Healthy individuals exhibit blood pressure variation over a 24-hour period with higher blood pressure during wakefulness and lower blood pressure during sleep. Loss or disruption of the blood pressure circadian rhythm has been linked to adverse health outcomes, for example, cardiovascular disease, dementia, and chronic kidney disease. However, the current diagnostic and therapeutic approaches lack sufficient attention to the circadian rhythmicity of blood pressure. Sleep patterns, hormone release, eating habits, digestion, body temperature, renal and cardiovascular function, and other important host functions as well as gut microbiota exhibit circadian rhythms, and influence circadian rhythms of blood pressure. Potential benefits of nonpharmacologic interventions such as meal timing, and pharmacologic chronotherapeutic interventions, such as the bedtime administration of antihypertensive medications, have recently been suggested in some studies. However, the mechanisms underlying circadian rhythm-mediated blood pressure regulation and the efficacy of chronotherapy in hypertension remain unclear. This review summarizes the results of the National Heart, Lung, and Blood Institute workshop convened on October 27 to 29, 2021 to assess knowledge gaps and research opportunities in the study of circadian rhythm of blood pressure and chronotherapy for hypertension.

ARIC (Atherosclerosis Risk In Communities) initiated community-based surveillance in 1987 for myocardial infarction and coronary heart disease (CHD) incidence and mortality and created a prospective cohort of 15,792 Black and White adults ages 45 to 64 years. The primary aims were to improve understanding of the decline in CHD mortality and identify determinants of subclinical atherosclerosis and CHD in Black and White middle-age adults. ARIC has examined areas including health disparities, genomics, heart failure, and prevention, producing more than 2,300 publications. Results have had strong clinical impact and demonstrate the importance of population-based research in the spectrum of biomedical research to improve health.

Vascular contributions to cognitive impairment and dementia (VCID) are characterized by the aging neurovascular unit being confronted with and failing to cope with biological insults due to systemic and cerebral vascular disease, proteinopathy including Alzheimer's biology, metabolic disease, or immune response, resulting in cognitive decline. This report summarizes the discussion and recommendations from a working group convened by the National Heart, Lung, and Blood Institute and the National Institute of Neurological Disorders and Stroke to evaluate the state of the field in VCID research, identify research priorities, and foster collaborations. As discussed in this report, advances in understanding the biological mechanisms of VCID across the wide spectrum of pathologies, chronic systemic comorbidities, and other risk factors may lead to potential prevention and new treatment strategies to decrease the burden of dementia. Better understanding of the social determinants of health that affect risks for both vascular disease and VCID could provide insight into strategies to reduce racial and ethnic disparities in VCID.

The National Heart, Lung, and Blood Institute convened a multidisciplinary working group of hypertension researchers on December 6 to 7, 2018, in Bethesda, MD, to share current scientific knowledge in hypertension and to identify barriers to translation of basic into clinical science/trials and implementation of clinical science into clinical care of patients with hypertension. The goals of the working group were (1) to provide an overview of recent discoveries that may be ready for testing in preclinical and clinical studies; (2) to identify gaps in knowledge that impede translation; (3) to highlight the most promising scientific areas in which to pursue translation; (4) to identify key challenges and barriers for moving basic science discoveries into translation, clinical studies, and trials; and (5) to identify roadblocks for effective dissemination and implementation of basic and clinical science in real-world settings. The working group addressed issues that were responsive to many of the objectives of the National Heart, Lung, and Blood Institute Strategic Vision. The working group identified major barriers and opportunities for translating research to improved control of hypertension. This review summarizes the discussion and recommendations of the working group.

