Risk Of Heart Disease Mortality Research Articles

TEMPORARY REMOVAL: Estimated doses to the heart, lungs and oesophagus and risks from typical UK radiotherapy for early breast cancer during 2015-2023

PurposeBreast cancer radiotherapy can increase the risks of heart disease, lung cancer and oesophageal cancer. At present, the best dosimetric predictors of these risks are mean doses to the whole heart, lungs and oesophagus, respectively. We aimed to estimate typical doses to these organs and resulting risks from UK breast cancer radiotherapy. MethodsA systematic review and meta-analysis was conducted of planned or delivered mean doses to the whole heart, lungs or oesophagus from UK breast cancer radiotherapy in studies published during 2015-2023. Average mean doses were summarised for combinations of laterality and clinical targets. Heart disease and lung cancer mortality risks were then estimated using established models. ResultsFor whole heart, thirteen studies reported 2893 doses. Average mean doses were higher in left than in right-sided radiotherapy and increased with extent of clinical targets. For left-sided radiotherapy, average mean heart doses were: 2.0 Gy (range 1.2-8.0 Gy) breast/chest wall, 2.7 Gy (range 0.6-5.6 Gy) breast/chest wall with either axilla or supraclavicular nodes and 2.9 Gy (range 1.3-4.7 Gy) breast/chest wall with nodes including internal mammary. For right-sided radiotherapy, average mean heart doses were: 1.0 Gy (range 0.3-1.0 Gy) breast/chest wall and 1.2 Gy (range 1.0-1.4 Gy) breast/chest wall with either axilla or supraclavicular nodes. There were no whole heart dose estimates from right internal mammary radiotherapy.For whole lung, six studies reported 2230 doses. Average mean lung doses increased with extent of targets irradiated: 2.6 Gy (range 1.4-3.0 Gy) breast/chest wall, 3.0 Gy (range 0.9-5.1 Gy) breast/chest wall with either axilla or supraclavicular nodes and 7.1 Gy (range 6.7-10.0 Gy) breast/chest wall with nodes including internal mammary.For whole oesophagus, two studies reported 76 doses. Average mean oesophagus doses increased with extent of targets irradiated: 1.4 Gy (range 1.0-2.0 Gy) breast/chest wall with either axilla or supraclavicular nodes and 5.8 Gy (range 1.9-10.0 Gy) breast/chest wall with nodes including internal mammary. ConclusionThe typical doses to these organs may be combined with dose-response relationships to estimate radiation risks. Estimated 30-year absolute lung cancer mortality risks from modern UK breast cancer radiotherapy for patients irradiated when aged 50 years were 2 to 6% for long-term continuing smokers, and <1% for non-smokers. Estimated 30-year mortality risks for heart disease were <1%.

Association of Disrupted Delta Wave Activity During Sleep With Long-Term Cardiovascular Disease and Mortality

BackgroundDelta wave activity is a prominent feature of deep sleep, which is significantly associated with sleep quality. ObjectivesThe authors hypothesized that delta wave activity disruption during sleep could predict long-term cardiovascular disease (CVD) and CVD mortality risk. MethodsThe authors used a comprehensive power spectral entropy-based method to assess delta wave activity during sleep based on overnight polysomnograms in 4,058 participants in the SHHS (Sleep Heart Health Study) and 2,193 participants in the MrOS (Osteoporotic Fractures in Men Study) Sleep study. ResultsDuring 11.0 ± 2.8 years of follow-up in SHHS, 729 participants had incident CVD and 192 participants died due to CVD. During 15.5 ± 4.4 years of follow-up in MrOS, 547 participants had incident CVD, and 391 died due to CVD. In multivariable Cox regression models, lower delta wave entropy during sleep was associated with higher risk of coronary heart disease (SHHS: HR: 1.46; 95% CI: 1.02-2.06; P = 0.03; MrOS: HR: 1.79; 95% CI: 1.17-2.73; P < 0.01), CVD (SHHS: HR: 1.60; 95% CI: 1.21-2.11; P < 0.01; MrOS: HR: 1.43; 95% CI: 1.00-2.05; P = 0.05), and CVD mortality (SHHS: HR: 1.94; 95% CI: 1.18-3.18; P < 0.01; MrOS: HR: 1.66; 95% CI: 1.12-2.47; P = 0.01) after adjusting for covariates. The Shapley Additive Explanations method indicates that low delta wave entropy was more predictive of coronary heart disease, CVD, and CVD mortality risks than conventional sleep parameters. ConclusionsThe results suggest that delta wave activity disruption during sleep may be a useful metric to identify those at increased risk for CVD and CVD mortality.

