OBJECTIVE:To determine the effects of intensive blood pressure treatment on orthostatic hypertension. DESIGN:Systematic review and individual participant data meta-analysis. DATA SOURCES:MEDLINE, Embase, and Cochrane CENTRAL databases through 13 November 2023. INCLUSION CRITERIA:Population: ≥500 adults, age ≥18 years with hypertension or elevated blood pressure; intervention: randomized trials of more intensive antihypertensive drug treatment (lower blood pressure goal or active agent) with duration ≥6 months; control: less intensive antihypertensive drug treatment (higher blood pressure goal or placebo); outcome: measured standing blood pressure. MAIN OUTCOMES:Orthostatic hypertension, defined as an increase in systolic blood pressure ≥20 mm Hg or diastolic blood pressure ≥10 mm Hg after changing from sitting to standing. DATA SYNTHESIS:Two investigators independently abstracted articles. Individual participant data from nine trials identified during the systematic review were appended together as a single dataset. RESULTS:Of 31 124 participants with 315 497 standing blood pressure assessments, 9% had orthostatic hypotension (that is, a drop in blood pressure after standing of systolic ≥20 mm Hg or diastolic ≥10 mm Hg), 17% had orthostatic hypertension, and 3.2% had both a rise in systolic blood pressure and standing blood pressure ≥140 mm Hg at baseline. The effects of more intensive treatment were similar across trials with odds ratios for orthostatic hypertension ranging from 0.85 to 1.08 (I2=38.0%). During follow-up, 17% of patients assigned to more intensive treatment had orthostatic hypertension, whereas 19% of those assigned less intensive treatment had orthostatic hypertension. Compared with less intensive treatment, the risk of orthostatic hypertension was lower with more intensive blood pressure treatment (odds ratio 0.93, 95% confidence interval 0.90 to 0.96). Effects were greater among non-black versus black adults (odds ratio 0.86 v 0.97; P for interaction=0.003) and adults without diabetes versus those with diabetes (0.88 v 0.96; P for interaction=0.05) but did not differ by age ≥75 years, sex, baseline seated blood pressure ≥130/≥80 mm Hg, obesity, stage 3 kidney disease, stroke, cardiovascular disease, standing systolic blood pressure ≥140 mm Hg, or pre-randomization orthostatic hypertension (P for interactions ≥0.05). CONCLUSIONS:In this pooled cohort of adults with elevated blood pressure or hypertension, orthostatic hypertension was common and more intensive blood pressure treatment modestly reduced the occurrence of orthostatic hypertension. These findings suggest that approaches generally used for seated hypertension may also prevent hypertension on standing. STUDY REGISTRATION:Prospero CRD42020153753 (original proposal).

Hypertension impacts most older adults as one of many multiple chronic conditions. A thorough evaluation is required to assess overall health, cardiovascular status, and comorbid conditions that impact treatment targets. In the absence of severe frailty or dementia, intensive treatment prevents more cardiovascular events than standard treatment and may slow cognitive decline. "Start low and go slow" is not the best strategy for many older adults as fewer cardiovascular events occur when hypertension is controlled within the first 3 to 6 months of treatment.

BackgroundThe Ohio Cardiovascular and Diabetes Health Collaborative (Cardi-OH) unites general and subspecialty medical staff at the 7 medical schools in Ohio with community and public health partnerships to improve cardiovascular and diabetes health outcomes and eliminate disparities in Ohio’s Medicaid population. Although statewide collaboratives exist to address health improvements, few deploy needs assessments to inform their work. ObjectiveCardi-OH conducts an annual needs assessment to identify high-priority clinical topics, screening practices, policy changes for home monitoring devices and referrals, and preferences for the dissemination and implementation of evidence-based best practices. The results of the statewide needs assessment could also be used by others interested in disseminating best practices to primary care teams. MethodsA cross-sectional survey was distributed electronically via REDCap (Research Electronic Data Capture; Vanderbilt University) to both Cardi-OH grant-funded and non–grant-funded members (ie, people who have engaged with Cardi-OH but are not funded by the grant). ResultsIn total, 88% (103/117) of Cardi-OH grant-funded members and 8.14% (98/1204) of non–grant-funded members completed the needs assessment survey. Of these, 51.5% (53/103) of Cardi-OH grant-funded members and 47% (46/98) of non–grant-funded members provided direct clinical care. The top cardiovascular medicine and diabetes clinical topics for Cardi-OH grant-funded members (clinical and nonclinical) were lifestyle prescriptions (50/103, 48.5%), atypical diabetes (38/103, 36.9%), COVID-19 and cardiovascular disease (CVD; 38/103, 36.9%), and mental health and CVD (38/103, 36.9%). For non–grant-funded members, the top topics were lifestyle prescriptions (53/98, 54%), mental health and CVD (39/98, 40%), alcohol and CVD (27/98, 28%), and cardiovascular complications (27/98, 28%). Regarding social determinants of health, Cardi-OH grant-funded members prioritized 3 topics: weight bias and stigma (44/103, 42.7%), family-focused interventions (40/103, 38.8%), and adverse childhood events (37/103, 35.9%). Non–grant-funded members’ choices were family-focused interventions (51/98, 52%), implicit bias (43/98, 44%), and adverse childhood events (39/98, 40%). Assessment of other risk factors for CVD and diabetes across grant- and non–grant-funded members revealed screening for social determinants of health in approximately 50% of patients in each practice, whereas some frequency of depression and substance abuse screening occurred in 80% to 90% of the patients. Access to best practice home monitoring devices was challenging, with 30% (16/53) and 41% (19/46) of clinical grant-funded and non–grant-funded members reporting challenges in obtaining home blood pressure monitoring devices and 68% (36/53) and 43% (20/46) reporting challenges with continuous glucose monitors. ConclusionsCardi-OH grant- and non–grant-funded members shared the following high-priority topics: lifestyle prescriptions, CVD and mental health, family-focused interventions, alcohol and CVD, and adverse childhood experiences. Identifying high-priority educational topics and preferred delivery modalities for evidence-based materials is essential for ensuring that the dissemination of resources is practical and useful for providers.