Background Central arterial stiffening and increased pulsatility, with consequent cerebral hypoperfusion, may result in structural brain damage and cognitive impairment. Methods and Results We analyzed a cross‐sectional sample of ARIC‐NCS (Atherosclerosis Risk in Communities–Neurocognitive Study) participants (aged 67–90 years, 60% women) with measures of cognition (n=3703) and brain magnetic resonance imaging (n=1255). Central arterial hemodynamics were assessed as carotid‐femoral pulse wave velocity and pressure pulsatility (central pulse pressure). We derived factor scores for cognitive domains. Brain magnetic resonance imaging using 3‐Tesla scanners quantified lacunar infarcts; cerebral microbleeds; and volumes of white matter hyperintensities, total brain, and the Alzheimer disease signature region. We used logistic regression, adjusted for demographics, apolipoprotein E ɛ4, heart rate, mean arterial pressure, and select cardiovascular risk factors, to estimate the odds of lacunar infarcts or cerebral microbleeds. Linear regression, additionally adjusted for intracranial volume, estimated the difference in log‐transformed volumes of white matter hyperintensities, total brain, and the Alzheimer disease signature region. We estimated the mean difference in cognitive factor scores across quartiles of carotid‐femoral pulse wave velocity or central pulse pressure using linear regression. Compared with participants in the lowest carotid‐femoral pulse wave velocity quartile, participants in the highest quartile of carotid‐femoral pulse wave velocity had a greater burden of white matter hyperintensities (P=0.007 for trend), smaller total brain volumes (−18.30 cm3; 95% CI, −27.54 to −9.07 cm3), and smaller Alzheimer disease signature region volumes (−1.48 cm3; 95% CI, −2.27 to −0.68 cm3). These participants also had lower scores in executive function/processing speed (β=−0.04 z score; 95% CI, −0.07 to −0.01 z score) and general cognition (β=−0.09 z score; 95% CI, −0.15 to −0.03 z score). Similar results were observed for central pulse pressure. Conclusions Central arterial hemodynamics were associated with structural brain damage and poorer cognitive performance among older adults.

The recent release of the Strategic Plan for NIH Nutrition Research (SPNR) provides a unique opportunity for advancements in nutrition science and research through investigator-initiated efforts. This presentation provides a broad overview of the nutrition measures collected in NHLBI cohort studies and presents information on available resources through the NHLBI Biologic Specimen and Data Repository Information Coordinating Center (BioLINCC). Leveraging existing NHLBI cohort studies, which include diverse study populations, is a cost-effective approach for investigators, including early stage investigators, to develop new research questions. A landscape analysis was conducted to evaluate the nutrition measures collected in eight, multi-site NHLBI-funded cohort studies including over 163,000 participants (ages 18 −100 y+). These datasets include the Coronary Artery Risk Development in Young Adults (CARDIA), the Framingham Heart Study, the Jackson Heart Study (JHS), the Women’s Health Initiative (WHI), the Multi-Ethnic Study of Atherosclerosis (MESA), the Atherosclerosis Risk in Communities Study (ARIC), the Hispanics Community Health Study/Study of Latinos (SOL), and the Cardiovascular Health Study (CHS). Information from BioLINCC provided an additional resource to identify nutrition measures collected. Most of the cohort studies used food frequency questionnaires to assess diet, with a smaller number using 24-hr recall methodology. Concentration biomarkers largely varied by study, including carotenoid and vitamin D concentrations to serum calcium and potassium levels. Lipids and blood pressure measurements were consistently collected across all cohort studies and some studies collected inflammatory markers (e.g., C reactive protein, interleukin-6) and used more invasive and costly cardiac imaging outcomes (e.g., carotid IMT, coronary calcium). This preliminary study identified variable nutrition measures and nutrition-related clinical outcomes in NHLBI-funded cohort studies, which are available on BioLINCC for future analysis by investigators. Additionally, these findings can help with implementation of the NIH SPNR by identifying key research gaps and possible focus areas for future research. National Institutes of Health.

BACKGROUND:Accurate assessment of the burden of stroke, a major cause of disability and death, is crucial. We aimed to estimate rates of validated ischaemic stroke hospitalizations in the USA during 1998-2011.METHODS:We used the Atherosclerosis Risk in Communities (ARIC) study cohort's adjudicated stroke data for participants aged ≥55 years, to construct validation models for each International Classification of Diseases (ICD)-code group and patient covariates. These models were applied to the Nationwide Inpatient Sample (NIS) data to estimate the probability of validated ischaemic stroke for each eligible hospitalization. Rates and trends in NIS using ICD codes vs estimates of validated ischaemic stroke were compared.RESULTS:After applying validation models, the estimated annual average rate of validated ischaemic stroke hospitalizations in the USA during 1998-2011 was 3.37 [95% confidence interval (CI): 3.31, 3.43) per 1000 person-years. Validated rates declined during 1998-2011 from 4.7/1000 to 2.9/1000; however, the decline was limited to 1998-2007, with no further decline subsequently through 2011. Validation models showed that the false-positive (∼23% of strokes) and false-negative rates of ICD-9-CM codes in primary position for ischaemic stroke approximately cancel. Therefore, estimates of ischaemic stroke hospitalizations did not substantially change after applying validation models.CONCLUSIONS:Overall, ischaemic stroke hospitalization rates in the USA have declined during 1998-2007, but no further decline was observed from 2007 to 2011. Validated ischaemic stroke hospitalizations estimates were similar to published estimates of hospitalizations with ischaemic stroke ICD codes in primary position. Validation of national discharge data using prospective chart review data is important to estimate the accuracy of reported burden of stroke.