Weight change and all-cause and cause-specific mortality: A 25-year follow-up study.

Whether the dynamic weight change is an independent risk factor for mortality remains controversial. This study aimed to examine the association between weight change and risk of all-cause and cause-specific mortality based on the Linxian Nutrition Intervention Trial (NIT) cohort. Body weight of 21,028 healthy residents of Linxian, Henan province, aged 40-69 years was measured two times from 1986 to 1991. Outcome events were prospectively collected up to 2016. Weight maintenance group (weight change <2kg) or stable normal weight group was treated as the reference. Cox proportional hazard model was performed to calculate hazard ratios (HRs) and 95% confidence intervals (95% CIs) to estimate the risk of mortality. A total of 21,028 subjects were included in the final analysis. Compared with the weight maintenance group, subjects with weight loss ≥2kg had an increased risk of death from all-cause (HR All-cause =1.14, 95% CI: 1.09-1.19, P <0.001), cancer (HR Cancer =1.12, 95% CI: 1.03-1.21, P =0.009), and heart disease (HR Heart diseases =1.21, 95% CI: 1.11-1.31, P <0.001), whereas subjects with weight gain ≥5kg had 11% (HR Cancer =0.89, 95% CI: 0.79-0.99, P =0.033) lower risk of cancer mortality and 23% higher risk of stroke mortality (HR Stroke =1.23,95% CI: 1.12-1.34). For the change of weight status, both going from overweight to normal weight and becoming underweight within 5 years could increase the risk of total death (HR Overweight to normal = 1.18, 95% CI: 1.09-1.27; HR Becoming underweight = 1.35, 95% CI: 1.25-1.46) and cancer death (HR Overweight to normal = 1.20, 95% CI: 1.04-1.39; HR Becoming underweight = 1.44, 95% CI: 1.24-1.67), while stable overweight could increase the risk of total death (HR Stable overweight = 1.11, 95% CI: 1.05-1.17) and death from stroke (HR Stable overweight = 1.44, 95% CI: 1.33-1.56). Interaction effects were observed between age and weight change on cancer mortality, as well as between baseline BMI and weight change on all-cause, heart disease, and stroke mortality (all Pinteraction <0.01). Weight loss was associated with an increased risk of all-cause, cancer, and heart disease mortality, whereas excessive weight gain and stable overweight were associated with a higher risk of stroke mortality. Efforts of weight management should be taken to improve health status. NCT00342654, https://classic.clinicaltrials.gov/ .

Inflammation and poverty as individual and combined predictors of 15-year mortality risk in middle aged and older adults in the US.

Chronic systemic inflammation and poverty are both linked to an increased mortality risk. The goal of this study was to determine if there is a synergistic effect of the presence of inflammation and poverty on the 15-year risk of all-cause, heart disease and cancer mortality among US adults. We analyzed the nationally representative National Health and Nutrition Examination Survey (NHANES) 1999 to 2002 with linked records to the National Death Index through the date December 31, 2019. Among adults aged 40 and older, 15-year mortality risk associated with inflammation, C-reactive protein (CRP), and poverty was assessed in Cox regressions. All-cause, heart disease and cancer mortality were the outcomes. Individuals with elevated CRP at 1.0 mg/dL and poverty were at greater risk of 15-year adjusted, all-cause mortality (HR = 2.45; 95% CI 1.64, 3.67) than individuals with low CRP and were above poverty. For individuals with just one at risk characteristic, low inflammation/poverty (HR = 1.58; 95% CI 1.30, 1.93), inflammation/above poverty (HR = 1.59; 95% CI 1.31, 1.93) the mortality risk was essentially the same and substantially lower than the risk for adults with both. Individuals with both elevated inflammation and living in poverty experience a 15-year heart disease mortality risk elevated by 127% and 15-year cancer mortality elevated by 196%. This study extends the past research showing an increased mortality risk for poverty and systemic inflammation to indicate that there is a potential synergistic effect for increased mortality risk when an adult has both increased inflammation and is living in poverty.

Predicted visceral adiposity index in relation to risk of coronary heart disease and all-cause mortality: insights from NHANES.

