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Importance Elevated low-density lipoprotein cholesterol (LDL-C) is a modifiable risk factor for cardiovascular disease, the leading cause of premature death worldwide. Assessing the LDL-C–related burden is critical for guiding prevention and treatment strategies. Objectives To estimate the global, regional, and national burden of ischemic heart disease and ischemic stroke attributable to elevated LDL-C (relative to 35-54 mg/dL) from 1990 to 2023 and to quantify the contributions of population growth, aging, risk-deleted burden, and exposure changes to burden trends. Design, Setting, and Population This comparative risk assessment, part of the Global Burden of Disease Study 2023, estimated population-level LDL-C exposure and associated health loss in 204 countries and territories. Mean LDL-C levels were estimated using spatiotemporal gaussian process regression based on 806 studies across 161 countries. Relative risks were derived from meta-analyses of 38 randomized clinical trials. Population-attributable fractions for deaths and disability-adjusted life-years (DALYs) were estimated by age and sex for adults aged 25 years or older from 1990 to 2023, with 95% uncertainty intervals. Exposure Population-level LDL-C concentrations. Main Outcomes and Measures Population-attributable fractions, counts, and rates (all ages and age standardized per 100 000) of LDL-C–attributable deaths and DALYs from ischemic heart disease and ischemic stroke, with uncertainty intervals. Results In 2023, elevated LDL-C accounted for 3.6 million deaths (95% uncertainty interval, 2.2-5.4 million; 6.0% of global mortality) and 90.7 million DALYs (95% uncertainty interval, 58.9-123.3 million; 3.2% of DALYs). Although global all-ages rates remained stable, age-standardized death and DALY rates decreased by 45.6% and 39.5%, respectively, since 1990. In 2023, age-standardized LDL-C–attributable DALY rates were highest in Eastern Europe and lowest in high-income Asia-Pacific. One-third of the global LDL-C burden occurred in India and China. Population growth and aging drove the increasing burden, with notable regional disparities in LDL-C exposure and risk-deleted DALY rates shifting toward middle-sociodemographic settings. Conclusions and Relevance Despite declining age-standardized rates, the absolute LDL-C burden has increased since 1990 due to demographic changes and has shifted toward middle-sociodemographic countries. Measurement and surveillance gaps persist. Strengthened prevention, diagnosis, and treatment access strategies are essential to mitigate the health burden of LDL-C.

Background/Objectives: In the United States, HF prevalence is projected to progressively rise by 2030. Prior research suggests a strong association between reduced sleep duration and increased cardiovascular disease and HF risk. This study introduces an alternative parameter, the weekend sleep recovery (WSR), measured by the weekend-to-weekday sleep duration ratio (SDR), to evaluate its association with HF risk. Methods: We conducted a cross-sectional analysis of NHANES (National Health and Nutrition Examination Survey) 2017–2023 to examine self-reported sleep patterns. Participants were classified as WSR (SDR > 1) or non-WSR (SDR ≤ 1). Multivariate logistic regression assessed the association between WSR and HF, adjusting for demographics and comorbidities. Results: Among 8320 participants included in the fully adjusted analysis, WSR was associated with lower odds of HF compared with non-WSR (adjusted OR 0.73, 95% CI 0.55–0.96; p = 0.026). A significant interaction was observed between WSR and weekday sleep duration (P for interaction = 0.003), whereas no interaction was found with weekend sleep duration. In exploratory subgroup analyses, nominally significant associations were observed in several clinical subgroups; however, after correction for multiple comparisons, only participants without dyslipidemia retained statistical significance. No significant effect modification by race/ethnicity was observed (P for interaction = 0.436). Conclusions: Weekend sleep recovery was associated with lower odds of HF in this cross-sectional study. The association varied according to weekday sleep duration but was generally consistent across racial/ethnic groups. Given the observational design, these findings should be interpreted as associative rather than causal and warrant confirmation in prospective studies.