Key Points In the Systolic Blood Pressure Intervention Trial (SPRINT), the longer-term incidence of needing dialysis or transplantation was low and primarily associated with baseline kidney function.Rates of dialysis or transplantation were higher with intensive versus standard treatment, though the differences were not statistically significant. Background The Systolic Blood Pressure Intervention Trial (SPRINT) showed that intensive lowering of systolic BP increased the risk of incident CKD and episodes of AKI. Whether intensive treatment changes the risk of kidney failure is unknown. The goal of this study was to estimate the legacy effect of intensive versus standard systolic BP lowering on the longer-term incidence of kidney failure. Methods This study is a secondary analysis of a randomized, open-label clinical trial with observational follow-up. Between 2010 and 2013, patients 50 years and older with hypertension and higher cardiovascular risk excluding those with diabetes mellitus, history of stroke, proteinuria >1 g/d, or polycystic kidney disease were recruited from 102 clinic sites in the United States and Puerto Rico. Participants were randomized to a systolic BP goal of <120 mm Hg (intensive treatment) or <140 mm Hg (standard treatment group). We linked participants with the United States Renal Data System to ascertain kidney failure (initiation of dialysis therapy or transplantation) and the US National Death Index to ascertain all-cause mortality through 2020. Results Based on analysis of 9279 (99.1%) of 9361 randomized participants, 101 cases of kidney failure occurred over a median follow-up of 8.6 years (interquartile range, 8.0–9.1 years), with the majority occurring in 74 (73.3%) participants with an eGFR <45 ml/min per 1.73 m2 at baseline. Intensive treatment did not significantly increase the risk of kidney failure either overall (cause-specific hazard ratio, 1.20; 95% confidence interval, 0.81 to 1.78) or in the subgroup of participants with baseline eGFR <45 ml/min per 1.73 m2 (cause-specific hazard ratio, 1.43; 95% confidence interval, 0.89 to 2.30). Conclusions Overall, and in patients with eGFR <45 ml/min per 1.73 m2, there were higher rates of dialysis or transplantation among SPRINT participants randomized to intensive treatment, but the modest differences observed were not statistically significant. Clinical Trial registry name and registration number: SPRINT, NCT01206062.

A growing appreciation of the pathophysiological interrelatedness of metabolic risk factors such as obesity and diabetes, chronic kidney disease, and cardiovascular disease has led to the conceptualization of cardiovascular-kidney-metabolic syndrome. The confluence of metabolic risk factors and chronic kidney disease within cardiovascular-kidney-metabolic syndrome is strongly linked to risk for adverse cardiovascular and kidney outcomes. In addition, there are unique management considerations for individuals with established cardiovascular disease and coexisting metabolic risk factors, chronic kidney disease, or both. An extensive body of literature supports our scientific understanding of, and approach to, prevention and management for individuals with cardiovascular-kidney-metabolic syndrome. However, there are critical gaps in knowledge related to cardiovascular-kidney-metabolic syndrome in terms of mechanisms of disease development, heterogeneity within clinical phenotypes, interplay between social determinants of health and biological risk factors, and accurate assessments of disease incidence in the context of competing risks. There are also key limitations in the data supporting the clinical care for cardiovascular-kidney-metabolic syndrome, particularly in terms of early-life prevention, screening for risk factors, interdisciplinary care models, optimal strategies for supporting lifestyle modification and weight loss, targeting of emerging cardioprotective and kidney-protective therapies, management of patients with both cardiovascular disease and chronic kidney disease, and the impact of systematically assessing and addressing social determinants of health. This scientific statement uses a crosswalk of major guidelines, in addition to a review of the scientific literature, to summarize the evidence and fundamental gaps related to the science, screening, prevention, and management of cardiovascular-kidney-metabolic syndrome.

Cardiovascular-kidney-metabolic health reflects the interplay among metabolic risk factors, chronic kidney disease, and the cardiovascular system and has profound impacts on morbidity and mortality. There are multisystem consequences of poor cardiovascular-kidney-metabolic health, with the most significant clinical impact being the high associated incidence of cardiovascular disease events and cardiovascular mortality. There is a high prevalence of poor cardiovascular-kidney-metabolic health in the population, with a disproportionate burden seen among those with adverse social determinants of health. However, there is also a growing number of therapeutic options that favorably affect metabolic risk factors, kidney function, or both that also have cardioprotective effects. To improve cardiovascular-kidney-metabolic health and related outcomes in the population, there is a critical need for (1) more clarity on the definition of cardiovascular-kidney-metabolic syndrome; (2) an approach to cardiovascular-kidney-metabolic staging that promotes prevention across the life course; (3) prediction algorithms that include the exposures and outcomes most relevant to cardiovascular-kidney-metabolic health; and (4) strategies for the prevention and management of cardiovascular disease in relation to cardiovascular-kidney-metabolic health that reflect harmonization across major subspecialty guidelines and emerging scientific evidence. It is also critical to incorporate considerations of social determinants of health into care models for cardiovascular-kidney-metabolic syndrome and to reduce care fragmentation by facilitating approaches for patient-centered interdisciplinary care. This presidential advisory provides guidance on the definition, staging, prediction paradigms, and holistic approaches to care for patients with cardiovascular-kidney-metabolic syndrome and details a multicomponent vision for effectively and equitably enhancing cardiovascular-kidney-metabolic health in the population.