The Visceral Adiposity Index (VAI) is a straightforward and gender-specific marker that combines anthropometric measurements with lipid profiles. The objective of this study was to evaluate the relationship between VAI and coronary heart disease (CHD). The study examined data collected from adults during the NHANES 1999-2018 cycle. The analyses were weighted, and multivariable logistic regression models were employed to investigate the association between VAI and CHD. Additionally, subgroup analyses stratified by age were conducted. To evaluate the impact of VAI levels on survival outcomes, the study utilized the Kaplan-Meier method and performed the log-rank test to evaluate the survival outcome of participants with different VAI levels. The study findings revealed a significant association between VAI and CHD, indicating a non-linear relationship where an increase in VAI was associated with an elevated risk of CHD. High levels of VAI were linked to an increased prevalence of CHD (Q4 vs Q1, OR 1.50, 95% CI 1.12-2.01, P=0.01). Additionally, higher levels of VAI were associated with a poorer overall prognosis in terms of survival outcomes. There were no statistically significant differences in survival outcomes among the population with CHD. The results of this study highlighted a significant association between VAI and CHD, with a non-linear relationship observed. High VAI levels were associated with an increased risk of CHD and poor survival outcomes, emphasizing the importance of understanding and managing this risk factor, particularly in older age groups.

Sleep duration and mortality in patients with chronic noncommunicable disease: a population-based cohort study.

Inadequate sleep behaviors may confer a higher risk of premature death, however, evidence in patients with chronic noncommunicable disease (NCD) is scarce. To investigate the relationship between sleep duration and mortality from all-cause and heart diseases in NCD patients from a prospective cohort. Totally, 14,171 participants with at least one NCD, including 8275 with hypertension, 7547 with high cholesterol, 4065 with diabetes, and 5815 with chronic renal failure were enrolled from the National Health and Nutrition Examination Survey during 2005-2014. Cox proportional hazard models were performed to estimate the hazard ratio (HR) for sleep duration and mortality after adjusting for potential confounding factors. After a median follow-up of 9 years, 2514 all-cause deaths were identified. Compared with sleeping 7-8 h/day, sleeping over 8 h/day was significantly associated with a higher risk of all-cause mortality, where the multivariable-HRs were 1.29 (1.11, 1.50) for hypertension, 1.23 (1.01, 1.51) for high cholesterol, 1.44 (1.13, 1.82) for diabetes, and 1.36 (1.10, 1.68) for chronic renal failure. Similar patterns were observed for heart disease mortality. A nonlinear association was detected between sleep duration and mortality in patients with NCD. Age modified the association in patients with hypertension (P-interaction: 0.036). Trouble sleeping modified the association in patients with diabetes (P-interaction: 0.042). Long sleep duration was associated with higher risks of all-cause and heart disease mortality in patients with chronic NCD. Our findings highlight that improving sleep behaviors may decrease the risk of premature deaths and help to NCD tertiary prevention.

Calcium - a scoping review for Nordic Nutrition Recommendations 2023.

The aim of this scoping review was to conduct evidence-based documentations between calcium (Ca) intake and health outcomes for updating dietary reference values (DRVs) and food-based dietary guidelines (FBDGs) in the sixth edition of Nordic Nutrient Recommendations (NNR2023). The systematic literature search was limited to reviews on human data published between 2011 and June 2021. Systematic reviews (SRs) and original publications of relevance for this scoping review were included. A common practice of designing studies on health outcomes related to Ca supplement intake is to examine combined Ca and vitamin D, and therefore, a combination of Ca with vitamin D (CaD) was included in this review. In total, 27 studies addressing the association between dietary or supplemental Ca on bone health, bone mineral density (BMD), pregnancy-related outcomes, cardiovascular diseases (CVD), cancers, obesity, and mortality were reviewed. SRs showed that both dietary and supplemental Ca intakes were positively associated with BMD, but evidence did not support the benefit in fracture prevention. Current evidence did not support that Ca or CaD supplementation increases risk of coronary heart disease or all-cause mortality in older adults, but that Ca may be beneficial for hypertension, especially in young people. Increasing Ca intake may be beneficial during pregnancy, especially for those at high risk of pre-eclampsia due to ethnicity, age, high BMI, and those with low baseline Ca intake. The associations between high Ca intake and cancers were varied, with strong evidence that high consumption of dairy products is protective against colorectal cancer and limited-suggestive evidence that dairy products and diets high in Ca might also be protective against breast cancer. Moreover, there is limited-suggestive evidence that dairy products and diets high in Ca increase the risk of prostate cancer. Based on current evidence, Ca intake is beneficial or neutral in relation to most of the outcomes evaluated in this review. Data from the Nordic countries show that average Ca intake is around the same as previously recommended by NNR. However, the average Ca intake in the Baltic countries is below the recommendations.

