Family planning program has been globally shown to reduce maternal mortality by reducing both total and high-risk pregnancies. Despite the national implementation of this program since the 1970s, Indonesia still faces many challenges in achieving family planning goals. Low modern contraceptive prevalence rate (mCPR) remains a problem that impacts public health, population growth, economy, and welfare issues. It should be tackled, especially in rural areas, with multifactorial causes and diverse needs. Various programs have been developed globally to overcome this problem; however, each region has different characteristics and demands that should be understood. This feminist qualitative study, embedding participatory action research principles and adapting the first three steps of the six essential steps for quality intervention development (6SQuID), aims to develop a theory of change by understanding the rural population's needs and actively collaborating with multiple participant groups to increase modern contraceptive uptake. The target location is West Sumba Regency, one of Indonesia's 100 lowest mCPR regencies and located in East Nusa Tenggara, which has the highest total fertility rate in Indonesia. Consisting of two rounds of data collection, this study includes different participant groups: rural women, men, mothers-in-law, religious figures, cultural leaders, community health workers, family planning educators, and family planning decision-makers with different strategies. We aim to recruit approximately 45 participants through purposive sampling, selecting participants based on the criteria for each group. The data collection methods are focus groups and semi-structured interviews. This study will encourage the community to collaborate and empower rural women to overcome their problems by identifying the reasons behind modern contraceptive refusal and developing a theory of change to reach the final goal: to create a meaningful change in modern contraceptive services. By understanding the diverse contexts and specific needs of the rural population, this study will be essential to transforming family planning programs. In doing so, it will significantly enhance reproductive and women's health while also addressing and reducing health disparities in rural communities. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement Yes ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: The College of Medical, Veterinary, and Life Sciences (MVLS) Research Ethics Committee of the University of Glasgow, United Kingdom, issued ethical approval in August 2025 (200240450), and the Public Health Faculty of the University of Nusa Cendana, Indonesia, issued ethical approval in May 2025 (001922/KEPK FKM UNDANA/2025). I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes Datasets have not been fully generated or analysed during the current study. Deidentified research data will be made available under the University of Glasgow, following the University’s Code of Good Practice and ethical standards, upon completion of the study and publication.

Body mass index (BMI) is widely used to assess obesity-related risk, but it does not capture ectopic fat deposition. Muscle fat infiltration (MFI), an MRI-derived marker of ectopic adiposity, may provide additional insight into type 2 diabetes (T2D) risk (1) . We examined sex-specific associations of MFI and BMI with incident T2D in a large population-based cohort. This prospective analysis included 17,482 women and 19,610 men free of T2D at baseline with available MRI data. Incident T2D cases (468 in women and 270 in men) were identified using linked primary care records, with a median follow-up of 12.1 years. BMI and MRI-derived MFI were standardized (z-scores) and additionally categorized into sex-specific quintiles. Sex-stratified Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) per 1-SD increase and across quintiles, adjusting for age, deprivation index, ethnicity, physical activity, smoking status, and alcohol intake. For a 1-SD increase in MFI, the risk of T2D was higher in both women (HR: 1.53; 95% CI: 1.42–1.64) and men (HR: 1.49; 95% CI: 1.41–1.57). Corresponding associations for BMI were stronger (women: HR 2.10; 95% CI: 1.93–2.28; men: HR 2.06; 95% CI: 1.93–2.20). Comparing the highest versus lowest quintile, women in the highest BMI quintile had a markedly higher risk of T2D (HR: 19.5; 95% CI: 9.12–41.6), while the highest quintile of MFI was associated with a 9.07-fold higher risk (95% CI: 4.54–18.1). Among men, the highest quintile of MFI was associated with an 8.35-fold higher risk (95% CI: 5.33–13.1), whereas the highest quintile of BMI was associated with an 11.5-fold higher risk (95% CI: 7.33–18.0). Muscle fat infiltration, an MRI-derived marker of ectopic adiposity, is strongly associated with future risk of type 2 diabetes in both women and men. However, BMI showed consistently stronger associations with T2D risk, particularly at the extremes of the distribution. These findings suggest that while MRI-derived measures such as MFI capture important aspects of metabolic risk, BMI remains a robust and powerful predictor of T2D in population settings. Advanced imaging may nevertheless offer complementary value for understanding ectopic fat–related mechanisms and refining risk stratification.