Background Hypertension control is critical to reducing cardiovascular disease, challenging to achieve, and exacerbated by socioeconomic inequities. Few states have established statewide quality improvement (QI) infrastructures to improve blood pressure (BP) control across economically disadvantaged populations. In this study, we aimed to improve BP control by 15% for all Medicaid recipients and by 20% for non-Hispanic Black participants. Methodology This QI study used repeated cross-sections of electronic health record data and, for Medicaid enrollees, linked Medicaid claims data for 17,672 adults with hypertension seen at one of eight high-volume Medicaid primary care practices in Ohio from 2017 to 2019. Evidence-based strategies included (1) accurate BP measurement; (2) timely follow-up; (3) outreach; (4) a standardized treatment algorithm; and (5) effective communication. Payers focused on a 90-day supply (vs. 30-day) of BP medications, home BP monitor access, and outreach. Implementation efforts included an in-person kick-off followed by monthly QI coaching and monthly webinars. Weighted generalized estimating equations were used to estimate the baseline, one-year, and two-year implementation change in the proportion of visits with BP control (<140/90 mm Hg) stratified by race/ethnicity. Results For all practices, the percentage of participants with controlled BP increased from 52% in 2017 to 60% in 2019. Among non-Hispanic Whites, the odds of achieving BP control in year one and year two were 1.24 times (95% confidence interval: 1.14, 1.34) and 1.50 times (1.38, 1.63) higher relative to baseline, respectively. Among non-Hispanic Blacks, the odds for years one and two were 1.18 times (1.10, 1.27) and 1.34 times (1.24, 1.45) higher relative to baseline, respectively. Conclusions A hypertension QI project as part of establishing a statewide QI infrastructure improved BP control in practices with a high volume of disadvantaged patients. Future efforts should investigate ways to reduce inequities in BP control and further explore factors associated with greater BP improvements and sustainability.

