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Objectives: Arterial calcification contributes to cardiovascular mortality. Based on a recent animal study, we hypothesized that higher dietary potassium intake was associated with less abdominal aortic calcification (AAC) and lower arterial stiffness among adults in the United States., Methods: Cross-sectional analyses were performed on participants over 40 years old from the National Health and Nutrition Examination Survey 2013-2014. Dietary potassium intake was categorized into quartiles (Q1: <1911, Q2: 1911-2461, Q3: 2462-3119, and Q4: >3119 mg/d). Primary outcome AAC was quantified using the Kauppila scoring system. AAC scores were categorized into no AAC (AAC = 0, reference group), mild/moderate (AAC >0 to ≤ 6), and severe AAC (AAC >6). Pulse pressure was used as a surrogate for arterial stiffness and examined as a secondary outcome., Results: Among 2,418 participants, there was not a linear association between dietary potassium intake and AAC. Higher dietary potassium intake was associated with less severe AAC when comparing dietary potassium intake in Q2 with Q1 (odds ratio 0.55; 95% confidence interval: 0.34 to 0.92; P = .03). Higher dietary potassium intake was significantly associated with lower pulse pressure (P = .007): per 1000 mg/d higher dietary potassium intake, pulse pressure was 1.47 mmHg lower in the fully adjusted model. Compared to participants with dietary potassium intake in Q1, pulse pressure was 2.84 mmHg lower in Q4 (P = .04)., Conclusions: We did not find a linear association between dietary potassium intake and AAC. Dietary potassium intake was negatively associated with pulse pressure., (Copyright © 2023 National Kidney Foundation, Inc. All rights reserved.)

Background Hypertension is a highly prevalent cardiovascular risk factor. It is possible that air pollution, also an established cardiovascular risk factor, may contribute to cardiovascular disease through increasing blood pressure. Previous studies evaluating associations between air pollution and blood pressure have had mixed results. Methods We examined the association between long-term (one-year moving average) air pollutant exposures, prevalent hypertension and blood pressure in 4121 older Americans (57+ years) enrolled in the National Social Life, Health, and Aging Project. We estimated exposures to PM 2.5 using spatio-temporal models and used logistic regression accounting for repeated measures to evaluate the association between long-term average PM 2.5 and prevalence odds of hypertension. We additionally used linear regression to evaluate the associations between air pollutants and systolic, diastolic, mean arterial, and pulse pressures. Health effect models were adjusted for a number of demographic, health and socioeconomic covariates. Results An inter-quartile range (3.91 μg/m 3 ) increase in the one-year moving average of PM 2.5 was associated with increased: Odds of prevalent hypertension (POR 1.24, 95% CI: 1.11, 1.38), systolic blood pressure (0.93 mm Hg, 95% CI: 0.05, 1.80) and pulse pressure (0.89 mm Hg, 95% CI: 0.21, 1.58). Dose-response relationships were also observed. Conclusions PM 2.5 was associated with increased odds of prevalent hypertension, and increased systolic pressure and pulse pressure in a cohort of older Americans. These findings add to the growing evidence that air pollution may be an important risk factor for hypertension and perturbations in blood pressure. [ABSTRACT FROM AUTHOR]

Abstract: Most definitions of frailty utilize US populations in their development. The concept of frailty has not been well studied in Japan, which has the largest percentage of older patients (per capita) in the world. We created a 5-year prospective cohort study of community-dwelling older Japanese adults. Participants were not frail at baseline, based on our definition adapted from the Canadian Study for Health and Aging Clinical Frailty Scale. Participants underwent a comprehensive geriatric assessment (CGA) at baseline, and final assessments were either in person or via mailed survey. We enrolled 407 individuals (184 men, mean age 78±4years; 223 women, mean age 77±4years). Sixty-five participants met criteria for frailty by the end of the study. In univariate analyses, eighteen separate parameters were associated with frailty, some of which included: age, gender, handgrip, timed walk, systolic blood pressure, pulse pressure, cognitive status, living alone, and hearing deficits. In multivariate analyses, the following elements remained associated with frailty: timed walk, pulse pressure, cognition deficits and hearing deficits. We established cut-off points for timed walk (5m/3s) and pulse pressure (60mmHg). We then created a simple additive score for these four factors (present = 1; absent = 0). A score of 0 had a 93% negative predictive value for frailty while a score of 4 had a 70% positive predictive value. While further study is needed, this work creates an easy-to-administer tool that may be generalizable to other populations. [Copyright &y& Elsevier]

