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Emerging evidence links the Endothelial Activation and Stress Index (EASIX) and mortality risk in coronary artery disease, but its relevance in hypertensive patients remains unclear. This study examines the association between EASIX and all‐cause and cardiovascular mortality in hypertensive individuals. The analysis included 6138 hypertensive patients from seven National Health and Nutrition Examination Survey (NHNES) cycles (2003–2016), with mortality data obtained from the National Death Index (NDI). Over a median follow‐up of 98 months, 1435 (23.4%) participants died, including 400 (6.5%) from cardiovascular causes. Restricted cubic spline analysis revealed a positive association between EASIX and both all‐cause and cardiovascular mortality. Weighted multivariable Cox regression indicated that each 1‐unit increase in EASIX corresponding to a 25% and 23% rise in mortality risk, respectively. Based on the optimal cutoff value determined using the maximally selected rank statistics method, participants were stratified into higher (>0.79) and lower (≤0.79) EASIX groups. Higher EASIX was significantly associated with increased all‐cause mortality risk (HR 1.46, 95% CI 1.23–1.73, p < 0.0001). Higher EASIX scores were associated with increased cardiovascular mortality, especially in former/current smokers and those with diabetes/prediabetes. Time‐dependent receiver operating characteristic analysis assessed the predictive accuracy of EASIX, yielding area under the curve (AUC) for 1‐, 3‐, 5‐, and 10‐year survival of 0.71, 0.67, 0.67, and 0.67 for all‐cause mortality and 0.79, 0.73, 0.73, and 0.71 for cardiovascular mortality. In conclusion, elevated EASIX is independently associated with increased all‐cause and cardiovascular mortality in hypertensive patients, suggesting its potential as a predictive biomarker in clinical practice.

Background Numerous studies support the association of exercise training, physical activity (PA) and sedentary behaviour (SB) with both mortality and morbidity outcomes. The results across studies have been inconsistent, and no umbrella reviews have yet been conducted on this topic. Methods We conducted an umbrella review of meta‐analyses of observational studies by screening articles in PubMed/MEDLINE, EMBASE and Web of Science databases from inception to 30 April 2024. Quality appraisal of each included meta‐analysis was done using the AMSTAR 2 tool, with evidence certainty evaluated based on statistical significance, study size, heterogeneity, small‐study effects, prediction intervals (PI) and potential biases. Results Frothy‐eight meta‐analyses were included (AMSTAR 2 ratings: high 25, moderate 10, low 2 and critically low 11). No evidence was highly suggestive or convincing. Suggestive evidence linked any PA and SB to lower and higher risks of all‐cause, cardiovascular and cancer mortality. Suggestive evidence indicated a significant association between self‐reported and device‐measured total PA (equivalent odds ratio [eOR] 0.78 [0.70–0.86] and eHR = 0.50 [0.38–0.65], respectively), self‐reported leisure time PA (eHR = 0.73 [0.66–0.80]), device‐measured daily steps (eHR = 0.44 [0.35–0.56]) and aerobic plus resistance training (eHR = 0.60 [0.56–0.64]) with lower all‐cause mortality. Weak evidence supported links between self‐reported and device‐measured SB and higher mortality (eHR = 1.3 [1.22–1.38] and eHR = 2.16 [1.09–4.28], respectively). Suggestive evidence was noted for the association between self‐reported leisure time PA (eHR = 0.74 [0.69–0.80]) and resistance training (eHR = 0.82 [0.81–0.84]) with cardiovascular mortality. Suggestive evidence was also found for the association between self‐reported leisure time PA (eHR = 0.87 [0.83–0.91]) with cancer mortality. Associations between self‐reported running time and mortality from all causes, cardiovascular diseases (CVD) and cancer did not reach statistical significance nor did the association between low skeletal muscle mass and all‐cause mortality. Meta‐regression analyses showed that physical activity reduces mortality risk, with age reducing the protective effects against all‐cause, CVD and cancer mortality. We also found that combined exercise training (aerobic plus resistance) most effectively reduces all‐cause and CVD mortality. Conclusions Converging evidence supports that physical activity and sedentary behaviour are associated with lower and higher rates of all‐cause, cardiovascular and cancer mortality. More high‐quality prospective studies are needed for a better understanding of the associations between running time and also TV‐viewing time and health‐related outcomes.