HomeCirculationVol. 148, No. 3Historical Neighborhood Redlining and Cardiovascular Risk in Patients With Chronic Kidney Disease Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBHistorical Neighborhood Redlining and Cardiovascular Risk in Patients With Chronic Kidney Disease Sadeer Al-Kindi, Issam Motairek, Catherine Kreatsoulas, Jackson T. Wright Jr, Mirela Dobre, Mahboob Rahman and Sanjay Rajagopalan Sadeer Al-KindiSadeer Al-Kindi Correspondence to: Sadeer Al-Kindi, MD, Assistant Professor of Medicine, University Hospitals Harrington Heart and Vascular Institute, Case Western Reserve University School of Medicine, 11100 Euclid Ave, Cleveland, OH 44106. Email E-mail Address: [email protected] https://orcid.org/0000-0002-1122-7695 Harrington Heart and Vascular Institute, University Hospitals, Cleveland, OH (S.A.-K., I.M., S.R.). , Issam MotairekIssam Motairek https://orcid.org/0000-0003-3294-8659 Harrington Heart and Vascular Institute, University Hospitals, Cleveland, OH (S.A.-K., I.M., S.R.). , Catherine KreatsoulasCatherine Kreatsoulas https://orcid.org/0000-0001-9542-8453 Harvard School of Public Health, Harvard University, Boston, MA (C.K.). , Jackson T. Wright JrJackson T. Wright Jr https://orcid.org/0000-0003-2557-7239 Division of Nephrology and Hypertension, University Hospitals Cleveland Medical Center, OH (J.T.W., M.D., M.R.). , Mirela DobreMirela Dobre https://orcid.org/0000-0002-9059-9998 Division of Nephrology and Hypertension, University Hospitals Cleveland Medical Center, OH (J.T.W., M.D., M.R.). , Mahboob RahmanMahboob Rahman https://orcid.org/0000-0001-9025-7413 Division of Nephrology and Hypertension, University Hospitals Cleveland Medical Center, OH (J.T.W., M.D., M.R.). and Sanjay RajagopalanSanjay Rajagopalan https://orcid.org/0000-0001-6669-8163 Harrington Heart and Vascular Institute, University Hospitals, Cleveland, OH (S.A.-K., I.M., S.R.). Originally published17 Jul 2023https://doi.org/10.1161/CIRCULATIONAHA.123.064215Circulation. 2023;148:280–282The leading cause of death among individuals with chronic kidney disease (CKD) is cardiovascular disease (CVD). Social risk factors, including the effects of neighborhoods and systemic racism, have been associated with CVD risk. During the 1930s, the US government–sponsored Home Owners' Loan Corporation (HOLC) implemented a grading system to evaluate neighborhood risk for mortgage applications.1 Neighborhoods rated A—depicted in green— represented the wealthiest areas; areas rated D—depicted in red—represented the poorest neighborhoods and were referred to as redlined. This practice resulted in residential segregation and has contributed to persistent systemic racism.1 We previously demonstrated a link between redlining and increased neighborhood-level cardiometabolic risk, including CVD and CKD, throughout the United States.2 This study aimed to investigate the association between redlining and the prevalence and incidence of CVD in a contemporary prospective cohort of patients with CKD.The data that support the findings of this study are available from the corresponding author. Data were obtained from participants who enrolled in the Chronic Renal Insufficiency Cohort in 2003 through 2008. The study protocol was approved by institutional review boards at the participating institutions.3 All participants provided informed consent to participate in the study. In brief, adults with mild to moderate CKD were recruited from 7 sites and followed prospectively for incident CVD. Events are adjudicated by phone calls and review of medical records. The residential addresses of participants were geocoded into census block groups at study entry and linked to HOLC-graded maps generated from digitized maps. We examined the association of participant neighborhood HOLC grade with prevalent (logistic regression) and incident (Cox regression models in patients without prevalent CVD) CVD events (myocardial infarction, peripheral arterial disease, stroke, heart failure, atrial fibrillation, and all-cause death), adjusting for age, sex, race, ethnicity, estimated glomerular filtration rate, smoking, low-density lipoprotein cholesterol level, diabetes, systolic and diastolic blood pressure, and urine albumin–creatinine ratio. We used Bonferroni corrections to account for multiple comparisons.A total of 1720 participants were included (553 in HOLC group D). Worsening neighborhood HOLC grade was associated with an increased proportion of Black and Hispanic residents, younger age, higher proteinuria, higher systolic blood pressure, and higher high-sensitivity troponin levels (all P<0.01), as determined using ANOVA for continuous and χ2 for categorical variables. In multivariable-adjusted models, group B (odds ratio [OR], 2.34 [95% CI, 1.32 to 4.15]), group C (OR, 2.31 [1.34 to 3.98]), and group D (OR, 2.10 [1.21 to 3.65]) were associated with increased baseline CVD (reference, HOLC group A; Table 1). These relationships were not attenuated after further adjustment for household income and education (B vs A: OR, 2.31 [1.30 to 4.10]; C vs A: OR, 2.25 [1.30 to 3.88]; D vs A: OR, 2.04 [1.17 to 3.56]). Among 1118 participants without baseline CVD, group D was associated with increased risk for HF or all-cause death (adjusted hazard ratio, 2.63 [1.31 to 5.28]; Table 1), which remained unchanged after further adjustment for BNP (B-type natriuretic peptide) and high-sensitivity troponins (D vs A: hazard ratio, 2.55 [1.27 to 5.13]), or education and income (D vs A: hazard ratio, 2.42 [1.20 to 4.86]).Table 1. Association Between Home Owners' Loan Corporation Risk and Prevalent and Incident Cardiovascular DiseaseCVDModel 1Model 2B vs AC vs AD vs AB vs AC vs AD vs APrevalent CVD (logistic regression model; n=1720) Any2.08 (1.23–3.51); P=0.007*2.19 (1.33–3.61); P=0.002*1.96 (1.18–3.26); P=0.0092.34 (1.32–4.15); P=0.003*2.31 (1.34–3.98); P=0.003*2.10 (1.21–3.65); P=0.009 Myocardial infarction or revascularization2.42 (1.29–4.56); P=0.006*2.03 (1.11–3.73); P=0.0221.97 (1.06–3.66); P=0.0332.36 (1.22–4.57); P=0.0111.85 (0.98–3.50); P=0.0591.83 (0.96–3.51); P=0.069 Peripheral artery disease1.95 (0.55–6.87); P=0.2982.91 (0.88–9.63); P=0.0792.69 (0.80–9.03); P=0.109 Heart failure1.67 (0.75–3.73); P=0.211.52 (0.71–3.28); P=0.2831.54 (0.71–3.36); P=0.275 Stroke1.83 (0.74–4.56); P=0.1932.21 (0.93–5.25); P=0.0732.00 (0.83–4.82); P=0.121 Atrial fibrillation1.61 (0.86–2.98); P=0.1341.68 (0.93–3.02); P=0.0831.36 (0.74–2.49); P=0.319Incident CVD in patients without prevalent CVD (Cox model; n=1118) Myocardial infarction1.17 (0.31–4.32); P=0.821.47 (0.44–4.93); P=0.531.37 (0.40–4.71); P=0.614 Peripheral artery disease0.94 (0.18–4.92); P=0.9421.03 (0.22–4.74); P=0.9721.53 (0.32–7.24); P=0.592 Heart failure1.56 (0.52–4.71); P=0.4322.47 (0.89–6.88); P=0.0843.02 (1.08–8.51); P=0.0361.41 (0.47–4.28); P=0.5422.03 (0.73–5.68); P=0.1752.46 (0.87–6.94); P=0.089 Stroke0.92 (0.18–4.75); P=0.9160.84 (0.18–3.86); P=0.8221.03 (0.22–4.79); P=0.968 Atrial fibrillation1.12 (0.45–2.75); P=0.8091.52 (0.67–3.44); P=0.3161.74 (0.74–4.10); P=0.204 Composite outcome†1.31 (0.59–2.90); P=0.5051.73 (0.83–3.61); P=0.1462.07 (0.98–4.36); P=0.056 Death1.22 (0.57–2.59); P=0.6131.60 (0.80–3.23); P=0.1872.16 (1.07–4.39); P=0.0331.21 (0.54–2.70); P=0.6431.50 (0.71–3.15); P=0.2892.06 (0.97–4.36); P=0.061 Heart failure or death1.55 (0.77–3.13); P=0.2182.16 (1.12–4.16); P=0.0212.80 (1.45–5.43); P=0.002*1.55 (0.74–3.23); P=0.2461.99 (1.00–3.96); P=0.0512.63 (1.31–5.28); P=0.006*Model 1: age, sex, race, ethnicity, estimated glomerular filtration rate; model 2: model 1 + smoked at least 100 cigarettes in lifetime, low-density lipoprotein level, diabetes, systolic blood pressure, diastolic blood pressure, urine albumin–creatinine ratio. CVD indicates cardiovascular disease.* Significant after Bonferroni correction.† Heart failure, myocardial infarction, stroke, peripheral artery disease.Historical residential segregation policies continue to affect health risk in patients with CKD. This study suggests that patients with mild to moderate CKD who are residents of historically redlined neighborhoods have a twofold higher risk of HF, independently of established CVD risk factors. The mechanisms of these associations remain speculative. We previously demonstrated that residents of historically poor HOLC groups have increased adverse environmental exposures,4 which may mediate increased CVD risk. These conditions may constitute geographic footprints that significantly affect life expectancy and disease burden, even in high-income countries.5 As such, potential mechanisms linking redlining with intergenerational CVD risk, and interventions to reduce risk, need to be elucidated in future studies.This study has important implications for both policymaking and clinical practice. The results suggest that policies surrounding residential segregation can have a persistent, multigenerational effect on chronic health outcomes. As a result, the health effects of neighborhoods and mortgage legislation should be carefully considered, particularly among minority populations. The identification of high-risk neighborhoods through redlining highlights the need for targeted community engagement strategies and health care investments. Furthermore, neighborhood characteristics such as redlining risk should be considered in the assessment of individual patient risk for future events, allowing for the implementation of intensive risk reduction strategies. This may necessitate the incorporation of neighborhood disadvantage in risk prediction models and the establishment of calibration across different patient populations.This study should be interpreted within the context of its limitations. First, this is a relatively small study from 7 cities, and thus may not be generalizable to all patients with CKD. In addition, there is the potential for confounding factors to influence the relationship between HOLC risk and CVD risk. The OR for prevalent CVD in group D overlaps with those of groups B and C, making it challenging to discern a clear dose-dependent relationship. A larger cohort may be needed to detect a more pronounced association. Nevertheless, this analysis is strengthened by prospective design and adjudicated outcomes.ARTICLE INFORMATIONSources of FundingThis work was partly funded by the National Institute on Minority Health and Health Disparities Award P50MD017351 (Drs Al-Kindi and Rajagopalan) and the National Institute of Diabetes and Digestive and Kidney Diseases Award U01DK061021 (Dr Rahman).Nonstandard Abbreviations and AcronymsBNPB-type natriuretic peptideCKDchronic kidney diseaseCVDcardiovascular diseaseHOLCHome Owners' Loan CorporationORodds ratioDisclosures None.FootnotesFor Sources of Funding and Disclosures, see page 282.Circulation is available at www.ahajournals.org/journal/circCorrespondence to: Sadeer Al-Kindi, MD, Assistant Professor of Medicine, University Hospitals Harrington Heart and Vascular Institute, Case Western Reserve University School of Medicine, 11100 Euclid Ave, Cleveland, OH 44106. Email sadeer.al-kindi@uhhospitals.orgREFERENCES1. Aaronson D, Hartley D, Mazumder B. The effects of the 1930s HOLC "redlining" maps.Am Econ J Econ Policy. 2021; 13:355–392.CrossrefGoogle Scholar2. Motairek I, Lee EK, Janus S, Farkouh M, Freedman D, Wright J, Nasir K, Rajagopalan S, Al-Kindi S. Historical neighborhood redlining and contemporary cardiometabolic risk.J Am Coll Cardiol. 2022; 80:171–175. doi: 10.1016/j.jacc.2022.05.010CrossrefMedlineGoogle Scholar3. Feldman HI, Appel LJ, Chertow GM, Cifelli D, Cizman B, Daugirdas J, Fink JC, Franklin-Becker ED, Go AS, Hamm LL, et al; Chronic Renal Insufficiency Cohort (CRIC) Study Investigators. The Chronic Renal Insufficiency Cohort (CRIC) Study: design and methods.J Am Soc Nephrol. 2003; 14:S148–S153. doi: 10.1097/01.asn.0000070149.78399.ceCrossrefMedlineGoogle Scholar4. Motairek I, Chen Z, Makhlouf MH, Rajagopalan S, Al-Kindi S. Historical neighbourhood redlining and contemporary environmental racism.Local Environ. 2022; 1:11.Google Scholar5. Ladoy A, Vallarta-Robledo JR, De Ridder D, Sandoval JL, Stringhini S, Da Costa H, Guessous I, Joost S. Geographic footprints of life expectancy inequalities in the state of Geneva, Switzerland.Sci Rep. 2021; 11:23326. doi: 10.1038/s41598-021-02733-xCrossrefMedlineGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetails July 18, 2023Vol 148, Issue 3 Advertisement Article InformationMetrics © 2023 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.123.064215PMID: 37459405 Originally publishedJuly 17, 2023 Keywordsenvironmentheart disease risk factorsresidence characteristicssocial determinants of healthPDF download Advertisement SubjectsDisparitiesHealth Equity