Importance In 2010, the Institute of Medicine (now the National Academy of Medicine) recommended collecting 24-hour urine to estimate US sodium intake because previous studies indicated 90% of sodium consumed was excreted in urine. Objective To estimate mean population sodium intake and describe urinary potassium excretion among US adults. Design, Setting, and Participants In a nationally representative cross-sectional survey of the US noninstitutionalized population, 827 of 1103 (75%) randomly selected, nonpregnant participants aged 20 to 69 years in the examination component of the National Health and Nutrition Examination Survey (NHANES) collected at least one 24-hour urine specimen in 2014. The overall survey response rate for the 24-hour urine collection was approximately 50% (75% [24-hour urine component response rate] × 66% [examination component response rate]). Exposures 24-hour collection of urine. Main Outcomes and Measures Mean 24-hour urinary sodium and potassium excretion. Weighted national estimates of demographic and health characteristics and mean electrolyte excretion accounting for the complex survey design, selection probabilities, and nonresponse. Results The study sample (n = 827) represented a population of whom 48.8% were men; 63.7% were non-Hispanic white, 15.8% Hispanic, 11.9% non-Hispanic black, and 5.6% non-Hispanic Asian; 43.5% had hypertension (according to 2017 hypertension guidelines); and 10.0% reported a diagnosis of diabetes. Overall mean 24-hour urinary sodium excretion was 3608 mg (95% CI, 3414-3803). The overall median was 3320 mg (interquartile range, 2308-4524). In secondary analyses by sex, mean sodium excretion was 4205 mg (95% CI, 3959-4452) in men (n = 421) and 3039 mg (95% CI, 2844-3234) in women (n = 406). By age group, mean sodium excretion was 3699 mg (95% CI, 3449-3949) in adults aged 20 to 44 years (n = 432) and 3507 mg (95% CI, 3266-3748) in adults aged 45 to 69 years (n = 395). Overall mean 24-hour urinary potassium excretion was 2155 mg (95% CI, 2030-2280); by sex, 2399 mg (95% CI, 2253-2545) in men and 1922 mg (95% CI, 1757-2086) in women; and by age, 1986 mg (95% CI, 1878-2094) in adults aged 20 to 44 years and 2343 mg (95% CI, 2151-2534) in adults aged 45 to 69 years. Conclusions and Relevance In cross-sectional data from a 2014 sample of US adults, estimated mean sodium intake was 3608 mg per day. The findings provide a benchmark for future studies.

BackgroundBoth excessive sodium intake and obesity are risk factors for hypertension and cardiovascular disease. The association between sodium intake and obesity is unclear, with few studies assessing sodium intake using 24-h urine collection.ObjectivesOur objective was to assess the association between usual 24-h sodium excretion and measures of adiposity among US adults.MethodsCross-sectional data were analyzed from a sample of 730 nonpregnant participants aged 20-69 y who provided up to 2 complete 24-h urine specimens in the NHANES 2014 and had data on overweight or obesity [body mass index (kg/m2) ≥25] and central adiposity [waist circumference (WC): >88 cm for women, >102 cm for men]. Measurement error models were used to estimate usual sodium excretion, and multiple linear and logistic regression models were used to assess its associations with measures of adiposity, adjusting for sociodemographic, health, and dietary variables [i.e., energy intake or sugar-sweetened beverage (SSB) intake]. All analyses accounted for the complex survey sample design.ResultsUnadjusted mean ± SE usual sodium excretion was 3727 ± 43.5 mg/d and 3145 ± 55.0 mg/d among participants with and without overweight/obesity and 3653 ± 58.1 mg/d and 3443 ± 35.3 mg/d among participants with or without central adiposity, respectively. A 1000-mg/d higher sodium excretion was significantly associated with 3.8-units higher BMI (95% CI: 2.8, 4.8) and a 9.2-cm greater WC (95% CI: 6.9, 11.5 cm) adjusted for covariates. Compared with participants in the lowest quartile of sodium excretion, the adjusted prevalence ratios in the highest quartile were 1.93 (95% CI: 1.69, 2.20) for overweight/obesity and 2.07 (95% CI: 1.74, 2.46) for central adiposity. The associations also were significant when adjusting for SSBs, instead of energy, in models.ConclusionsHigher usual sodium excretion is associated with overweight/obesity and central adiposity among US adults.