Estimating dose-response relationships for vitamin D with coronary heart disease, stroke, and all-cause mortality: observational and Mendelian randomisation analyses

Randomised trials of vitamin D supplementation for cardiovascular disease and all-cause mortality have generally reported null findings. However, generalisability of results to individuals with low vitamin D status is unclear. We aimed to characterise dose-response relationships between 25-hydroxyvitamin D (25[OH]D) concentrations and risk of coronary heart disease, stroke, and all-cause mortality in observational and Mendelian randomisation frameworks. Observational analyses were undertaken using data from 33 prospective studies comprising 500 962 individuals with no known history of coronary heart disease or stroke at baseline. Mendelian randomisation analyses were performed in four population-based cohort studies (UK Biobank, EPIC-CVD, and two Copenhagen population-based studies) comprising 386 406 middle-aged individuals of European ancestries, including 33 546 people who developed coronary heart disease, 18 166 people who had a stroke, and 27 885 people who died. Primary outcomes were coronary heart disease, defined as fatal ischaemic heart disease (International Classification of Diseases 10th revision code I20-I25) or non-fatal myocardial infarction (I21-I23); stroke, defined as any cerebrovascular disease (I60-I69); and all-cause mortality. Observational analyses suggested inverse associations between incident coronary heart disease, stroke, and all-cause mortality outcomes with 25(OH)D concentration at low 25(OH)D concentrations. In population-wide genetic analyses, there were no associations of genetically predicted 25(OH)D with coronary heart disease (odds ratio [OR] per 10 nmol/L higher genetically-predicted 25(OH)D concentration 0·98, 95% CI 0·95-1·01), stroke (1·01, [0·97-1·05]), or all-cause mortality (0·99, 0·95-1·02). Null findings were also observed in genetic analyses for cause-specific mortality outcomes, and in stratified genetic analyses for all outcomes at all observed levels of 25(OH)D concentrations. Stratified Mendelian randomisation analyses suggest a lack of causal relationship for 25(OH)D concentrations with both cardiovascular and mortality outcomes for individuals at all levels of 25(OH)D. Our findings suggest that substantial reductions in mortality and cardiovascular morbidity due to long-term low-dose vitamin D supplementation are unlikely even if targeted at individuals with low vitamin D status. British Heart Foundation, Medical Research Council, National Institute for Health Research, Health Data Research UK, Cancer Research UK, and International Agency for Research on Cancer.

Competing Risks of Coronary Heart Disease Mortality versus Other Causes of Death in 10 Cohorts of Middle-Aged Men of the Seven Countries Study Followed for 60 Years to Extinction.

To assess whether competing risks help explain why regions with initially high serum cholesterol have higher mortality from coronary heart disease (CHD) and lower mortality from stroke and other major heart diseases, while the reverse is found for those with initially lower serum cholesterol. Ten cohorts of men (N = 9063) initially aged 40-59 in six countries were examined and followed for fatal outcomes for 60 years. Major cardiovascular disease (CVD) groups were CHD, stroke, and other Heart Diseases of Uncertain Etiology (HDUE), or the combination of stroke and HDUE (STHD), along with all other causes of death. Fine-Gray competing risk analysis was applied with CHD versus all other causes of death or STHD (direct mode) and all other causes of death or STHD versus CHD (inverse mode), and the effects of 19 covariates (of which 3 references) on the cause-specific hazard of the outcomes were assessed, thus investigating potential etiologic roles. A systematic comparison with results obtained by running the Cox model in direct and inverse modes with the same end-point results was also performed and illustrated graphically. CHD mortality is bound to different risk factor relationships when compared with all other causes of death and with STHD. The role of serum cholesterol is crucial since, in both comparisons, by Fine-Gray, its coefficients are positive and significant for CHD and negative and significant for all other causes of death and STHD. Risk factor capabilities in specific outcome types of the CVD domain (CHD versus STHD) are different depending on the outcome types considered. Risk factor coefficients are smaller in Fine-Gray modelling and larger in the Cox model. Fine-Gray detects different risk factors whose coefficients may have opposite algebraic signs. This is the first report whereby a large group of risk factors are investigated in connection with life-long CVD outcomes by Fine-Gray competing risk analysis, and a systematic comparison is performed with results obtained by Cox models in both direct and inverse modes. Subtypes of CVD mortality should be summed with full awareness that some risk factors vary by pathology, and they should at least be disentangled into CHD and STHD.

Multidimensional Sleep Health Problems Across Middle and Older Adulthood Predict Early Mortality.