Background: Orthostatic hypertension (OHTN) is associated with cardiovascular disease (CVD). We previously demonstrated how more intensive blood pressure (BP) treatment reduced orthostatic hypotension (OH) via a net increase in BP upon standing. Whether this effect also increased OHTN was not examined. Methods: We used pooled data from an individual participant data meta-analysis of 9 randomized BP pharmacologic treatment trials with seated and standing BP (search conducted through May 13, 2022). OHTN was defined as an increase in SBP ≥20 or DBP ≥10 mm Hg after changing from sitting to standing. Effects were examined overall and by baseline characteristics. Results: Of 31,124 participants with 315,497 standing BP assessments, 9% had OH, and 20% had OHTN at baseline. Trial effects were similar ( I 2 = 38.0%). During follow-up, 17% of those assigned more intensive treatment had OHTN, while 19% of those assigned less intensive treatment had OHTN. Intensive BP treatment significantly lowered OHTN risk (OR 0.93; 95% CI: 0.90, 0.96) ( Figure ). Effects were significantly greater among non-Black adults (OR 0.86 vs 0.97, P -interaction =0.003) and adults without diabetes (OR 0.88 vs 0.96; P -interaction =0.047). Effects did not differ by age≥75 years, sex, baseline seated BP≥130/≥80 mm Hg, obesity, stage 3 kidney disease, stroke, cardiovascular disease, standing SBP ≥140 mm Hg, or pre-randomization OHTN ( P -interactions ≥0.05). Conclusion: In this pooled cohort of adults with hypertension or higher CVD risk, OHTN was more common than OH and more intensive BP treatment reduced OHTN risk. The relationship between this effect with respect to CVD should be a focus of subsequent research.