Background: 24-h urine collections are the suggested method to measure daily urinary potassium excretion (uK) but are costly and burdensome to implement. Objective: This study tested how well existing equations with the use of spot urine samples can estimate 24-h uK and if accuracy varies by timing of spot urine collection, age, race, or sex. Design: This cross-sectional study used data from 407 participants aged 18-39 y from the Washington, DC area in 2011 and 554 participants aged 45-79 y from Chicago in 2013. Spot urine samples were collected in individual containers for 24 h, and 1 for each timed period (morning, afternoon, evening, and overnight) was selected. For each selected timed spot urine, 24-h uK was predicted through the use of published equations. Difference (bias) between predicted and measured 24-h uK was calculated for each timed period and within age, race, and sex subgroups. Individual-level differences were assessed through the use of Bland-Altman plots and correlation tests. Results: For all equations, regardless of the timing of spot urine, mean bias was usually significantly different than 0. No one prediction equation was unbiased across all sex, race, and age subgroups. With the use of the Kawasaki and Tanaka equations, 24-h uKwas overestimated at low levels and underestimated at high levels, whereas observed differential bias with the Mage equation was in the opposite direction. Depending on prediction equation and timing of urine sample, 61-75% of individual 24-h uKs were misclassified among 500-mg incremental categories from <1500 to >= 3000 mg. Correlations between predicted and measured 24-h uK were poor to moderate (0.19-0.71). Conclusion: Because predicted 24-h uK accuracy varies by timing of spot urine collection, published prediction equations, and within age-race-sex subgroups, study results making use of predicted 24-h uK in association with health outcomes should be interpreted with caution. It is possible that a more accurate prediction equation can be developed leading to different results.

Background: Higher levels of sodium and lower levels of potassium intake are associated with higher blood pressure. However, the shape and magnitude of these associations can vary by study participant characteristics or intake assessment method. Twenty-four–hour urinary excretion of sodium and potassium are unaffected by recall errors and represent all sources of intake, and were collected for the first time in a nationally representative US survey. Our objective was to assess the associations of blood pressure and hypertension with 24-hour urinary excretion of sodium and potassium among US adults. Methods: Cross-sectional data were obtained from 766 participants age 20 to 69 years with complete blood pressure and 24-hour urine collections in the 2014 National Health and Nutrition Examination Survey, a nationally representative survey of the US noninstitutionalized population. Usual 24-hour urinary electrolyte excretion (sodium, potassium, and their ratio) was estimated from ≤2 collections on nonconsecutive days, adjusting for day-to-day variability in excretion. Outcomes included systolic and diastolic blood pressure from the average of 3 measures and hypertension status, based on average blood pressure ≥140/90 and antihypertensive medication use. Results: After multivariable adjustment, each 1000-mg difference in usual 24-hour sodium excretion was directly associated with systolic (4.58 mm Hg; 95% confidence interval [CI], 2.64–6.51) and diastolic (2.25 mm Hg; 95% CI, 0.83–3.67) blood pressures. Each 1000-mg difference in potassium excretion was inversely associated with systolic blood pressure (–3.72 mm Hg; 95% CI, –6.01 to –1.42). Each 0.5 U difference in sodium-to-potassium ratio was directly associated with systolic blood pressure (1.72 mm Hg; 95% CI, 0.76–2.68). Hypertension was linearly associated with progressively higher sodium and lower potassium excretion; in comparison with the lowest quartile of excretion, the adjusted odds of hypertension for the highest quartile was 4.22 (95% CI, 1.36–13.15) for sodium, and 0.38 (95% CI, 0.17–0.87) for potassium ( P <0.01 for trends). Conclusions: These cross-sectional results show a strong dose-response association between urinary sodium excretion and blood pressure, and an inverse association between urinary potassium excretion and blood pressure, in a nationally representative sample of US adults.