BackgroundIndividuals with impaired lung function have an elevated risk of cardiovascular events. Improved understanding of the factors associated with increased cardiovascular risk in the setting of lung function impairment is needed. We set out to determine in a nationwide population-based cohort whether impaired lung function as measured by forced expiratory volume in 1 s (FEV1) is associated with evidence of increased arterial stiffness measured by peripheral pulse pressure, a risk factor for cardiovascular events.MethodsCross-sectional study of adults ≥20 years of age in the Third National Health and Nutrition Examination Survey (NHANES III) who had valid and reproducible FEV1 data and serial blood pressure measurements allowing for the calculation of a mean pulse pressure, a measure of central arterial stiffness (n = 13,090).ResultsThere was a significant negative correlation between FEV1 and mean pulse pressure (r = −0.37). After controlling for demographic variables and confounders including cardiovascular risk factors, smoking history, and lung disease, the negative relationship between pulse pressure and FEV1 varies with age and becomes apparent only after age 40. In individuals aged 40–59 and ≥60 years, there was respectively a 2 and 3 mm Hg increment in pulse pressure for every one standard deviation decrement in FEV1.ConclusionsFEV1 is significantly related to pulse pressure, a clinically important measure of arterial stiffness, among those aged ≥40 years. This relationship may help to explain the increased risk of cardiovascular events found in individuals with impaired lung function.American Journal of Hypertension 2010; doi:10.1038/ajh.2010.37 [ABSTRACT FROM AUTHOR]

Presents several studies related to epidemiology. "Unexpectedly Poor Blood Pressure Control in an Unselected Cohort of Hospitalised Patients," by Syed U. Ahmed et al; "Treatment Patterns and Goal Attainment Among Hypertensive Patients With and Without Dyslipidemia and/or Diabetes," by Farhan Aslam; "Are There Disparities in Hypertension Treatment and Control Among Insured Adults in the U.S.? NHANES, 1999-2002," by Carma Ayala et al.

Background The associations of chronic cigarette smoking with blood pressure (BP) remain mixed. It is unclear whether a lack of examination of racial differences contributed to the mixed findings in previous studies. Black smokers metabolize nicotine at a slower rate than White smokers and racial discrimination contributes to nicotine dependence and higher BP among Black smokers. Methods and Results We studied the association between cigarette smoking and longitudinal (30-year) changes in systolic BP, diastolic BP, and pulse pressure (PP) in 4786 Black and White individuals from the CARDIA (Coronary Artery Risk Development in Young Adults) study using repeated-measures regression models. Neither systolic BP, nor diastolic BP differed between Black consistent smokers compared with Black never smokers, although Black consistent smokers had higher PP than Black never smokers (β=1.01 mm Hg, P =0.028). White consistent smokers had similar systolic BP, but lower diastolic BP (β=-2.27 mm Hg, P <0.001) and higher PP (β=1.59 mm Hg, P <0.001) compared with White never smokers. There were no differences in systolic BP, diastolic BP, or PP between Black or White long-term former smokers compared with never smokers (all P >0.05). Conclusions Although the associations of cigarette smoking with alterations in BP are small, the greater PP observed in consistent smokers may contribute in part to the higher cardiovascular disease risk observed in this group because PP is a strong predictor of cardiovascular disease risk after middle age.