Purpose: Vitamin K2 supplementation has emerged as a strategy to enhance recovery and modulate post-exercise physiological responses. This study aimed to assess the effects of vitamin K2 on recovery from muscle-damaging exercise in young and older adults. Methods: Healthy young (18-40 years) and older (65+ years) adults were randomly assigned to either vitamin K2 (menaquinone 7, MK-7, 240 μg/day) or placebo (cellulose) for 12 weeks in this double-blind randomised controlled trial. Before and after supplementation, knee extensor maximal torque, functional ability, muscle soreness, and systemic blood markers of muscle damage and inflammation were measured before (0h) and 3h, 24h, 48h, and 72h post-exercise. Data were analysed using regression and mixed models. Results: Seventy-one participants (35 young and 36 older) completed the study, with 12 weeks of vitamin K2 supplementation increasing circulating MK-7 levels (p-value <0.001). There were no supplement*time effects for any variables. Significant supplement*time*older age interaction effects were noted for electromechanical delay (EMD) (p-value = 0.03), electromyography root mean square (RMS) (p-value = 0.01), IL-6 concentrations (p-value <0.001), and creatine kinase (CK) levels (p-values = 0.02). In older adults, after 12 weeks, EMD appeared lower at all time points and RMS higher post exercise in the vitamin K2 group. No clear pattern in IL-6 or CK were observed, but at 72h post-exercise CK was lower in older adults in the Vitamin K2 group. Conclusions: Vitamin K2 supplementation had no effect on muscle strength, physical function, muscle soreness or inflammatory responses in the recovery period after a bout of resistance exercise. Effects of supplementation were observed on EMD, RMS, IL-6 and CK by age, and warrant further investigation. Trial registration: Prospectively registered on 21st December 2020, trial registration clinicaltrials.gov ID NCT04676958 https://clinicaltrials.gov/ct2/show/NCT04676958.

Background:Families with parents with health conditions often experience socioeconomic hardship, caregiving strain, and elevated exposure to family violence. However, differences in family polyvictimization (FPV) between these families and those without health conditions remain underexplored. This study examined disparities in FPV exposure and associated family-level risk factors. Methods:A cross-sectional household survey was conducted with 1,400 Hong Kong families with children under 18. Measures included FPV (FPV Screen), social support (MSPSS), family hierarchy (PRP), health (SF-12v2, PedsQoL), and mental health (DASS-21). Logistic regression models were used to examine associations between family characteristics and having parents with health conditions, as well as differences in FPV exposure between the two family groups. Results:Families with parents with health conditions had significantly higher FPV prevalence, with elder victimization remaining significant after adjustment (aOR = 1.89, 95% CI: 1.08-3.29). These families also showed greater odds of co-occurring disadvantages, including caregiving responsibilities for children with special educational needs (aOR = 3.81) or older relatives (aOR = 1.71), lower household income (aOR = 1.71), reduced physical functioning (aOR = 0.93), limited social support (aOR = 0.83), and heightened exposure to violence socialization (aOR = 1.48). Conclusions:FPV is more prevalent in families with parents with health conditions, especially when combined with caregiving strain, economic disadvantage, and relational stress. These findings support integrating FPV screening and family-centered support into disability and caregiving services, with attention to elder victimization and low-social-support households.