PURPOSE:Despite well-documented associations of socioeconomic status with incident heart failure (HF) hospitalization, little information exists on the relationship of socioeconomic status with HF diagnosed in the outpatient (OP) setting. METHODS:We used Poisson models to examine the association of area-level indicators of educational attainment, poverty, living situation, and density of primary care physicians with incident HF diagnosed in the inpatient (IP) and OP settings among a cohort of Medicare beneficiaries (n = 109,756; 2001-2013). RESULTS:The age-standardized rate of HF incidence was 35.8 (95% confidence interval [CI], 35.1-36.5) and 13.9 (95% CI, 13.5-14.4) cases per 1000 person-years in IP and OP settings, respectively. The incidence rate differences (IRDs) per 1000 person-years in both settings suggested greater incidence of HF in high- compared to low-poverty areas (IP IRD = 4.47 [95% CI, 3.29-5.65], OP IRD = 1.41 [95% CI, 0.61-2.22]) and in low- compared to high-education areas (IP IRD = 3.73 [95% CI, 2.63-4.82], OP IRD = 1.72 [95% CI, 0.97-2.47]). CONCLUSIONS:Our results highlight the role of area-level social determinants of health in the incidence of HF in both the IP and OP settings. These findings may have implications for HF prevention policies.

PurposeThe aim of this study was to quantify the influence of the length of the look-back period on misclassification of heart failure (HF) incidence in Medicare claims available for participants of a population-based cohort.MethodsAtherosclerosis Risk in Communities participants with 3years of continuous fee-for-service Medicare enrollment from 2000 to 2012 was assigned an index date 36months after enrollment separating the time-in-observation period into the look-back and the incidence periods. Incident HF events were identified using ICD-9-CM code algorithms as the first observed hospitalization claim or the second of two HF outpatient claims occurring within 12months. Using 36months as a referent, the look-back period was reduced by 6-month increments. For each look-back period, we calculated the incidence rate, percent of prevalent HF events misclassified as incident, and loss in sample size.ResultsWe identified 9568 Atherosclerosis Risk in Communities participants at risk for HF. For hospitalized and outpatient HF, the number of events misclassified as incident increased, and the total number of incident events decreased with increased length of the look-back period. The incident rate (per 1000 person years) decreased with increased length of the look-back period from 6 to 36months and had a greater impact on outpatient HF; for example, from 11.2 to 10.6 for ICD-9-CM 428.xx hospitalization in the primary position and 10.5 to 7.9 for outpatient HF.ConclusionOur estimates can be used to optimize trade-offs between the degree of misclassification and number of events in the estimation of incident HF from administrative claims data, as pertinent to different study questions. Copyright (c) 2017 John Wiley & Sons, Ltd.

We examined the population distribution of urinary sodium concentrations and the validity of existing equations predicting 24-hour sodium excretion from a single spot urine sample among older adults with and without hypertension. In 2013, 24-hour urine collections were obtained from 554 participants in the Multi-Ethnic Study of Atherosclerosis and the Coronary Artery Risk Development in Young Adults study, who were aged 45-79 years and of whom 56% were female, 58% were African American, and 54% had hypertension, in Chicago, Illinois. One-third provided a second 24-hour collection. Four timed (overnight, morning, afternoon, and evening) spot urine specimens and the 24-hour collection were analyzed for sodium and creatinine concentrations. Mean 24-hour sodium excretion was 3,926 (standard deviation (SD), 1,623) mg for white men, 2,480 (SD, 1,079) mg for white women, 3,454 (SD, 1,651) mg for African-American men, and 3,397 (SD, 1,641) mg for African-American women, and did not differ significantly by hypertensive status. Mean bias (difference) in predicting 24-hour sodium excretion from the timed spot urine specimens ranged from -182 (95% confidence interval: -285, -79) to 1,090 (95% confidence interval: 966, 1,213) mg/day overall. Although the Tanaka equation using the evening specimen produced the least bias overall, no single equation worked well across subgroups of sex and race/ethnicity. A single spot urine sample is not a valid indicator of individual sodium intake. New equations are needed to accurately estimate 24-hour sodium excretion for older adults.

Introduction: Both excessive sodium intake and obesity are risk factors for hypertension and cardiovascular disease. The association between sodium intake and obesity is unclear, with few studies a...