Anemia and acute heart failure (AHF) frequently coexist. Several published studies have investigated the association of anemia with all‐cause mortality and all‐cause heart failure events in AHF patients, but their findings remain controversial. This study is intended to evaluate the relationship between anemia and AHF. We systematically searched PubMed, Medline, the Cochrane Library, Embase, and Elsevier's ScienceDirect databases until July 30, 2023, and selected prospective or retrospective cohort studies to evaluate anemia for AHF. A total of nine trials involving 29 587 AHF patients were eventually included. Pooled analyses demonstrated anemia is associated with a higher risk of all‐cause heart failure event rate (OR: 1.82, 95% CI: 1.58−2.10, p < .01) and all‐cause mortality, both for short‐term (30 days) all‐cause mortality (OR: 1.91, 95% CI: 1.31−2.79, p < .01) and long‐term (1 year) all‐cause mortality (OR: 1.72, 95% CI: 1.27−2.32, p < .01). The evidence from this meta‐analysis suggested that anemia may be an independent risk factor for all‐cause mortality and all‐cause heart failure events in patients with AHF and might emphasize the importance of anemia correction before discharge. A total of nine trials involving 29 587 acute heart failure patients were eventually included. Pooled analyses demonstrated anemia is associated with a higher risk of all‐cause heart failure event rate (OR: 1.82, 95% CI: 1.58−2.10, p < .01) and all‐cause mortality, both for short‐term (30 days) all‐cause mortality (OR: 1.91, 95% CI: 1.31−2.79, p < .01) and long‐term (1 year) all‐cause mortality (OR: 1.72, 95% CI: 1.27−2.32, p < .01).

Although most drugs currently approved are meant to treat specific diseases or symptoms, it has been hypothesized that some might bear a beneficial effect on lifespan in healthy older individuals, outside of their specific disease indication. Such drugs include, among others, metformin, SGLT2 inhibitors and rapamycin. Since 2006, the UK biobank has recorded prescription medication and mortality data for over 500′000 participants, aged between 40 and 70 years old. In this work, we examined the impact of the top 406 prescribed medications on overall mortality rates within the general population of the UK. As expected, most drugs were linked to a shorter lifespan, likely due to the life‐limiting nature of the diseases they are prescribed to treat. Importantly, a few drugs were associated with increased lifespans, including notably Sildenafil, Atorvastatin, Naproxen and Estradiol. These retrospective results warrant further investigation in randomized controlled trials. The UK Biobank has collected data on prescription medications and mortality for over 500,000 participants aged 40–70 years. We analyzed the effects of the top 406 prescribed medications on overall mortality rates in the general population. Most drugs were linked to a shortened lifespan, likely due to the life‐limiting nature of the diseases they are prescribed to treat. However, a few medications, notably Sildenafil, Atorvastatin, Naproxen, and Estradiol, were associated with increased lifespans.