Importance There are ongoing concerns about the benefits of intensive vs standard blood pressure (BP) treatment among adults with orthostatic hypotension or standing hypotension. Objective To determine the effect of a lower BP treatment goal or active therapy vs a standard BP treatment goal or placebo on cardiovascular disease (CVD) or all-cause mortality in strata of baseline orthostatic hypotension or baseline standing hypotension. Data Sources Individual participant data meta-analysis based on a systematic review of MEDLINE, EMBASE, and CENTRAL databases through May 13, 2022. Study Selection Randomized trials of BP pharmacologic treatment (more intensive BP goal or active agent) with orthostatic hypotension assessments. Data Extraction and Synthesis Individual participant data meta-analysis extracted following PRISMA guidelines. Effects were determined using Cox proportional hazard models using a single-stage approach. Main Outcomes and Measures Main outcomes were CVD or all-cause mortality. Orthostatic hypotension was defined as a decrease in systolic BP of at least 20 mm Hg and/or diastolic BP of at least 10 mm Hg after changing position from sitting to standing. Standing hypotension was defined as a standing systolic BP of 110 mm Hg or less or standing diastolic BP of 60 mm Hg or less. Results The 9 trials included 29 235 participants followed up for a median of 4 years (mean age, 69.0 [SD, 10.9] years; 48% women). There were 9% with orthostatic hypotension and 5% with standing hypotension at baseline. More intensive BP treatment or active therapy lowered risk of CVD or all-cause mortality among those without baseline orthostatic hypotension (hazard ratio [HR], 0.81; 95% CI, 0.76-0.86) similarly to those with baseline orthostatic hypotension (HR, 0.83; 95% CI, 0.70-1.00; P = .68 for interaction of treatment with baseline orthostatic hypotension). More intensive BP treatment or active therapy lowered risk of CVD or all-cause mortality among those without baseline standing hypotension (HR, 0.80; 95% CI, 0.75-0.85), and nonsignificantly among those with baseline standing hypotension (HR, 0.94; 95% CI, 0.75-1.18). Effects did not differ by baseline standing hypotension ( P = .16 for interaction of treatment with baseline standing hypotension). Conclusions and Relevance In this population of hypertension trial participants, intensive therapy reduced risk of CVD or all-cause mortality regardless of orthostatic hypotension without evidence for different effects among those with standing hypotension.

Recently published national data demonstrate inadequate and worsening control of high blood pressure (HBP) in the United States, outcomes that likely have been made even worse by the coronavirus disease 2019 (COVID-19) pandemic. This major public health crisis exposes shortcomings of the US health care delivery system and creates an urgent opportunity to reduce mortality, major cardiovascular events, and costs for 115 million Americans. Ending this crisis will require a more coherent and systemic change to traditional patterns of care. The authors present an evidence-based Blueprint for Change for comprehensive health delivery system redesign based on current national clinical practice guidelines and quality measures. This innovative model includes a systems-based approach to ensuring proper BP measurement, assessment of cardiovascular risk, effective patient-centered team-based care, addressing social determinants of health, and shared decision-making. The authors also propose building on current national quality improvement initiatives designed to better control HBP.

Importance:The Systolic Blood Pressure Intervention Trial (SPRINT) showed that intensive blood pressure control reduced cardiovascular morbidity and mortality. However, the legacy effect of intensive treatment is unknown.Objective:To evaluate the long-term effects of randomization to intensive treatment with the incidence of cardiovascular and all-cause mortality approximately 4.5 years after the trial ended.Design, Setting, and Participants:In this secondary analysis of a multicenter randomized clinical trial, randomization began on November 8, 2010, the trial intervention ended on August 20, 2015, and trial close-out visits occurred through July 2016. Patients 50 years and older with hypertension and increased cardiovascular risk but without diabetes or history of stroke were included from 102 clinic sites in the US and Puerto Rico. Analyses were conducted between October 2021 and February 2022.Interventions:Randomization to systolic blood pressure (SBP) goal of less than 120 mm Hg (intensive treatment group; n = 4678) vs less than 140 mm Hg (standard treatment group; n = 4683).Main Outcomes and Measures:Extended observational follow-up for mortality via the US National Death Index from 2016 through 2020. In a subset of 2944 trial participants, outpatient SBP from electronic health records during and after the trial were examined.Results:Among 9361 randomized participants, the mean (SD) age was 67.9 (9.4) years, and 3332 (35.6%) were women. Over a median (IQR) intervention period of 3.3 (2.9-3.9) years, intensive treatment was beneficial for both cardiovascular mortality (hazard ratio [HR], 0.66; 95% CI, 0.49-0.89) and all-cause mortality (HR, 0.83; 95% CI, 0.68-1.01). However, at the median (IQR) total follow-up of 8.8 (8.3-9.3) years, there was no longer evidence of benefit for cardiovascular mortality (HR, 1.02; 95% CI, 0.84-1.24) or all-cause mortality (HR, 1.08; 95% CI, 0.94-1.23). In a subgroup of participants, the estimated mean outpatient SBP among participants randomized to intensive treatment increased from 132.8 mm Hg (95% CI, 132.0-133.7) at 5 years to 140.4 mm Hg (95% CI, 137.8-143.0) at 10 years following randomization.Conclusions and Relevance:The beneficial effect of intensive treatment on cardiovascular and all-cause mortality did not persist after the trial. Given increasing outpatient SBP levels in participants randomized to intensive treatment following the trial, these results highlight the importance of consistent long-term management of hypertension.Trial Registration:ClinicalTrials.gov Identifier: NCT01206062.