BACKGROUND:The association of central arterial stiffness and pressure pulsatility with mild cognitive impairment (MCI) and dementia is not well characterized in the population-based setting. OBJECTIVE:The aim of this study was to quantify the cross-sectional association of arterial stiffness and pressure pulsatility with MCI and dementia among 4,461 older white and black adults from the population-based Atherosclerosis Risk in Communities Study-Neurocognitive Study. METHODS:We used race-stratified multinomial logistic regression to evaluate associations of percentile cut points of carotid-femoral pulse wave velocity, central systolic blood pressure, central pulse pressure, and pulse pressure amplification with MCI and dementia versus no cognitive impairment. RESULTS:Among whites, those with carotid-femoral pulse wave velocity or central systolic blood pressure ≥75th percentile had a higher prevalence of MCI compared to participants <75th percentile (conditional odds ratio (OR); 95% confidence interval (CI): 1.27 (1.02, 1.56) and 1.28 (1.04, 1.57), respectively) and those with central pulse pressure ≥75th percentile had a higher prevalence of MCI (OR 1.27 (95% CI: 1.03, 1.58)) and dementia (OR 1.76 (95% CI: 1.06, 2.92) compared to participants <75th percentile. Also among whites, those with pulse pressure amplification ≤25th percentile had a higher prevalence of dementia compared to participants >25th percentile (OR 1.65; (95% CI: 1.01, 2.70). Weaker associations were seen among black participants. CONCLUSION:Higher arterial stiffness and pulsatility were associated with MCI and dementia in white participants. Longitudinal characterization of the observed associations is warranted to assess whether arterial stiffness and pressure pulsatility predict MCI and dementia among older adults.

Background: Although heart failure (HF) disproportionately affects older adults, little data exist regarding the prevalence of American College of Cardiology/American Heart Association HF stages among older individuals in the community. Additionally, the role of contemporary measures of longitudinal strain and diastolic dysfunction in defining HF stages is unclear. Methods: HF stages were classified in 6118 participants in the Atherosclerosis Risk in Communities study (67–91 years of age) at the fifth study visit as follows: A (asymptomatic with HF risk factors but no cardiac structural or functional abnormalities), B (asymptomatic with structural abnormalities, defined as left ventricular hypertrophy, dilation or dysfunction, or significant valvular disease), C1 (clinical HF without prior hospitalization), and C2 (clinical HF with earlier hospitalization). Results: Using the traditional definitions of HF stages, only 5% of examined participants were free of HF risk factors or structural heart disease (Stage 0), 52% were categorized as Stage A, 30% Stage B, 7% Stage C1, and 6% Stage C2. Worse HF stage was associated with a greater risk of incident HF hospitalization or death at a median follow-up of 608 days. Left ventricular (LV) ejection fraction was preserved in 77% and 65% in Stages C1 and C2, respectively. Incorporation of longitudinal strain and diastolic dysfunction into the Stage B definition reclassified 14% of the sample from Stage A to B and improved the net reclassification index ( P =0.028) and integrated discrimination index ( P =0.016). Abnormal LV structure, systolic function (based on LV ejection fraction and longitudinal strain), and diastolic function (based on e’, E/e’, and left atrial volume index) were each independently and additively associated with risk of incident HF hospitalization or death in Stage A and B participants. Conclusions: The majority of older adults in the community are at risk for HF (Stages A or B), appreciably more compared with previous reports in younger community-based samples. LV ejection fraction is robustly preserved in at least two-thirds of older adults with prevalent HF (Stage C), highlighting the burden of HF with preserved LV ejection fraction in the elderly. LV diastolic function and longitudinal strain provide incremental prognostic value beyond conventional measures of LV structure and LV ejection fraction in identifying persons at risk for HF hospitalization or death.

Background:Although heart failure (HF) disproportionately affects older adults, little data exist regarding the prevalence of American College of Cardiology/American Heart Association HF stages among older individuals in the community. Additionally, the role of contemporary measures of longitudinal strain and diastolic dysfunction in defining HF stages is unclear. Methods:HF stages were classified in 6118 participants in the Atherosclerosis Risk in Communities study (67–91 years of age) at the fifth study visit as follows: A (asymptomatic with HF risk factors but no cardiac structural or functional abnormalities), B (asymptomatic with structural abnormalities, defined as left ventricular hypertrophy, dilation or dysfunction, or significant valvular disease), C1 (clinical HF without prior hospitalization), and C2 (clinical HF with earlier hospitalization). Results:Using the traditional definitions of HF stages, only 5% of examined participants were free of HF risk factors or structural heart disease (Stage...