Having multiple sleep problems is common in adulthood. Yet, most studies have assessed single sleep variables at one timepoint, potentially misinterpreting health consequences of co-occurring sleep problems that may change over time. We investigated the relationship between multidimensional sleep health across adulthood and mortality. Participants from the Midlife in the United States Study reported sleep characteristics in 2004-2006 (MIDUS-2; M2) and in 2013-2014 (MIDUS-3; M3). We calculated a composite score of sleep health problems across 5 dimensions: Regularity, Satisfaction, Alertness, Efficiency, and Duration (higher = more problems). Two separate models for baseline sleep health (n = 5 140; median follow-up time = 15.3 years) and change in sleep health (n = 2 991; median follow-up time = 6.4 years) to mortality were conducted. Cox regression models controlled for sociodemographics and key health risk factors (body mass index, smoking, depressive symptoms, diabetes, and hypertension). On average, 88% of the sample reported having one or more sleep health problems at M2. Each additional sleep health problem at M2 was associated with 12% greater risk of all-cause mortality (hazard ratio [HR] = 1.12, 95% confidence interval [CI] = 1.04-1.21), but not heart disease-related mortality (HR = 1.14, 95% CI = 0.99-1.31). An increase in sleep health problems from M2 to M3 was associated with 27% greater risk of all-cause mortality (HR = 1.27, 95% CI = 1.005-1.59), and 153% greater risk of heart disease mortality (HR = 2.53, 95% CI = 1.37-4.68). More sleep health problems may increase the risk of early mortality. Sleep health in middle and older adulthood is a vital sign that can be assessed at medical checkups to identify those at greater risk.

Relationships of Total and Domain-Specific Moderate-to-Vigorous Physical Activity with All-Cause and Disease-Specific Mortality.

This study aimed to investigate the relationships of moderate-to-vigorous physical activity (MVPA) with all-cause and disease-specific mortality. We also investigated how the association between MVPA at leisure time (LT-MVPA) and health outcomes differs at different MVPA at work (WT-MVPA) levels. The 81,601 community-dwelling Japanese persons age 50-79 yr who responded to a questionnaire in 2000-2003 were followed until 2018. Cox proportional hazard model was used to examine the association of total MVPA with risks of all-cause, cancer, heart disease, stroke, and respiratory disease mortality. Then, we compared the mortality risk according to the tertile of LT-MVPA, stratified by the tertile of WT-MVPA. During the 15.1 yr of average follow-up, 16,951 deaths were identified. Even total MVPA below the recommended volume (i.e., 0.1-1.49 MET·h·d -1 ) was associated with 11% to 24% reductions in all-cause (hazard ratio [HR], 0.89; 95% confidence interval [CI], 0.82-0.96) and heart disease mortality (HR, 0.76; 95% CI, 0.61-0.94), compared with no MVPA at all. The further reduced risks were seen in MVPA up to 10 MET·h·d -1 . The inverse association between LT-MVPA and mortality risks was more evident at lower WT-MVPA, which was also inversely associated with the risks. Health benefits were observed at low levels of MVPA and up to 10 MET·h·d -1 , although the fine threshold for excessive MVPA was not clear. LT-MVPA had distinct health benefits especially for persons with lower WT-MVPA.

Association of sleep complaints with all-cause and heart disease mortality among US adults.

Compared with sleep disorders, no consensus has been reached on whether a subjective complaint of having trouble sleeping is associated with increased all-cause and heart disease mortality risk. Previous studies displayed considerable heterogeneity in population disease characteristics and duration of follow-up. Therefore, the aims of this study were to examine the relationship between sleep complaints and all-cause and heart disease mortality and whether the associations were influenced by follow-up time and population disease characteristics. In addition, we aimed to figure out the influence of the joint effects of sleep duration and sleep complaints on mortality risk. The present study utilized data from five cycles of the National Health and Nutrition Examination Survey (NHANES) (2005~2014) linked with the most updated 2019 National Death Index (NDI). Sleep complaints were determined by answers to "Have you ever told a doctor or other health professional that you have trouble sleeping?" and "Have you ever been told by a doctor or other health professional that you have a sleep disorder?". Those who answered 'Yes' to either of the aforementioned two questions were considered as having sleep complaints. A total of 27,952 adult participants were included. During a median follow-up of 9.25 years (interquartile range, 6.75-11.75 years), 3,948 deaths occurred and 984 were attributable to heart disease. A multivariable-adjusted Cox model revealed that sleep complaints were significantly associated with all-cause mortality risk (HR, 1.17; 95% CI, 1.07-1.28). Subgroup analysis revealed that sleep complaints were associated with all-cause (HR, 1.17; 95% CI, 1.05-1.32) and heart disease (HR, 1.24; 95% CI, 1.01-1.53) mortality among the subgroup with cardiovascular disease (CVD) or cancer. In addition, sleep complaints were more strongly associated with short-term mortality than long-term mortality. The joint analysis of sleep duration and sleep complaints showed that sleep complaints mainly increased the mortality risk in those with short (< 6 h/day, sleep complaints HR, 1.40; 95% CI, 1.15-1.69) or recommended (6-8 h/day, sleep complaints HR, 1.15; 95% CI, 1.01-1.31) sleep duration group. In conclusion, sleep complaints were associated with increased mortality risk, indicating a potential public benefit of monitoring and managing sleep complaints in addition to sleep disorders. Of note, persons with a history of CVD or cancer may represent a potentially high-risk group that should be targeted with a more aggressive intervention of sleep problems to prevent premature all-cause and heart disease death.