Multimorbidity is highly prevalent and a major driver of premature mortality (1–5) . While healthy lifestyle behaviours are known to reduce mortality risk in the general population (6,7) , it remains unclear to what extent individuals with multimorbidity benefit from sustained lifestyle improvements. We aimed to evaluate the association between lifestyle and mortality risk in people with multimorbidity, and whether it varied across the specific multimorbidity patterns. This prospective study included 475,706 UK Biobank participants. A lifestyle score (8) according to nine risk factors (smoking, alcohol, physical activity, sleep, TV viewing, fruit and vegetable intake, oily fish, red meat, processed meat) was established and categorised as healthy and unhealthy lifestyle. Specific multimorbidity patterns were defined as metabolic (≥2 of diabetes, stroke, heart disease), cardio-renal (≥2 of diabetes, stroke, heart disease, kidney disease), and overall (≥2 of 43 conditions) multimorbidity (9) . All-cause mortality was ascertained from death registries and hospital records. Cox proportional hazards models, with interaction terms, assessed associations between lifestyle and the outcome across multimorbidity types. Participants with missing covariates or implausible values of lifestyle risk factors were excluded. Models were adjusted for age, sex, ethnicity, deprivation, and BMI. All participants provided written informed consent (10) . Among participants, 44.5% reported an unhealthy lifestyle, and 1.9%, 1.7% and 32.8% had cardiovascular, cardio-renal and overall multimorbidity, respectively. Compared with those without multimorbidity, hazard ratios (HRs) for all-cause mortality were 4.63 (95% CI, 4.30-4.98) for metabolic multimorbidity and 4.84 (95% CI,4.51-5.20) for cardio-renal multimorbidity. Compared with people without diseases and with healthy lifestyle, participants with cardio-renal multimorbidity and an unhealthy lifestyle had a markedly elevated risk of HR 6.65 (95% CI, 6.10–7.25) for all-cause mortality. Significant multiplicative and additive interactions between lifestyle and multimorbidity were observed for all-cause mortality in overall multimorbidity. Lifestyle behaviours substantially modify the mortality risk among people with multimorbidity. The greatest benefit is observed in cardio-renal multimorbidity. Targeted, cluster-specific lifestyle interventions could markedly reduce premature mortality and support precision prevention strategies in people with high multimorbidity burden.

Background: Preventing multimorbidity requires understanding how long-term conditions begin to accumulate. Clinical management of a first long-term condition may provide an opportunity for secondary prevention of multimorbidity. Cardiovascular-kidney-metabolic (CKM) conditions share interconnected risk factors and established monitoring and risk-reduction pathways, but whether progression differs after a first CKM versus non-CKM condition remains unclear. Methods: We conducted a retrospective cohort study of adults aged 18 years and older in Japan, the UK, and Denmark, with no or one of 22 harmonised conditions most relevant in primary care. We used a continuous-time multistate framework to examine progression from a first condition to two conditions (MM2), then three or more conditions (MM3+), and death after MM2. We estimated three-year absolute risks and HRs, using time-split Cox models (0–1, 1–3, and ≥3 years), stratified by sex and adjusted for age and calendar year. Findings: We included 3 258 240 participants in Japan, 1 570 985 in the UK, and 3 391 192 in Denmark. Three-year absolute multimorbidity risk was higher after CKM first conditions than non-CKM first conditions: Japan: 44·7% versus 38·8%, UK: 32·9% versus 22·2%, Denmark: 40·2% versus 32·8%. CKM-first trajectories had higher hazards of progression to multimorbidity than non-CKM-first trajectories across all countries and time bands. Corresponding HRs for non-CKM versus CKM first conditions ranged from 0·84 to 0·97 in Japan, 0·69 to 0·86 in the UK, and 0·70 to 0·90 in Denmark. After MM2, associations with MM3+ varied by pattern, age, country, and time; the non-CKM-to-non-CKM pattern had the highest mortality hazard across countries. Interpretation: A first CKM condition was associated with faster progression to MM2, but absolute risk after a first non-CKM condition remained substantial. After MM2, further accumulation and mortality varied by disease composition and recorded sequence. Secondary prevention for multimorbidity should address both CKM-first and non-CKM-first trajectories.