Abstract BACKGROUND AND AIMS Circulating cardiac biomarkers implicated in the pathogenesis of heart disease may provide a non-invasive, more precise assessment of cardiovascular risk. In the Systolic Blood Pressure Intervention Trial (SPRINT), intensive blood pressure lowering was associated with a 25% reduction in cardiovascular events and a 27% reduction in all-cause mortality. We sought to assess whether the beneficial effect of lowering systolic blood pressure on clinical outcomes was accompanied by a reduction in serum biomarkers of myocardial fibrosis. METHOD SPRINT, a multicenter randomized controlled trial conducted in the United States, enrolled participants aged ≥ 50 years, at increased risk for cardiovascular disease and randomized them to intensive systolic blood pressure lowering (target < 120 mmHg) or standard blood pressure lowering (target < 140 mmHg). In a randomly selected subgroup of SPRINT participants, myocardial fibrosis was assessed by two collagen-derived serum peptides, C-terminal propeptide of procollagen type I (CICP) and N-terminal propeptide of procollagen type 3 (P3NP) and Galectin 3 measured at study baseline and at 24 months follow-up. Chronic kidney disease was defined as eGFR < 60 mL/min/1.73 m2. Analyses were based on linear mixed models including clinic site as a random effect, with adjustments for treatment group and baseline level of each respective biomarker. RESULTS A total of 742 SPRINT participants with and without CKD with available measurements of myocardial fibrosis biomarkers at study baseline and 24 months were included in the study. The median (IQR) Galectin 3, CICP and P3NP levels at study baseline and 24 months follow-up in the intensive versus standard group are presented in the Table 1. Intensive blood pressure lowering was not associated with longitudinal changes in CICP or P3NP (Table 1 and Figure 1). Intensive blood pressure lowering was associated with a statistically significant increase in Galectin 3 level [between group mean difference 0.47 (IQR: 0.03–0.92) ng/mL, P = 0.04]. All of the findings were generally consistent across participants with and without CKD (Table 1). CONCLUSION In a random sample of SPRINT participants, intensive versus standard blood pressure lowering was not associated with a reduction in circulating myocardial fibrosis biomarkers overtime in hypertensive individuals with and without CKD.

BACKGROUND:Effective management of hypertension (HTN) is a priority in primary care, necessary to decrease the costs, morbidity, and mortality associated with cardiovascular disease. Strategies to support quality improvement (QI) efforts in primary care are needed to make significant improvements in population health, especially for patients who experience socioeconomic inequalities. LOCAL PROBLEM:To address the high rate (>50%) of uncontrolled HTN in the state of Ohio, a statewide QI project was implemented in high-volume Medicaid practices, aimed at improving blood pressure control and addressing racial disparities. The initiative expanded to include coaching QI to support efforts in primary care practices. METHODS:The Model for Improvement guided development of Plan-Do-Study-Act (PDSA) cycles facilitated by QI coaching and APRN collaboration to implement key components of HTN guidelines: accurate blood pressure measurement, effective treatment, and timely follow-up. INTERVENTIONS:Interventions were implemented after PDSA cycles over 18 months in two practice sites to address HTN control. Linking multiple PDSA test cycles and review of data bimonthly allowed for reflection on the impact of interventions for non-Hispanic Black patients and the overall patient population. RESULTS:The percentage of patients with controlled HTN, repeat blood pressure measurement, and timely follow-up improved in an urban primary care practice associated with an academic medical center and in a rural federally qualified health center. CONCLUSIONS:Primary care practices can benefit from the external support of coaching when implementing QI processes to make meaningful change. APRNs are key collaborators for expanding QI efforts in primary care.

Antihypertensive treatments benefit cerebrovascular health and cognitive function in patients with hypertension, but it is uncertain whether an intensive blood pressure target leads to potentially harmful cerebral hypoperfusion.To investigate the association of intensive systolic blood pressure (SBP) control vs standard control with whole-brain cerebral blood flow (CBF).This substudy of the Systolic Blood Pressure Intervention Trial (SPRINT) randomized clinical trial compared the efficacy of 2 different blood pressure-lowering strategies with longitudinal brain magnetic resonance imaging (MRI) including arterial spin labeled perfusion imaging to quantify CBF. A total of 1267 adults 50 years or older with hypertension and increased cardiovascular risk but free of diabetes or dementia were screened for the SPRINT substudy from 6 sites in the US. Randomization began in November 2010 with final follow-up MRI in July 2016. Analyses were performed from September 2020 through December 2021.Study participants with baseline CBF measures were randomized to an intensive SBP target less than 120 mm Hg or standard SBP target less than 140 mm Hg.The primary outcome was change in whole-brain CBF from baseline. Secondary outcomes were change in gray matter, white matter, and periventricular white matter CBF.Among 547 participants with CBF measured at baseline, the mean (SD) age was 67.5 (8.1) years and 219 (40.0%) were women; 315 completed follow-up MRI at a median (IQR) of 4.0 (3.7-4.1) years after randomization. Mean whole-brain CBF increased from 38.90 to 40.36 (difference, 1.46 [95% CI, 0.08-2.83]) mL/100 g/min in the intensive treatment group, with no mean increase in the standard treatment group (37.96 to 37.12; difference, -0.84 [95% CI, -2.30 to 0.61] mL/100 g/min; between-group difference, 2.30 [95% CI, 0.30-4.30; P = .02]). Gray, white, and periventricular white matter CBF showed similar changes. The association of intensive vs standard treatment with CBF was generally similar across subgroups defined by age, sex, race, chronic kidney disease, SBP, orthostatic hypotension, and frailty, with the exception of an indication of larger mean increases in CBF associated with intensive treatment among participants with a history of cardiovascular disease (interaction P = .05).Intensive vs standard antihypertensive treatment was associated with increased, rather than decreased, cerebral perfusion, most notably in participants with a history of cardiovascular disease.ClinicalTrials.gov Identifier: NCT01206062.