Associations of the Healthy Eating Index-2010 with risk of all-cause and heart disease mortality among adults with hypertension: Results from the National Health and Nutrition Examination Survey 2007-2014.

Studies regarding the impact of the Healthy Eating Index-2010 (HEI-2010) on the mortality of adults with hypertension are lacking. This study aimed to prospectively explore the relationships between HEI-2010 and mortality from heart disease and all causes in adults with hypertension based on the National Health and Nutrition Examination Survey (NHANES), 2007-2014. This is a prospective cohort study including 6,690 adults with hypertension from NHANES (2007-2014). National Death Index data up to 31 December 2019 were used to determine the number of deaths due to heart disease and all other causes. We evaluated hazard ratios (HRs) and 95% confidence intervals (CIs) using the Cox proportional hazards model. A total of 1,259 deaths from all causes, including 338 due to heart disease, were documented over an average follow-up duration of 8.4 years. In comparison with the lowest quartile of HEI-2010 scores, multivariable-adjusted HRs (95% CIs) for all-cause mortality were 0.82 (0.70, 0.97), 0.78 (0.64, 0.95), and 0.68 (0.54, 0.85) for the second, third, and fourth quartiles of the HEI-2010 scores (P-trend < 0.001) and for heart disease mortality were 0.60 (0.44, 0.81), 0.59 (0.40, 0.89), and 0.53 (0.35, 0.80) (P-trend = 0.010). Each increment in natural-log-transformed HEI-2010 scores was linked to a 43% reduction in the risk of all-cause mortality (P < 0.001) and a 55% reduction in the risk of heart disease mortality (P = 0.003). Among the 12 components of HEI-2010, adherence to a higher intake of greens and beans, vegetables, total protein foods, seafood and plant proteins, and unsaturated fatty acids, as well as moderate consumption of empty calories, were related to a 21-29% lower risk of all-cause mortality. In the current study, there was a statistically significant inverse relationship between HEI-2010 and mortality from heart disease and all causes among adults with hypertension. Based on the findings, it may help guide the dietary intake for adults with hypertension.

Racial and ethnic disparities in treatment-related heart disease mortality among US breast cancer survivors

Racial and ethnic disparities in heart disease mortality by initial treatment type among breast cancer survivors have not been well described. We included 739 557 women diagnosed with first primary invasive breast cancer between 2000 and 2017 (aged 18-84 years, received surgery, survived ≥1 year, followed through 2018) in the Surveillance, Epidemiology, and End Results-18 database. Standardized mortality ratios (SMRs; observed over expected) were calculated by race and ethnicity (non-Hispanic/Latina Asian American, Native Hawaiians, and other Pacific Islanders [AANHPI]; non-Hispanic/Latina Black [Black]; Hispanic/Latina [Latina]; and non-Hispanic/Latina White [White]) and initial treatment (surgery only; chemotherapy with surgery; chemotherapy, radiotherapy, with surgery; and radiotherapy with surgery) compared with the racial- and ethnic-matched general population, and by clinical characteristics. Cumulative heart disease mortality was estimated accounting for competing risks. SMRs were elevated for Black and Latina women treated with surgery only and chemotherapy with surgery (SMR range = 1.15-1.21) and AANHPI women treated with chemotherapy, radiotherapy, with surgery (SMR = 1.29; 95% confidence interval [CI] = 1.11 to 1.48), whereas SMRs were less than 1 for White women (SMR range = 0.70-0.96). SMRs were especially high for women with advanced (regional or distant) stage among Black women for all treatment (range = 1.15-2.89) and for AANHPI and Latina women treated with chemotherapy with surgery (range = 1.28-3.61). Non-White women diagnosed at younger than age 60 years had higher SMRs, as did Black and AANHPI women diagnosed with estrogen receptor-positive breast cancers. Black women had the highest 10-year cumulative risk of heart disease mortality: aged younger than 60 years (Black: 1.78%, 95% CI = 1.63% to 1.94%) compared with White, AANHPI, and Latina women (<1%) and aged 60 years and older (Black: 7.92%, 95% CI = 7.53% to 8.33%) compared with White, AANHPI, and Latina women (range = 3.90%-6.48%). Our findings illuminated striking racial and ethnic disparities in heart disease mortality among Black, AANHPI, and Latina breast cancer survivors, especially after initial chemotherapy receipt.