Previous studies showed a significant association between screen time (ST) and health-related quality of life (HRQoL) in children. However, the mechanisms underlying the association are unclear. To determine the extent to which time spent (physical activities and sleep duration) and relationship factors (dysfunctional parent-child interaction and peer problems) mediate the association between children’s ST and their HRQoL. A population-representative sample of 1,033 parents of primary school children (49.3% female; Mage = 8.5, SDage = 1.9) in Hong Kong participated in the study over the course of one year (two waves). Children’s ST was reported by parents. The study outcome, children’s HRQoL, was assessed using the 23-item Pediatrics Quality of Life Inventory Parent-Proxy Report (PedsQL). Mediators, including dysfunctional parent-child interaction (PCDI), peer problems (SDQ-PP), weighted daily time spent in moderate-to-vigorous physical activity (MVPA), and weighted average of daily sleep duration, were assessed to test the displacement and relational hypotheses. Multilevel structural equation modeling with a 1-1-1 mediation framework showed a statistically significant direct effect (β = -0.77, 95% CI -1.02 to -0.53) of ST on PedsQL. The association was partially mediated by both relationship factors (PCDI: β = -0.09, 95% confidence interval [CI] -0.15 to -0.03; mediation proportion = 8.33%; SDQ-PP: β = -0.13, 95% CI -0.23 to -0.03; mediation proportion = 12.74%) at the within-person level, but not time spent factors (i.e., sleep duration and MVPA). Impairments in parent-child and peer relationships partially mediated the association between duration of screen time and children’s HRQoL. These findings suggest that relationship-focused intervention might buffer the negative associations of increased screen time on children’s functioning. Not applicable.

The associations between systemic inflammation biomarkers and cardiovascular disease (CVD) remain not well explored. This study aimed to investigate associations between different systemic inflammation biomarkers and incident CVD and main CVD subtypes - ischaemic heart disease (IHD), stroke, and heart failure - explore dose–response relationships, and compare their predictive performance. This prospective cohort study included 423,701 UK Biobank participants free of CVD at baseline. Baseline neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), platelet-to-lymphocyte ratio (PLR), systemic immune-inflammation index (SII), and system inflammation response index (SIRI) were derived. Cox-proportional regression models were used to investigate the associations. NLR, PLR, SII, and SIRI was positively and LMR was negatively associated with all four of the outcomes investigated. The relationships were non-linear for all biomarkers with CVD and were linear for NLR, SII, and SIRI and non-linear for LMR and PLR with IHD, stroke and heart failure. Compared with the more established biomarkers, all four of the novel biomarkers had statistically superior predictive performance for three of the outcomes investigated (CVD, IHD and heart failure) and three of them were superior at predicting stroke. Compared to a model of CVD prediction with classical risk factors (C-index = 0.702), discrimination was improved on the addition of inflammation markers for CVD (C-index change 0.0069, 95

Importance:Body mass index (BMI) is widely used to assess obesity-related health risks, but waist circumference (WC) and waist-to-height ratio (WHtR) are thought to better capture central adiposity and associated disease risk. Objective:To compare the associations of BMI, WC, and WHtR with the risk of 78 incident conditions, multiple long-term conditions (MLTCs), and mortality, and to evaluate whether waist-based measures improve risk identification over BMI and, if so, over which BMI range. Design Setting and Participants:This cohort study analyzed data from 495,911 adults in the UK Biobank with a mean follow-up of 13.7 years. Findings were replicated in the Whitehall II study (n = 7,973; mean follow-up, 28.6 years). Exposures:Obesity defined by BMI, WC, and WHtR. Main Outcomes and Measures:Associations of each adiposity measure with 78 incident conditions, MLTCs, and mortality were assessed using Cox proportional hazards models. Population attributable fractions (PAFs) were calculated to estimate the proportion of outcomes attributable to obesity defined by each measure. Results:Obesity defined by BMI, WC, or WHtR was associated with increased risk for most outcomes. WHtR-defined obesity generally showed the strongest associations, followed by WC and BMI, with some exceptions (e.g., osteoarthritis). However, PAFs for MLTCs for WC and WHtR were <1% percentage points higher than for BMI. Notably, meaningful gains in PAFs were observed only among individuals with BMI between 25.0 and 29.9. These findings were replicated in the Whitehall II cohort. Conclusions and Relevance:Replacing BMI with waist-based measures did not meaningfully improve risk identification for MLTCs in the general population when BMI was ≥30. However, waist-based measures may offer additional predictive value among individuals with BMI <30.