Introduction: Menopause is known to be associated with myocardial infarction (MI). However, the association between menopause age and MI onset in a nationally representative population remains unknown. Objective: To examine the correlation between age of menopause and age of MI onset in the general population and the association between early menopause (onset of menopause ≤ 40 years old) and early onset of MI (onset of MI ≤ 40 years old). Methods: A cross-sectional study was conducted using a population from the 2017-2020 National Health and Nutrition Examination Survey (NHANES). The questionnaire collected self-reported data on the participants' menopause age and their age of first MI. The relationship between these two parameters was analyzed by multivariate linear and logistic regression analyses. Multivariate analysis was adjusted for race, age, body mass index (BMI), smoking status, diabetes mellitus (DM), hypertension, and dyslipidemia status. Results: Among 2,200 postmenopausal females, 90 (4.1%) have had MI. The study involved 85 postmenopausal females who reported both menopause age and MI onset, with a mean ± SD age of 55 ± 13 years. This study found a significant association between menopause age and MI onset. After adjusting for confounders, it was found that every 1-year increase in the age of menopause will delay the onset of MI by 0.28 years, with a 95% CI of 0.013 to 0.552 (Table 1A, Graph 1A, Graph 1B). Additionally, early menopause carries an almost significantly increased risk of 2.11 times (95% CI: 1.00, 4.45) for early-onset MI. After adjusting for confounders, the magnitude of the association was lower and not statistically significant, but the direction remains (OR (95% CI): 2.08 (0.87, 4.95)). However, after stratification with comorbidities, DM status was identified as an effect modifier, with early MI significantly observed in patients with DM in both univariate and multivariate analyses, with OR (95% CI) of 3.03 (1.10, 8.37) and 4.88 (1.26, 18.96), respectively (Table 2A). Conclusion: This study demonstrated a positive association between menopause age and MI onset in a generally representative population. This suggests that prolonged estrogen exposure due to late menopause may delay the onset of MI. Additionally, early menopause was associated with early MI onset in the DM population. Further longitudinal studies are required to examine the potential mechanisms involved in menopause onset and MI onset.

Background: There is suspicion that estrogen may protect against atherosclerosis. Women who experience menarche earlier, and thus have earlier estrogen exposure, might develop atherosclerosis later. The relationship between menarche age and the onset of angina pectoris, a symptom of coronary artery disease, remains unknown. Goal: This study aims to find the correlation between menarche age and the onset age of angina pectoris, and the association between early menarche (onset of menarche ≤ 10 y/o) and early onset of angina pectoris (onset of angina pectoris ≤ 40 y/o). Methods: A cross-sectional study using a population from the 2017-2020 National Health and Nutrition Examination Survey (NHANES). The question collects self-reported data on onset of menarche and onset of angina pectoris. The relationship between menarche age and age in onset of angina pectoris was analyzed by linear and logistic regression analysis. Multivariate analysis adjusted for race, age, body mass index (BMI), smoking , diabetes mellitus (DM), hypertension, and dyslipidemia status. Results: Among 4,816 females who reported their menarche age, 88(1.8 %) have had an angina pectoris. The study involved 82 females who reported both the age of menarche and the age of onset of angina pectoris. The mean ± SD of the age at menarche and the age at onset of angina pectoris was 12.53 ± 1.79 y/o and 51.66 ± 15.16 y/o, respectively. The study found a significant association between the menarche age and the age at onset of angina pectoris. After adjusting for confounders, we found that every 1-year increase in the age of menarche will delay the onset of angina pectoris by 1.43 years, with a 95% CI of 0.01 to 2.86.(Table 1A,Graph 1A-1B) We also found that early menarche has a significantly increased risk 2.8 times (95%CI: 1.3, 6.2) of early onset of angina pectoris.After adjusting for confounders, the association became even stronger. The odds ratio (OR) increased to 3.3 (95%CI: 1.4, 8.0), indicating that women with early menarche were 3.3 times more likely to experience early angina pectoris compared to those with later menarche.(Table 2A) Conclusion: In contrast to our hypothesis, age at menarche is positively associated with onset of angina pectoris. The earlier onset of menarche is linked to the earlier onset of angina pectoris. We suspected that factors beyond estrogen levels may contribute to this unexpected finding. Additional studies are needed to examine the cause of this correlation.