Loss of a child and the risk of atrial fibrillation: a Danish population-based prospective cohort study

BackgroundSeveral studies suggest that bereavement is associated with increased risks of ischaemic heart disease, heart failure, stroke and cardiovascular mortality. Knowledge regarding the link between bereavement and the risk of...

Abstract 16: Maternal Coronary Heart Disease and Mortality Within 5 Years of Delivery Among Women With Hypertensive Disorders of Pregnancy and/or Diabetes

Introduction: Pre-pregnancy hypertension (HTN), hypertensive disorders of pregnancy (HDP), and diabetes are linked to increased risk of post-pregnancy coronary heart disease (CHD) and all-cause mortality, but the cumulative impact of pre-pregnancy HTN, HDP, and diabetes has yet to be fully investigated. We aimed to examine associations between HDP and diabetes with CHD and mortality ≤5 years of delivery stratified by race/ethnicity. Methods: This retrospective cohort study included women aged 12-49 with ≥1 singleton, live birth in South Carolina (2004-2016). After exclusions, 431,839 women remained: non-Hispanic White [NHW; 58.8%], non-Hispanic Black [NHB; 31.7%], and Hispanic [9.5%]. Birth certificates defined pre-pregnancy HTN, HDP (preeclampsia, eclampsia, gestational hypertension), and diabetes (pre-pregnancy, gestational); hospitalization/ED visit data also defined pre-pregnancy HTN and HDP. Hospitalization/ED visit data and death certificates defined incident CHD and all-cause mortality. Cox proportional hazard models adjusted for covariates assessed associations by condition and race/ethnicity. Results: Incident CHD risk was increased ≤5 years of delivery for women with diabetes (HR=1.79, CI: 1.40-2.29), HDP (HR=2.91, CI: 1.98-2.65), diabetes and HDP (HR=3.95 CI:3.09-5.05), pre-pregnancy HTN and HDP (HR=3.94, CI: 3.11-5.00), and all three conditions (HR=5.78, CI: 4.41-8.06) compared to none. All-cause mortality risk was increased for HDP (HR=1.31, CI: 1.08-1.58), diabetes and HDP (HR=1.93, CI: 1.30-2.87), pre-pregnancy HTN and HDP (HR=2.20, CI: 1.54-3.15), and all three conditions (HR=2.88, CI: 1.61-5.16), but not with diabetes. The table shows overall and race/ethnic-specific event rates and model results. Discussion: Women with HDP (regardless of pre-pregnancy HTN) and/or diabetes experienced higher incident CHD and all-cause mortality risk ≤5 years of delivery. Event rates were highest for women with two or three conditions, with all event rates higher for NHB than NHW women.

Association between personality and the risk of ischemic heart disease mortality before and after the Great East Japan Earthquake: Data from the Miyagi Cohort Study

The purpose of the present study was to investigate the association between personality and the risk of IHD mortality among Great East Japan Earthquake (GEJE) survivors, and to investigate whether personality traits affected the increase in IHD mortality observed after the GEJE. We analyzed data for 29,065 men and women in the Miyagi Cohort Study who were 40-64 years old at baseline. We divided the participants into quartiles based on scores for each of the four personality subscales (extraversion, neuroticism, psychoticism, and lie), using the Japanese version of the Eysenck Personality Questionnaire-Revised Short Form. We divided the eight years before and after the GEJE event (11 March 2011) into two period, and examined the relationship between personality traits and the risk of IHD mortality. Cox proportional hazards analysis was used to estimate the multivariate hazard ratios (HRs) and 95% confidence intervals (CIs) for the risk of IHD mortality according to each personality subscale category. In the four years before the GEJE, neuroticism was significantly associated with an increased risk of IHD mortality. Compared with the lowest category for neuroticism, the multivariate-adjusted HR (95% CI) for IHD mortality in the highest category was 2.19 (1.03-4.67) (p-trend=0.12). In contrast, no statistically significant association between neuroticism and IHD mortality was observed in the four years after the GEJE. This finding suggests that the observed increase in IHD mortality after the GEJE can be attributed to risk factors other than personality.

Nuts and Cardiovascular Disease Outcomes: A Review of the Evidence and Future Directions.