Aims/hypothesisThe aim of the study was to describe trends in all-cause and cause-specific mortality rates in Hong Kong Chinese people with diabetes from 2001 to 2016.MethodsThe Hong Kong Diabetes Surveillance Database (HKDSD) is a territory-wide diabetes cohort identified from the Hong Kong Hospital Authority electronic medical record system. Deaths between 2001 and 2016 were identified from linkage to the Hong Kong Death Registry. We used Joinpoint regression analysis to describe mortality patterns among people with diabetes by age and sex, and standardised mortality ratios (SMRs) to compare all-cause mortality rates in people with and without diabetes.ResultsBetween 2001 and 2016, a total of 390,071 men and 380,007 women aged 20 years or older with diabetes were included in the HKDSD. There were 96,645 deaths among men and 88,437 deaths among women. Mortality rates for all-cause, cardiovascular disease and cancer among people with diabetes declined by 52.3%, 72.2% and 65.1% in men, respectively, and by 53.5%, 78.5% and 59.6% in women, respectively. Pneumonia mortality rates remained stable. The leading cause of death in people with diabetes has shifted from cardiovascular disease to pneumonia in the oldest age group, with cancer remaining the most common cause of death in people aged 45–74 years. The all-cause SMRs for men declined from 2.82 (95% CI 2.72, 2.94) to 1.50 (95% CI 1.46, 1.54), and for women, they declined from 3.28 (95% CI 3.15, 3.41) to 1.67 (95% CI 1.62, 1.72). However, among people aged 20–44 years, the declines in all-cause mortality rates over the study period were not statistically significant for both men (average annual per cent change [AAPC]: −3.2% [95% CI −7.3%, 1.0%]) and women (AAPC: −1.2% [95% CI −6.5%, 4.4%]). The SMRs in people aged 20−44 years fluctuated over time, between 7.86 (95% CI 5.74, 10.5) in men and 6.10 (95% CI 3.68, 9.45) in women in 2001, and 4.95 (95% CI 3.72, 6.45) in men and 4.92 (95% CI 3.25, 7.12) in women in 2016.Conclusions/interpretationAbsolute and relative mortality has declined overall in people with diabetes in Hong Kong, with less marked improvements in people under 45 years of age, calling for urgent action to improve care in young people with diabetes.

Background Glycemic control is crucial in peritoneal dialysis (PD) patients with diabetes. Although fasting blood glucose (FBG) is the most commonly used index to measure blood glucose levels, there is currently no evidence supporting the association between FBG level and mortality risk in PD patients. Methods A total of 3548 diabetic PD patients between 2002 and 2018 were enrolled from the National Health Insurance Service database of Korea. We investigated the association between FBG levels and the risk of all‐cause and cause‐specific mortality. Results Patients with FBG levels 80–99 mg/dL exhibited the highest survival rates, whereas those with FBG levels ≥180 mg/dL had the lowest survival rates. Compared with FBG levels 80–99 mg/dL, the adjusted hazard ratios and 95% confidence interval for all‐cause mortality significantly increased as follows: 1.02 (0.87–1.21), 1.41 (1.17–1.70), 1.44 (1.18–2.75), and 2.05 (1.73–2.42) for patients with FBG 100–124 mg/dL, FBG 125–149 mg/dL, FBG 150–179 mg/dL, and FBG ≥180 mg/dL, respectively. The risk for all‐cause mortality also showed an increasing pattern in patients with FBG levels <80 mg/L. The risk of cardiovascular death significantly increased as FBG levels exceeded 125 mg/dL. However, the risk of infection‐related and malignancy‐related deaths did not show a significant increase with increasing FBG levels. Conclusion There was an increase in the risk of all‐cause mortality as FBG levels exceeded 125 mg/dL in PD patients with diabetes, and the risk of cardiovascular death showed a strong correlation with FBG levels compared with other causes of death. Highlights A clear association was observed between FBG levels and the risk of all‐cause mortality in PD patients, indicating that FBG is a significant indicator for quantifying the risk of all‐cause mortality in these patients. Although a higher FBG level was significantly associated with an increased risk of cardiovascular‐related death, there was no notable increase in the risk of death from cancer or infections as the FBG levels increased.