Abstract Background Short sleep is linked to increased acute myocardial infarction (MI) risk.However, the association of weekend-to-weekday sleep patterns with MI in a nationally representative population remains unknown. The goal is to investigate how weekday and weekend sleep durations affect myocardial infarction (MI) in the general population, and if longer weekend sleep can offset insufficient weekday sleep's effects. Methods A cross-sectional study utilized data from the 2017-2020 NHANES to examine the relationship between sleep patterns and MI. Participants self-reported their average sleep durations on weekdays (1) and weekends (2), along with the calculated weekend-to-weekday sleep duration ratio (SDR) (3). Logistic regression models, adjusting for various factors, including demographics and comorbidities, were employed to analyze the association. Those with SDR > 1 had more weekend sleep, while an SDR = 1 indicated equal sleep durations. Results The study involved 9,205 adult participants, with a mean ± SD age of 68.8 ± 10.8 years and 30.7% being female. Among them, 4.65% (428 patients) had a history of MI. The mean ± SD of weekday and weekend sleep hours was 7.6 ± 1.7 and 8.3 ± 1.8 hours, respectively. For weekday sleep duration, after univariate analysis, individuals compared to those in Q1 were statistically significant 0.72 times less likely in Q2 and 1.4 times more likely in Q4 to experience MI . While MI was 0.76 times less likely to occur among participants in Q3, it was not statistically significant (95% CI Q2: 0.54, 0.96; Q4: 1.05, 1.76; Q3:0.57, 1.00). After adjusting, participants only in Q3 were statistically significant 0.71 times less likely to develop MI.(Q3: 95% CI 0.51, 0.99). For weekend sleep duration, the univariate analysis showed that individuals in Q2, Q3, and Q4 were significantly less likely to experience MI (OR = 0.63, 0.67, and 0.69; 95% CIs: 0.48-0.82, 0.51-0.87, 0.53-0.90, respectively) After adjusting, only participants in Q2 were statistically significant less likely to develop MI (OR = 0.71; 95% CI 0.52 - 0.96). For the weekend-to-weekday sleep duration ratio (SDR), after univariate analysis, individuals were statistically significant 0.54 times less likely, and 1.5 times more likely to experience MI in those whose SDR is more than 1, and those whose SDR equals 1, respectively (95% CI SDR > 1: 1.14, 1.98; SDR = 1: 0.39, 0.72). After adjusting, participants with SDR more than 1 were statistically significant 0.69 times less likely to develop MI. Conclusions Moderate sleep durations on weekdays (in Q3), weekends (in Q2), along with SDR more than 1, were negatively linked with MI in a general population. This implies that sleep durations on both weekends and weekdays have comparable associations with MI. Additionally, full recovery sleep on weekends following sleep-deprived weekdays, might reduce MI risk. Further studies are needed to explore impact of weekend and weekday sleep patterns on MI.Histogram and Margins plotTable of Odd ratios

Background: Although BP is associated with kidney outcomes, its clinical significance in living kidney donors (LKD) is unknown. We aim to examine the association between pre-donation BP and the risk of kidney function decline in LKD. Methods: A retrospective cohort study using OPTN/SRTR including adult LKD, who underwent donation between 6/1972 and 9/2022, was utilized to examine the association of quartile (Q) of pre-donation SBP and DBP with time-to-event of ≥35% decline in post-donation eGFR from pre-donation eGFR by multiple Cox regression. Results: Of 174,311 adult LKD, mean±SD age was 41±12 years and 60% were female. Mean pre-donation SBP and DBP were 122±13 and 74±9 mmHg, respectively. Mean pre-donation SBP in Q 1, 2, 3, and 4 were 106±6, 117±2, 126±3, and 140±9 mmHg, respectively and the corresponding DBP were 62±5, 71±2, 78±2, and 86±5 mmHg, respectively. The median (IQR) of pre-donation eGFR was 91 (75, 111) mL/min/1.73 m2. Median(IQR) eGFR at immediate post-donation, 6-, 12-, and 24-months post-donation were 50 (40, 62), 54 (44, 67), 55 (45, 68), and 57 (47, 70) mL/min/1.73 m2, respectively. Out of 38,780 LKD with post-donation eGFR data at 6, 12, or 24 months, 31,054 had the event of ≥35% decline in post-donation eGFR from pre-donation eGFR with a median time to follow-up of 6.77 months(IQR 5.93, 12.67). The incidence rate of the event was 0.08 person-months. Compared to patients with SBP in Q 1, those with SBP in Q 2, 3, and 4 had a significantly increased risk for the event(HRSBP Q2,3,4 1.05, 1.08, and 1.15; P <0.001 – 0.003) but only patients with DBP in Q 3 and 4 had a significantly increased risk for the event (HRSBP Q3,4 1.04 and 1.09). After adjusting for age, gender, race/ethnicity, U.S. citizenship, education level, history of pre-donation HTN, diabetes, pre-donation BMI, DBP, and urine protein:creatinine ratio, there was a J-shaped association between pre-donation SBP and post-donation eGFR decline and only patients in the Q 2 became significantly associated with lower the risk for the event (HR 0.87, 95%CI 0.76, 0.99; Fig1). The pre-donation DBP – post-donation eGFR association was similar to the SBP – eGFR association but there was no statistically significant in all Q (Fig2). There was no effect-measured modifier for all covariates. Conclusions: Pre-donation SBP in a normal range(113 - 120 mmHg) is associated with the lowest risk for a post-donation eGFR decline. BP control in the normal range should be achieved for potential LKD.

