011). Patients with rising tertiles of SHR also had a significantly higher risk of MACE (tertile 1 as reference; tertile 2: HR 1.77, 95% CI: 1.14-2.73, p = 0.010; tertile 3: HR 2.64, 95% CI: 1.75-3.98, p < 0.001). SHR remained a robust predictor of MACE in patients with and without diabetes; whereas ABG was no longer associated with the MACE risk in diabetic patients. SHR showed an area under the curve of 0.63 for MACE prediction. By incorporating SHR to TIMI risk score, the combined model further improved the discrimination for MACE.

The SHR independently confers the cardiovascular risk after MINOCA, and may serve as a better predictor than glycemia at admission alone, particularly in those with diabetes.KEY MESSAGESStress hyperglycemia ratio (SHR) is independently associated with the prognosis in a distinct population with myocardial infarction with nonobstructive coronary arteries (MINOCA).SHR is a better predictor of prognosis than admission glycemia alone, especially in diabetic patients with MINOCA.SHR may serve as a prognostic marker for risk stratification as well as a potential target for tailored glucose-lowering treatment in MINOCA.

Among patients with acute coronary syndrome and percutaneous coronary intervention, stress hyperglycemia ratio (SHR) is primarily associated with short-term unfavorable outcomes. However, the relationship between SHR and long-term worsen prognosis in acute myocardial infarction (AMI) patients admitted in intensive care unit (ICU) are not fully investigated, especially in those with different ethnicity. This study aimed to clarify the association of SHR with all-cause mortality in critical AMI patients from American and Chinese cohorts.

Overall 4,337 AMI patients with their first ICU admission from the American Medical Information Mart for Intensive Care (MIMIC)-IV database (n = 2,166) and Chinese multicenter registry cohort Cardiorenal ImprovemeNt II (CIN-II, n = 2,171) were included in this study. The patients were divided into 4 groups based on quantiles of SHR in both two cohorts.

The total mortality was 23.8% (maximum follow-up time: 12.1 years) in American MIMIC-IV and 29.1% (maximum follow-up time: 14.1 years) in Chinese CIN-II. In MIMIC-IV cohort, patients with SHR of quartile 4 had higher risk of 1-year (adjusted hazard radio [aHR] = 1.87; 95% CI: 1.40-2.50) and long-term (aHR = 1.63; 95% CI: 1.27-2.09) all-cause mortality than quartile 2 (as reference). Similar results were observed in CIN-II cohort (1-year mortality: aHR = 1.44; 95%CI: 1.03-2.02; long-term mortality: aHR = 1.32; 95%CI: 1.05-1.66). In both two group, restricted cubic splines indicated a J-shaped correlation between SHR and all-cause mortality. In subgroup analysis, SHR was significantly associated with higher 1-year and long-term all-cause mortality among patients without diabetes in both MIMIC-IV and CIN-II cohort.

Among critical AMI patients, elevated SHR is significantly associated with and 1-year and long-term all-cause mortality, especially in those without diabetes, and the results are consistently in both American and Chinese cohorts.

Randomized, controlled trials have shown both benefit and harm from tight blood-glucose control in patients in the intensive care unit (ICU). Variation in the use of early parenteral nutrition and in insulin-induced severe hypoglycemia might explain this inconsistency.

We randomly assigned patients, on ICU admission, to liberal glucose control (insulin initiated only when the blood-glucose level was >215 mg per deciliter [>11.9 mmol per liter]) or to tight glucose control (blood-glucose level targeted with the use of the LOGIC-Insulin algorithm at 80 to 110 mg per deciliter [4.4 to 6.1 mmol per liter]); parenteral nutrition was withheld in both groups for 1 week. Protocol adherence was determined according to glucose metrics. The primary outcome was the length of time that ICU care was needed, calculated on the basis of time to discharge alive from the ICU, with death accounted for as a competing risk; 90-day mortality was the safety outcome.

Of 9230 patients who underwent randomization, 4622 were assigned to liberal glucose control and 4608 to tight glucose control. The median morning blood-glucose level was 140 mg per deciliter (interquartile range, 122 to 161) with liberal glucose control and 107 mg per deciliter (interquartile range, 98 to 117) with tight glucose control. Severe hypoglycemia occurred in 31 patients (0.7%) in the liberal-control group and 47 patients (1.0%) in the tight-control group. The length of time that ICU care was needed was similar in the two groups (hazard ratio for earlier discharge alive with tight glucose control, 1.00; 95% confidence interval, 0.96 to 1.04; P = 0.94). Mortality at 90 days was also similar (10.1% with liberal glucose control and 10.5% with tight glucose control, P = 0.51). Analyses of eight prespecified secondary outcomes suggested that the incidence of new infections, the duration of respiratory and hemodynamic support, the time to discharge alive from the hospital, and mortality in the ICU and hospital were similar in the two groups, whereas severe acute kidney injury and cholestatic liver dysfunction appeared less prevalent with tight glucose control.

In critically ill patients who were not receiving early parenteral nutrition, tight glucose control did not affect the length of time that ICU care was needed or mortality. (Funded by the Research Foundation-Flanders and others; TGC-Fast ClinicalTrials.gov number, NCT03665207.).

Sepsis remains a critical concern in healthcare, and its management is complicated when patients have pre-existing diabetes and varying body mass indexes (BMIs). This retrospective multicenter observational study, encompassing data from 15,884 sepsis patients admitted between 2012 and 2017, investigates the relationship between peak glucose levels and peak glycemic gap in the first 3 days of ICU admission, and their impact on mortality. The study reveals that maintaining peak glucose levels between 141-220 mg/dL is associated with improved survival rates in sepsis patients with diabetes. Conversely, peak glycemic gaps exceeding 146 mg/dL are linked to poorer survival outcomes. Patients with peak glycemic gaps below -73 mg/dL also experience inferior survival rates. In terms of predicting mortality, modified Sequential Organ Failure Assessment-Peak Glycemic Gap (mSOFA-pgg) scores outperform traditional SOFA scores by 6.8% for 90-day mortality in overweight patients. Similarly, the modified SOFA-Peak Glucose (mSOFA-pg) score demonstrates a 17.2% improvement over the SOFA score for predicting 28-day mortality in underweight patients. Importantly, both mSOFA-pg and mSOFA-pgg scores exhibit superior predictive power compared to traditional SOFA scores for patients at high nutritional risk. These findings underscore the importance of glycemic control in sepsis management and highlight the potential utility of the mSOFA-pg and mSOFA-pgg scores in predicting mortality risk, especially in patients with diabetes and varying nutritional statuses.