BACKGROUND:NICE guidelines recommend GPs use the kidney failure risk equation (KFRE) to identify people with chronic kidney disease (CKD) at higher risk of kidney failure. Albuminuria results are required to calculate KFRE. AIM:Analyse the implementation of KFRE into clinical practice and investigate if albuminuria testing varied amongst patients with CKD, particularly for underserved groups. DESIGN AND SETTING:Retrospective cohort study of 23,063 adults in Glasgow from 2013 to 2022. METHOD:We evaluated albuminuria testing rates and the predictive performance of KFRE in estimating 5-year kidney failure risk amongst people with CKD. Logistic regression models quantified associations between demographic/clinical variables and albuminuria testing. Amongst people who developed kidney failure, we retrospectively assessed the impact of KFRE on the timing of meeting criteria for referral to renal services. RESULTS:Albuminuria testing was performed in 44.5% of 10,874 adults with CKD. Females (adjusted odds ratio (aOR) 0.86: 95% CI 0.79-0.93) and those with hypertension (aOR 0.69: 95% CI 0.63-0.77) were less likely to have albuminuria testing. Those aged 40-50 years (aOR 1.83: 95% CI 1.15-2.91), with diabetes (aOR 2.35: 95% CI 2.14-2.58) and living in the least socioeconomically deprived areas (aOR 1.11: 95% CI 1.00-1.23) were more likely to have albuminuria testing. Of 1,352 individuals with incident kidney failure, incorporating KFRE into referral guidelines helped identify high-risk patients early. CONCLUSION:KFRE could be calculated for less than half of people due to lack of albuminuria testing. Focus should be given to improving albuminuria testing and inequities identified to allow wider implementation of KFRE.

AIMS:Genetic predisposition to adiposity is associated with type 2 diabetes (T2D), even in the absence of phenotypic adiposity (obesity and central obesity). We aimed to quantify the overall contribution of obesity and modifiable lifestyle factors to the association between genetic predisposition to adiposity and the development of T2D. METHODS:This prospective cohort study involved 220 703 White British participants from the UK Biobank. It examined the associations between genetic predisposition to adiposity [body mass index polygenic risk (BMI-PRS) and waist-hip ratio polygenic risk (WHR-PRS)] and incident T2D, as well as interactions and mediation via lifestyle factors (diet quality, physical activity levels, total energy intake, sleep duration, and smoking and alcohol intake) and phenotypic adiposity. RESULTS:People with high phenotypic adiposity and high adiposity PRS values (>1 SD above the mean) had the highest risk of incident T2D (versus non-obese/central obese and non-high PRS). This was the case for BMI-PRS [hazard ratio (HR) = 3.72] and WHR-PRS (HR = 4.17). Lifestyle factors explained 30.5% of the BMI-PRS/T2D association (2.0% mediation; 28.5% effect modification), and lifestyle and obesity together explained 92.1% (78.8% mediation; 13.3% effect modification). Lifestyle factors explained 20.4% of the WHR-PRS/T2D association (3.4% mediation; 17.0% effect modification), and lifestyle and central obesity together explained 72.8% (41.1% mediation; 31.7% effect modification). CONCLUSIONS:Whilst phenotypic adiposity explains a large proportion of the association between BMI-PRS/WHR-PRS and T2D, modifiable lifestyle factors also make contributions. Promoting healthy lifestyles among people prone to adiposity is important in reducing the global burden of T2D.

Physical activity (PA) is consistently associated with lower risk of long-term conditions. Preliminary evidence suggested the associations could be modified by air pollution. This study aims to examine whether air pollution levels modify the associations of PA with all-cause mortality and incident cancer, major adverse cardiovascular events (MACE), type 2 diabetes, and chronic obstructive pulmonary disease (COPD). A total of 414,644 UK Biobank participants were included in the analyses. PA was self-reported and objectively measured using accelerometers. PA was self-reported with IPAQ and objectively measured using accelerometers. Annual PM2.5, PM10, and NO air pollutant concentrations in 2010 were measured using a European land use regression model. Cox proportional hazard models were used to examine the associations of PA and air pollution with health outcomes. Multiplicative and additive interactions were estimated. During the study period from 2006 to 2022, 31,765 (7.7