Introduction: Accurate monitoring of population intake is essential for evaluating the impact of sodium reduction strategies, such as sodium targets for manufactured and restaurant foods. Previous nationally representative estimates of U.S. sodium intake were based on dietary recalls rather than 24-h urine collections, the gold standard measure for sodium intake given about 90% is excreted in urine. In contrast, 60%-90% of potassium consumed is excreted in urine. Hypothesis: We hypothesized most U.S. adults aged 20-69 years consume excess sodium and inadequate potassium. Methods: We used 24-h urinary excretion based on complete, timed, collections from a nationally-representative sample of NHANES participants aged 20-69 y in 2014 (n=827, 75% of selected respondents). We estimated usual 24-h sodium and potassium excretion and their ratio. Within-individual, day-to-day variation in 24-h excretion was adjusted using measurement error models with a repeat 24-h urine collection, 4-11 days from the first, among 436 participants. Results: Overall, mean 24-h urinary sodium excretion was 3,662 mg (95% confidence interval [CI], 3,502, 3,822 mg); 89% (95% CI, 84, 93%) of U.S. adults aged 20-69 y excreted ≥2,300 mg (Tolerable Upper Intake). Sodium excretion differed by sex (men, 4,207 mg, 95% CI, 3,984, 4430, mg; women, 3,142 mg, 95% CI, 2,985, 3,299 mg), but not age, race-ethnicity, income, education, body mass index, physical activity, or hypertension. Among pre-hypertensive and hypertensive adults who may benefit from lowering intake further, 99% excreted >1500 mg. Mean 24-h urinary potassium excretion was 2,202 mg (95% CI, 2,098, 2,306 mg) much less than 4700 mg (Adequate Intake). Potassium excretion differed by sex (men, 2,422 mg; women, 1,973 mg) and race-ethnicity (non-Hispanic black, 1,781 mg; non-Hispanic white, 2,328 mg; non-Hispanic white; 2,133 mg non-Hispanic Asian; 2,055 mg Hispanic), but not other examined characteristics. Conclusions: These first nationally-representative estimates of 24-h urinary excretion indicate that most U.S. adults consume excess sodium, potentially benefiting from population sodium reduction. Average 24-h urinary potassium excretion is low, suggesting that intake is low, and varies by race-ethnicity.

Introduction: One in three US adults has hypertension, a major risk factor for cardiovascular disease. We aimed to assess the associations between 24-h urinary excretion of sodium, potassium, and sodium-potassium ratio with blood pressure and hypertension status among US adults. Hypothesis: We hypothesized that urine sodium excretion and urine sodium-potassium ratio would be positively and urine potassium excretion would be inversely associated with blood pressure and hypertension. Methods: Cross-sectional data on up to two 24-h complete urine collections were analyzed from 765 non-institutionalized participants aged 20-69 y in the 2014 US National Health and Nutrition Examination Survey (NHANES). Urine collection started and stopped in the NHANES mobile examination center. Approximately half of participants had two complete collections; usual sodium and potassium excretion, and sodium-potassium ratio, were estimated using measurement error models accounting for day-to-day variability. Analyses adjusted for age, sex, race/ethnicity, body mass index, history of cardiovascular disease, diabetes, chronic kidney disease, smoking status, and physical activity, as well as the complex survey design. Results: In fully adjusted linear regression models, sodium excretion was positively associated with systolic (4.43 mmHg per 1000 mg/day, 95% CI 2.31,6.56) and diastolic (1.93 mmHg, 95% CI 0.34,3.51) blood pressure. Sodium-potassium ratio was also positively associated with systolic blood pressure (2.86 mmHg per .5 unit increase, 95% CI 1.15,4.56), and potassium excretion was inversely associated with systolic blood pressure (-3.39 mmHg per 1000mg/day increase, 95% CI -6.05,0.72). Adjusted odds ratios for hypertension, for excretion in the highest compared to the lowest quartiles, were 4.34 (95% CI 1.37,13.79) for sodium and 0.39 (95% CI 0.17,0.88) for potassium. Results were robust in sensitivity analyses restricted to persons not taking antihypertensive medications. Conclusions: Using a nationally-representative sample of US adults and a “gold-standard” urine biomarker, these data further support the strong relationship of higher sodium and lower potassium excretion with higher blood pressure and hypertension risk.