Background: High dietary sodium intake may induce a small, yet physiologically relevant rise in serum sodium concentration, which associates with increased systolic blood pressure. Cellular data suggest that this association is mediated by increased endothelial cell stiffness. We hypothesized that higher serum sodium levels were associated with greater arterial stiffness in participants in the Systolic Blood Pressure Intervention Trial (SPRINT)., Methods: Multivariable linear regression was used to examine the association between baseline serum sodium level and (i) pulse pressure (PP; n = 8,813; a surrogate measure of arterial stiffness) and (ii) carotid-femoral pulse wave velocity (CFPWV; n = 591 in an ancillary study to SPRINT)., Results: Baseline mean ± SD age was 68 ± 9 years and serum sodium level was 140 ± 2 mmol/L. In the PP analysis, higher serum sodium was associated with increased baseline PP in the fully adjusted model (tertile 3 [≥141 mmol] vs. tertile 2 [139-140 mmol]; β = 0.87, 95% CI = 0.32 to 1.43). Results were similar in those with and without chronic kidney disease. In the ancillary study, higher baseline serum sodium was not associated with increased baseline CFPWV in the fully adjusted model (β = 0.35, 95% CI = -0.14 to 0.84)., Conclusions: Among adults at high risk for cardiovascular events but free from diabetes, higher serum sodium was independently associated with baseline arterial stiffness in SPRINT, as measured by PP, but not by CFPWV. These results suggest that high serum sodium may be a marker of risk for increased PP, a surrogate index of arterial stiffness., (© American Journal of Hypertension, Ltd 2019. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Objective: To investigate whether pulse pressure (PP) in anesthetized patients undergoing cardiac surgery before and after cardiopulmonary bypass (CPB) is associated with higher postoperative acute kidney injury (AKI) stage., Design: Retrospective cohort of 597 patients undergoing cardiac surgery., Setting: Single academic health care center., Participants: Adult patients undergoing cardiac surgery requiring CPB (coronary artery bypass grafting, valve, aortic, or combined surgery)., Interventions: Pulse pressure was assessed during 3 time periods: pre- and post-CPB, and in the first postoperative hour in the intensive care unit. Pulse pressure, patient characteristics, and intraoperative variables were evaluated using univariable generalized estimating equation analysis for a relationship with AKI stage. Significant risk factors from the univariable analysis then were evaluated in a multivariable generalized estimating equation analysis. Acute kidney injury stage was defined using the Acute Kidney Injury Network criteria., Primary Outcome: Stage of postoperative AKI., Measurements and Main Results: Intraoperative prebypass PP was associated independently and significantly with postoperative AKI stage (odds ratio 1.0107; 95% Confidence Interval, 1.0046-1.0168; p = 0.0005). For every 1-mmHg increase in PP, the odds of a higher AKI stage increased 1.07%. The 2 other periods were not found to be significant predictors of AKI stage., Conclusion: During general anesthesia prior to initiation of CPB, elevated PP is significantly predictive of postoperative AKI stage. This finding merits further research., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Purpose: The objective of this study was to determine individual and joint effects of pulse pressure and blood pressure treatment intensity on serious adverse events in the Systolic Blood Pressure Intervention Trial., Methods: Pulse pressure was calculated by subtracting diastolic blood pressure from systolic blood pressure. Blood pressure treatment intensity goal was ≤140mm Hg in the control arm and ≤120mm Hg in the intensive arm. The primary outcome was a 5-point composite of hypotension, syncope, electrolyte abnormalities, acute renal insufficiency, or injurious falls., Results: In 9361 trial participants, the incident rate for the primary outcome per 1000 person-years increased with higher pulse pressure category: ≤49 mmHg: 20.4 (17.2-24.1), 50-59 mmHg: 24.5 (21.3-28.2), 60-69 mmHg: 31.7 (27.7-36.2), ≥70 mmHg: 44.6 (39.8-49.9; P trend < .0001; hazard ratio [HR] of pulse pressure [every 10mm Hg] 1.23; 95% confidence interval [CI], 1.18-1.28). The intensive treatment arm had a higher incidence rate of serious adverse events than the control arm (34.2, 95% CI, 31.2-37.3, vs 26.0, 95% CI, 23.4-28.8, P = .0001; HR 1.32; 95% CI, 1.15-1.51). The combined effect was not significant in the relative risk scale (HR 0.97, P interaction  = .48) but was significant in the risk difference scale (P = .027), contributing 2.5 additional serious adverse events per 1000 person-years for every 10mm Hg increase in pulse pressure in excess of the individual effects of pulse pressure and treatment intensity., Conclusions: Wider pulse pressure and intensive blood pressure treatment were individually associated with the composite adverse event outcome. A modest effect modification of pulse pressure and treatment intensity led to additional adverse events when both were present. Clinicians should use caution when treating older patients with elevated pulse pressure to an intensive blood pressure treatment target., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Background: Pulse pressure (PP) is a potential risk factor of stroke. The relationship of incident stroke with systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and PP was examined., Methods: Data were from the REasons for Geographic And Racial Differences in Stroke national cohort study of 30,239 black and white participants aged ≥45 years, enrolled between 2003 and 2007. PP (SBP-DBP) and MAP (MAP = DBP + 1/3*PP) were calculated. Telephone follow-up occurred every six months for self or proxy-reported suspected stroke events, confirmed using expert adjudication. Cox-proportional hazards models examined the association of incident stroke for the different BP measurements with multivariable adjustment for sociodemographic and clinical risk factors including gender and race., Results: Men and women without prevalent stroke at baseline were analyzed (n = 25,462). During follow-up (mean 6.3±2.3 years, maximum 10 years), 916 strokes occurred. Unadjusted PP (hazard ratio [HR] = 1.30; 95% confidence interval [CI] 1.24-1.35), SBP (HR = 1.22; 95% CI 1.18-1.32), MAP (HR = 1.24; 95% CI 1.16-1.32), and DBP (HR = 1.09; 95% CI 1.01-1.17) were associated with stroke risk; however, after adjustment for SBP and other risk factors, the association with PP was attenuated (HR = 0.98; 95% CI 0.90-1.07), whereas SBP persisted as a predictor (HR = 1.14; 95% CI 1.06-1.23). These associations were consistent across age (younger vs. older >70 years) and race (black vs. white)., Conclusions: PP is positively associated with incident stroke, but not independently from SBP; and, there were no significant gender, racial, or regional differences in that association., (© American Journal of Hypertension, Ltd 2015. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Background: Serum fibroblast growth factor-23 (FGF-23) is associated with cardiovascular disease (CVD), yet the mechanisms remain uncertain. Our objective was to determine whether higher FGF-23 concentrations are associated with arterial stiffness., Methods: In this cross-sectional study, serum FGF-23 concentrations were measured in 5977 participants without known CVD in the Multi-Ethnic Study of Atherosclerosis. The primary outcomes of interest were large (LAE) and small artery elasticity (SAE), pulse pressure and ankle-brachial index (ABI) > 1.30. LAE and SAE were measured by pulse contour analysis of the radial artery. Pulse pressure was measured with an automated sphygmomanometer using the average of two resting blood pressure measurements. ABI was calculated as the ratio of the ankle and brachial systolic blood pressures., Results: Serum FGF-23 concentrations were not significantly associated with LAE [relative difference (RD) per doubling: 0%; 95% confidence interval (CI): -2-1%], SAE (RD per doubling: 0%; 95% CI: -3-2%), pulse pressure (β per doubling: 0.44; 95% CI: -0.31-1.19), or a high ABI (odds ratio per doubling: 1.14; 95% CI: 0.84-1.55). Findings were similar irrespective of chronic kidney disease status., Conclusions: Higher serum FGF-23 concentrations are not associated with arterial stiffness, as measured by pulse pressure, LAE, SAE or high ABI, in a community-based population without CVD., (Published by Oxford University Press on behalf of ERA-EDTA 2014. This work is written by (a) US Government employee(s) and is in the public domain in the US.)