Telomere length (TL) is an important indicator of cellular aging. Shorter TL is associated with several age‐related diseases including coronary heart disease, heart failure, diabetes, osteoporosis, and cancer. Recently, a DNA methylation‐based TL (DNAmTL) estimator has been developed as an alternative method for directly measuring TL. In this study, we examined the association of DNAmTL with cancer prevalence and mortality risk among people with and without HIV in the Veterans Aging Cohort Study Biomarker Cohort (VACS, N = 1917) and Women's Interagency HIV Study Cohort (WIHS, N = 481). We profiled DNAm in whole blood (VACS) or in peripheral blood mononuclear cells (WIHS) using an array‐based method. Cancer prevalence was estimated from electronic medical records and cancer registry data. The VACS Index was used as a measure of physiologic frailty. Models were adjusted for self‐reported race and ethnicity, batch, smoking status, alcohol consumption, and five cell types (CD4, CD8, NK, B cell, and monocyte). We found that people with HIV had shorter average DNAmTL than those without HIV infection [beta = −0.25, 95% confidence interval (−0.32, −0.18), p = 1.48E‐12]. Greater value of VACS Index [beta = −0.002 (−0.003, −0.001), p = 2.82E‐05] and higher cancer prevalence [beta = −0.07 (−0.10, −0.03), p = 1.37E‐04 without adjusting age] were associated with shortened DNAmTL. In addition, one kilobase decrease in DNAmTL was associated with a 40% increase in mortality risk [hazard ratio: 0.60 (0.44, 0.82), p = 1.42E‐03]. In summary, HIV infection, physiologic frailty, and cancer are associated with shortening DNAmTL, contributing to an increased risk of all‐cause mortality. Telomere length (TL) serves as a key indicator of cellular aging, with shorter TL linked to various age‐related diseases. A DNA methylation‐based TL (DNAmTL) estimator has been developed as an alternative method for direct TL measurement. In this study, we observed that people living with HIV exhibit shorter DNAmTL. Furthermore, a reduction of DNAmTL is linked to greater physical frailty, higher prevalence of cancer, and a heightened risk of all‐cause mortality in our studied population.

The platelet‐to‐lymphocyte ratio (PLR) has been proposed as a promising inflammatory biomarker, with potential implications for cardiovascular prognosis. However, its association with mortality outcomes in hypertensive individuals is not fully elucidated. This investigation sought to clarify the linkage between PLR and both overall and cardiovascular mortality in hypertensive individuals. Data from 15 483 hypertensive adults in the NHANES (2005–2018) were analyzed. Mortality data, including all‐cause and cardiovascular deaths, were sourced from the National Death Index (NDI) up to December 31, 2019. The linkage between PLR and mortality risk was depicted using restricted cubic spline (RCS) models. Cox proportional hazards regression models assessed the independent association of PLR with mortality risk, with adjustments incrementally applied: Model 1 without adjustments; Model 2 adjusted for age and sex; Model 3 adjusted further for age, gender, race, marital status, diabetes, alcohol intake, smoking status, body mass index (BMI), history of cardiovascular disease (CVD), high‐density lipoprotein cholesterol (HDL), low‐density lipoprotein cholesterol (LDL), total cholesterol (TC), triglyceride (TG), and creatinine (CR). Over a median follow‐up of 79 months, there were 2820 all‐cause deaths and 758 cardiovascular deaths. The multivariate Cox analysis showed that those in the highest PLR quartile had significantly elevated risks of all‐cause mortality (Model 1: HR = 1.28, 95% CI 1.16–1.42, p < 0.001; Model 2: HR = 1.14, 95% CI 1.03–1.26, p = 0.014; Model 3: HR = 1.16, 95% CI 1.05–1.29, p = 0.004)and cardiovascular mortality (Model 1: HR = 1.59, 95% CI 1.30–1.94, p < 0.001; Model 2: HR = 1.38, 95% CI 1.13–1.68, p = 0.001; Model 3: HR = 1.47, 95% CI 1.20–1.80, p < 0.001). The study reveals a U‐shaped relationship between PLR and all‐cause mortality, alongside a linear association with cardiovascular mortality. A PLR threshold of 118.83 has been identified as indicative of an adverse prognosis for all‐cause mortality. Elevated PLR independently predicts heightened risks of both all‐cause and cardiovascular mortality among hypertensive patients.