Nuts are nutrient-rich foods that contain many bioactive compounds that are beneficial for cardiovascular health. Higher consumption of nuts has been associated with a reduced risk of several cardiovascular diseases (CVD) in prospective cohort studies, including a 19% and 25% lower risk of CVD incidence and mortality, respectively, and a 24% and 27% lower risk of coronary heart disease incidence and mortality, respectively. An 18% lower risk of stroke mortality, a 15% lower risk of atrial fibrillation, and a 19% lower risk of total mortality have also been observed. The role of nuts in stroke incidence, stroke subtypes, peripheral arterial disease and heart failure has been less consistent. This narrative review summarizes recommendations for nuts by clinical practice guidelines and governmental organizations, epidemiological evidence for nuts and CVD outcomes, nut-containing dietary patterns, potential mechanisms of nuts and CVD risk reduction, and future research directions, such as the use of biomarkers to help better assess nut intake. Although there are still some uncertainties around nuts and CVD prevention which require further research, as summarized in this review, there is a substantial amount of evidence that supports that consuming nuts will have a positive impact on primary and secondary prevention of CVD.

Dietary fatty acids and mortality risk from heart disease in US adults: an analysis based on NHANES

We investigated the association of dietary intake of major types of fatty acids with heart disease mortality in a general adult cohort with or without a prior diagnosis of myocardial infarction (MI). This cohort study included US adults who attended the National Health and Nutrition Examination Surveys from 1988 to 2014. Heart disease mortality was ascertained by linkage to the National Death Index records through 31 December 2015. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of fatty acid intake for heart disease mortality. This cohort included 45,820 adults among which 1,541 had a prior diagnosis of MI. Participants were followed up for 532,722 person-years (mean follow-up, 11.6 years), with 2,313 deaths recorded from heart disease being recorded. Intake of saturated (SFAs) and monounsaturated fatty acids (MUFAs) was associated with heart disease mortality after adjustment for all the tested confounders. In contrast, a 5% higher calorie intake from polyunsaturated fatty acids (PUFAs) was associated with a 9% (HR, 0.91; 95% CI 0.83–1.00; P = 0.048) lower multivariate-adjusted risk of heart disease mortality. Sub-analyses showed that this inverse association was present in those without a prior diagnosis of MI (HR,0.89; 95% CI 0.80–0.99) but not in those with the condition (HR, 0.94; 95% CI 0.75–1.16). The lack of association in the MI group could be due to a small sample size or severity and procedural complications (e.g., stenting and medication adherence) of the disease. Higher PUFA intake was associated with a favourable lipid profile. However, further adjustment for plasma lipids did not materially change the inverse association between PUFAs and heart disease mortality. Higher intake of PUFAs, but not SFAs and MUFAs, was associated with a lower adjusted risk of heart disease mortality in a large population of US adults supporting the need to increase dietary PUFA intake in the general public.

Dairy Food Consumption Is Associated with Reduced Risk of Heart Disease Mortality, but Not All-Cause and Cancer Mortality in US Adults.

Previous evidence has linked animal protein intake, including dairy foods, with an increased risk in mortality from all-causes and certain chronic diseases, including cancer and heart disease. The objective of the current analysis was to examine associations between total dairy consumption with mortality from all-causes, cancer, and heart disease. Data for adults (≥19 y; n = 54,830) from the Third National Health and Nutrition Examination Survey (NHANES) and NHANES 1999-2014 were linked with mortality data through 2015. Individual usual intake for dairy foods were estimated using the National Cancer Institute method. Hazard ratio (HR) models were fit for mortality types (all cause, cancer, heart disease) and measures of usual intakes of dairy. Multivariable analysis further adjusted for age, gender, ethnicity, waist circumference, smoking status, education level, chronic condition status (i.e., based on cancer, myocardial infarct, and diabetes/diabetes medication reported), weight loss attempts, and % kcal from animal protein. No associations were seen between dairy food intake and mortality risk from all-causes [HR = 0.97; confidence intervals (CI): 0.85-1.11; p = 0.67], and cancer [HR = 0.95; CI: 0.75-1.20; p = 0.65] when comparing the lowest quartile to the highest quartile of consumption. Dairy food consumption was associated with a 26% reduced risk for heart disease mortality when comparing the lowest quartile to the highest quartile [HR = 0.74; CI: 0.54-1.01; p = 0.05]. Further analyses in different age groups showed that dairy food consumption was associated with 39% and 31% reduced risk for heart disease mortality in older adults 51-70 and ≥51 y, respectively [adults 51-70 y: HR = 0.61; CI: 0.41-0.91; p = 0.01; adults ≥51 y: HR = 0.69; CI: 0.54-0.89; p = 0.004]. These results contradict previous findings that have linked dairy foods to increased mortality risk. Further, dairy foods as part of a healthy dietary pattern, may help lower heart disease mortality risk.