Background: Somatic growth in childhood is accompanied by substantial remodeling of the aorta. Obesity is associated with increased aortic stiffness and flow and may interfere with aortic remodeling during growth. Wide pulse pressure (PP) indicates mismatch between aortic impedance and pulsatile flow and increases risk for future systolic hypertension and cardiovascular disease (CVD). We hypothesized that the rise of pediatric obesity would be associated with a temporal trend to higher PP., Methods and Results: We analyzed demographic, anthropometric, and blood pressure (BP) data for 8- to 17-year-old children (N=16 457) from the cross-sectional National Health and Nutrition Examination Surveys (NHANES) for 1976 through 2008. Multivariable adjusted survey regression was used to examine temporal trends in PP and mean arterial pressure (MAP) and the relation to obesity. Across this period, unadjusted PP was higher (0.29 mm Hg/y, 95% CI 0.26 to 0.33 mm Hg/y; P<0.0001), while MAP was lower (-0.24 mm Hg/y, 95% CI -0.27 to -0.20 mm Hg/y; P<0.0001) across examinations. Adjusting for body mass index partially attenuated the temporal trend for PP by 32% (P<0.0001). Obesity amplified the relation between taller height and higher PP (from 0.23 [95% CI 0.19 to 0.28] to 0.27 [95% CI 0.21 to 0.34] mm Hg/cm height in boys and from 0.08 [95% CI 0.04 to 0.13] to 0.22 [95% CI 0.13 to 0.31] mm Hg/cm height in girls; P<0.01 for both)., Conclusions: PP has increased during the rise of pediatric obesity. Higher PP may indicate mismatch between aortic diameter, wall stiffness, and flow in obese children during a period of rapid somatic growth when the aorta is already under considerable remodeling stress.