Liver disease is a leading cause of death worldwide. Nucleated red blood cells (NRBCs) are associated with high mortality and poor outcomes in patients with severe illnesses. However, the relationship between NRBCs and severe liver disease remains unclear. Potential confounding effects were managed using propensity score matching. The association between NRBCs and clinical outcomes in patients with liver disease was clarified using Cox proportional hazards regression analysis and smoothing splines. Differences in NRBCs between 30‐day survivors and non‐survivors within the pre‐matched cohort during the first 30 days after ICU admission were assessed using generalised additive mixed models. Compared to the 30‐day survivors, the 30‐day non‐survivors had significantly higher NRBC counts. Higher NRBC counts were significantly correlated with an augmented risk of 30‐day, 90‐day and in‐hospital mortality, with concurrently decreased hospitalisation durations. Inpatients with liver disease, progressive increases in the 30‐day mortality risk were associated with increased NRBC counts. The association between NRBCs and enhanced 30‐day mortality rates was consistent across stages and etiologies. Moreover, 30‐day non‐survivors experienced average daily increases in NRBC counts of 0.31% compared with 30‐day survivors. Elevated NRBC counts correlated with increased 30‐, 90‐day and in‐hospital mortality in patients with liver disease.

Background Limited studies have explored the association between visceral adipose tissue (VAT) mass and fat‐to‐muscle mass ratio (FMR) and mortality. We aimed to evaluate the sex‐specific association of VAT and FMR with all‐cause and cause‐specific mortality by age. Methods A total of 438 896 participants (49.8% men, mean age ± standard deviation: 57 ± 8 years for men; 56 ± 8 years for women) were included from the UK Biobank cohort. The nature of VAT was predictive, as obtained by sex‐stratified, non‐linear prediction models. Fat and muscle mass were estimated using a bioelectrical impedance assessment device. FMR was calculated as the fat mass divided by the muscle mass in the whole body. VAT and FMRs were divided into quintiles in ascending order, and the 3rd quintile was used as the reference. Cox regression analyses were used to estimate the associations between VAT, FMR and mortality. Results During a median of 12.4 years of follow‐up, we documented 29 903 deaths. After adjusting for various covariates, the individuals in the highest quintiles of VAT and FMR had the highest hazard ratios (HRs) of all‐cause mortality [1.24 (95% confidence interval: 1.17–1.33) for VAT and 1.24 (1.17–1.31) for FMR in men; and 1.11 (1.03–1.21) for VAT in women], except that the 1st quintile of FMR in women had the greatest HR [1.18 (1.09–1.27)]. Significant interactions were observed in both sexes according to age category (P for interaction < 0.05). Among men <50 years, participants in the 1st and 5th quintiles of VAT and FMR had significantly higher risks of mortality [1.30 (1.02–1.66) and 1.67 (1.27–2.19) in VAT; 1.25 (0.99–1.56) and 1.41 (1.11–1.79) in FMR, respectively]; in women, this phenomenon was observed in the ≥60 age group [1.16 (1.06–1.27) and 1.19 (1.08–1.31) in VAT; 1.18 (1.08–1.29) and 1.11 (1.01–1.22) in FMR, respectively]. VAT showed a linear positive association with mortality in women <60 years and a J‐shaped association from respiratory disease in both sexes ≥60 years. FMR showed a linear positive association with mortality from cancer in men <60 years and a J‐shaped association with mortality from cause‐specific mortality in both sexes ≥60 years, except for mortality from cardiovascular disease in men. Conclusions Most associations of VAT and FMR with all‐cause mortality were J‐shaped and were significantly modified by age status (<50, 50–59 and ≥60 years). The clinical implication is that regarding body composition and VAT mass, different health strategies may be adopted for people of different sexes and ages.