Background: Hypertension is well known for its association with cardiovascular events and arthritis. However, epidemiological data on the direct relationship between heart failure and arthritis in hypertensive patients is limited. This study examines the hypothesis that arthritis increases the risk of heart failure among patients with hypertension. Additionally, the effect of gender on these outcomes was assessed. Method: In our study, we analyzed data from 6,789 adults with hypertension aged 18 to 80 years, sourced from the National Health and Nutrition Examination Survey (NHANES) for the years 2017-2018. Arthritis was defined based on participants’ self-reported diagnosis by a doctor. We utilized logistic regression to explore the relationship between arthritis and the presence of heart failure across three different models. The first model included heart failure alone, the second model included age, gender, education, race, body mass index (BMI), smoking, and drinking, and the third model additionally included coronary artery disease and stroke. Result: The prevalence of heart failure among individuals with both arthritis and hypertension stands at 6.0%. Investigation into gender reveals a notable prevalence in males at 8.2% compared to 4.5% in females [Fig 1]. The analysis revealed a positive correlation between the two conditions across the entire population, with correlation coefficients of 2.38 (95% CI: 1.68-3.37), 1.61 (95% CI: 1.11-2.34), and 1.51 (95% CI: 1.01-2.25) for the three models, respectively. Specifically, in males, there was a notably increased association in the first and second models, with correlation coefficients of 2.77 (95% CI: 1.76-4.35) and 1.69 (95% CI: 1.05-2.74), respectively. Conversely, among females, a significant association was observed only in the first model, with a correlation coefficient of 2.24 (95% CI: 1.29-3.89) [Fig 2]. Conclusion: A robust positive correlation between arthritis and heart failure was observed in hypertensive U.S. patients. Gender was found to be a factor influencing this relationship, with males having a higher risk and prevalence of heart failure compared to the overall population.

AbstractWell‐selected patients with kidney disease and diabetes mellitus who undergo simultaneous kidney‐pancreas transplantation often experience dramatic improvements in quality of life and long‐term survival compared to those who remain on medical therapy. Over the past several years the importance of frailty in the pancreas transplant candidate and recipient populations has grown. More patients with advanced age have entered the waitlist, and complications from prolonged diabetes, even in younger patients, have created increased evidence of risk for frailty. Given these concerns, and the broad challenges facing pancreas transplantation volumes overall, we generated this review to help establish the impact and implications. We summarize the interplay of immunological factors, aging, environmental factors, diabetes mellitus, and chronic kidney disease that put these patients at risk for frailty. We discuss its measurement and recommend a combination of two instruments (both well‐validated and one entirely objective). We describe the outcomes for patients before and after pancreas transplantation who may have frailty, and what interventions can be taken to mitigate its effects. Broader investigation into frailty in the pancreas transplant population is needed to better understand how to select patients for pancreas transplantation and to how manage its consequences thereafter.

AbstractBackgroundDue to a substantial decline in pancreas transplantation (PT) across the United States over the past 15 years, we sought to understand the perceptions and practices of US PT programs.MethodsSurveys were sent to members of the American Society of Transplantation Surgeons and the American Society of Transplantation by email and professional society postings between August 2019 and November 2019.ResultsOne hundred twenty three responses were recorded from 56 unique programs. Program characteristics were obtained from the Scientific Registry of Transplant Recipients. Respondents were transplant surgeons (71%), transplant nephrologists (17%), trainees (9%), and allied professionals (3%). Programs were defined according to annual volume as: low (<5 PT/year), intermediate (6–20), or high (>20). High‐volume programs reported that these factors were most important for increased PT: expansion of recipient selection, more aggressive donor utilization, and hiring of PT program‐specific personnel. At both the program and national level, the vast majority (82% and 79%, respectively) felt the number of PTs currently performed are not in balance with patients' needs.ConclusionsOverall, programs reported that the option of PT is not offered adequately to diabetic patients and that strategies to maintain higher PT volume are most evident at intermediate, and especially, high‐volume programs.