AIMS:Pain is associated with cardiovascular disease; however, its association with incident arrhythmias is unclear. We assessed associations between different pain characteristics (pain type, chronic pain, chronic widespread pain [chronic widespread pain], chronic musculoskeletal pain [chronic musculoskeletal pain], and number of chronic pain and chronic musculoskeletal pain sites) and incident cardiac arrhythmias, overall and by subtype. METHODS:The study included 422,654 UK Biobank participants. Pain was ascertained via a touchscreen questionnaire. The outcomes were incident arrhythmias: all cardiac arrhythmias, atrial fibrillation (AF), other (non-AF) cardiac arrhythmias, bradyarrhythmias, and ventricular arrhythmias. Multivariable Cox-proportional regression was used to investigate the associations. RESULTS:Over a mean (SD) follow-up of 13.19 (1.96) years, 36,860 (8.72%) participants developed arrhythmia. Compared with those without pain, those with chronic localized pain and chronic widespread pain had increased risk of all cardiac arrhythmias (hazard ratio [HR] 1.13, 95% confidence interval [CI], 1.10-1.17; 1.34, 1.19-1.51), AF (1.09, 1.05-1.14; 1.33, 1.15-1.55), and other cardiac arrhythmias (1.17, 1.12-1.22; 1.41, 1.20-1.66). There was evidence of a dose-relationship between number of chronic pain sites and risk of all cardiac arrhythmias, AF and bradyarrhythmias. Effect estimates were significantly larger among participants aged <60 years than those aged ≥60 years, and larger in women than men. CONCLUSIONS:Chronic pain was associated with cardiac arrhythmias. Whilst causation cannot be assumed in any observational study, there was evidence of both a temporal relationship and dose-relationship. These findings reinforce the need for pain management approaches that include a broad assessment of individuals' risk factors, wider health status, and appropriate vigilance for emerging conditions.

Maternal adversity (e.g., adverse childhood experiences, ACEs) and health (e.g., depressive symptoms and chronic illness) negatively impact offspring's health. One possible mechanism is via premature/accelerated biological aging, as indicated in telomere length. In this 3-year longitudinal study, we examined the association between maternal adversity and health and children's buccal telomere length (bTL) at age 3. Data from 122 mother-child dyads were analyzed. Maternal history of ACEs and chronic illness were collected at baseline (during 20-24 weeks of gestation). Their depressive symptoms across three periods (during pregnancy, 4 weeks after childbirth, and 3 years after childbirth) were also collected. Children's TL were extracted from their buccal swab samples at age 3. The children's bTL was quantified using the quantitative PCR method and expressed in T/S ratio (the ratio of telomere repeats copy numbers to single-copy gene numbers). Results showed pregnant women experienced distinctive trajectories of depressive symptoms over time. Children of mothers with relapsing/remitting depressive symptoms had shorter bTL (β = -0.19, 95% CI = -0.14 to -0.005) than mothers who had low-stable symptoms. This finding remained significant even after accounting for maternal ACEs and chronic illness. Additionally, maternal ACEs, together with depressive symptoms, may affect children's bTL. This study provides relatively comprehensive evidence on the effects of maternal stressors, highlighting the relevance of maternal adversity and depressive symptom patterns as predictors of offspring telomere biology.

Clinical guidelines recommend use of (1) antiplatelet, (2) lipid-lowering, and (3) beta blocker medication, and (4) angiotensin-converting enzyme inhibitor or angiotensin receptor blocker (ACEi/ARB) for secondary prevention following myocardial infarction (MI). This study examines whether sociodemographic factors and comorbidity were associated with receipt of guideline-recommended medication, and whether receipt was associated with all-cause mortality. A cohort study was conducted on West of Scotland patients aged 53 years or above who were discharged from hospital alive after an incident MI between 2014 and 2022. Receipt of guideline-directed therapy was defined as relevant medications dispensed within 3 months of discharge. Age, sex, area-deprivation, care/nursing home residence, year of incident MI, and pre-existing conditions were included as predictors of non-receipt and covariates in the analysis of the association between non-receipt and death. Among 12,204 MI survivors, 7898 (64.72