HomeHypertensionVol. 79, No. 12Ambient Air Pollution and Pulse Wave Velocity in Patients With Hypertension Treated With Intensive Versus Standard Blood Pressure Control Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBAmbient Air Pollution and Pulse Wave Velocity in Patients With Hypertension Treated With Intensive Versus Standard Blood Pressure Control Sadeer G. Al-Kindi, Robert D. Brook, Mirela Dobre, Mahboob Rahman, Jackson T. Wright and Sanjay Rajagopalan Sadeer G. Al-KindiSadeer G. Al-Kindi Correspondence to: Sadeer Al-Kindi, University Hospitals Harrington Heart and Vascular Institute, Case Western Reserve University School of Medicine, 11100 Euclid Ave, Cleveland, OH 44106. Email E-mail Address: [email protected] https://orcid.org/0000-0002-1122-7695 Division of Cardiovascular Medicine (S.G.A.-K., S.R.), Department of Medicine, Case Western Reserve University/University Hospitals Cleveland Medical Center, Cleveland, OH. Search for more papers by this author , Robert D. BrookRobert D. Brook https://orcid.org/0000-0002-8521-7262 Cardiovascular Disease Prevention, Wayne State University, Detroit, MI (R.D.B.). Search for more papers by this author , Mirela DobreMirela Dobre https://orcid.org/0000-0002-9059-9998 Division of Nephrology and Hypertension (M.D., M.R., J.T.W.), Department of Medicine, Case Western Reserve University/University Hospitals Cleveland Medical Center, Cleveland, OH. Search for more papers by this author , Mahboob RahmanMahboob Rahman https://orcid.org/0000-0001-9025-7413 Division of Nephrology and Hypertension (M.D., M.R., J.T.W.), Department of Medicine, Case Western Reserve University/University Hospitals Cleveland Medical Center, Cleveland, OH. Search for more papers by this author , Jackson T. WrightJackson T. Wright https://orcid.org/0000-0003-2557-7239 Division of Nephrology and Hypertension (M.D., M.R., J.T.W.), Department of Medicine, Case Western Reserve University/University Hospitals Cleveland Medical Center, Cleveland, OH. Search for more papers by this author and Sanjay RajagopalanSanjay Rajagopalan Correspondence to: Sanjay Rajagopalan, Cardiovascular Research Institute, University Hospitals Harrington Heart and Vascular Institute, Case Western Reserve University School of Medicine, 11100 Euclid Ave, Cleveland, OH 44106. Email E-mail Address: [email protected] https://orcid.org/0000-0001-6669-8163 Division of Cardiovascular Medicine (S.G.A.-K., S.R.), Department of Medicine, Case Western Reserve University/University Hospitals Cleveland Medical Center, Cleveland, OH. Search for more papers by this author Originally published29 Sep 2022https://doi.org/10.1161/HYPERTENSIONAHA.122.19779Hypertension. 2022;79:e144–e146Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: September 30, 2022: Ahead of Print Ambient air pollution (especially fine particulate matter <2.5 µm, PM2.5) has been linked to increased cardiovascular risk.1 Increase in blood pressure has been hypothesized to be one mechanism and has indeed been noted in both humans and experimental models.1 In the SPRINT (Systolic BP Intervention Trial), we have previously shown that the cardiovascular risk reduction due to intensive BP lowering was more robust among individuals living in areas with higher air pollution levels.2 We sought to investigate the link between ambient particulate matter (PM2.5) and change in pulse wave velocity (PWV), a marker of arterial stiffness, and the impact of intensive BP lowering in SPRINT participants. We hypothesized that differential responsiveness of arterial stiffness to BP lowering in relation to chronic PM2.5 exposure may shed light on mechanisms by which air pollution modulates BP and cardiovascular risk.A subset of SPRINT participants underwent PWV measurements at baseline, and at 3 years using the Sphygmocor CPV system (AtCor Medical, Naperville, IL)3 and using unattended BP measurements performed at the randomization visit. Using residential ZIP code of participant’s residence, we linked participants with integrated satellite-based ambient PM2.5. PM2.5 estimates were derived from a model that includes satellite-based methods (aerosol optical depth), chemical transport models, and adjustment for ground monitors as we previously described.2 We analyzed patients by PM2.5 levels as a continuous variable and using threshold (<12 versus ≥12 µg/m3) corresponding to annual National Ambient Air Quality Standards (NAAQS). Paired t-tests were used to analyze changes over time in PWV. Spearman correlations and linear regression analyses were performed to investigate the association between PM2.5 (both at entry and mean annual levels during the trial), baseline PWV, and change in PWV through year 3 (ΔPWV). Three linear regression models were performed to evaluate the association between PM2.5 and ΔPWV: unadjusted model, model 1 (adjusted for age, sex, race), and model 2 (model 1 + total cholesterol, baseline systolic and diastolic BP, Clinical/subclinical cardiovascular disease, baseline estimated glomerular filtration rate, smoking status, and randomization arm, body mass index, heart rate, and baseline PWV).A total of 517 participants were included (259 randomized to standard BP, and 258 to intensive BP). Mean PM2.5 was 9.5±1.8 μg/m3 and mean baseline PWV was 10.7±2.7 m/s. Over 3 years, PWV increased by a mean of 0.27 m/s from baseline (P=0.016). There was no correlation between PM2.5 and PWV at baseline (Spearman ρ=0.01, P=0.84). PM2.5, however, significantly correlated with ΔPWV (Spearman ρ=0.26, P<0.001). The associations between PM2.5 and ΔPWV were similar in the intensive (Spearman ρ=0.29, P<0.001) and standard BP arms (Spearman ρ=0.25, P<0.001), Figure [A]. No significant interaction was noted between PM2.5 and trial assignment (intensive versus standard BP control) with respect to ∆PWV (PM2.5×Assignment, Pinteraction=0.74). Participants living in areas with PM2.5 levels above the NAAQS threshold of 12 μg/m3 (n=61) had higher ΔPWV compared with participants living below NAAQS threshold (n=456), ΔPWV 1.3 m/s versus 0.13 m/s, P=0.001. After multiple adjustments (model 2), entry and mean PM2.5 remained associated with ΔPWV (per 1 μg/m3 of PM2.5, entry PM2.5: [β 0.408, SE 0.058, P<0.001]; mean PM2.5: [β 0.315, SE 0.053, P<0.001]; Figure [B]).Download figureDownload PowerPointFigure. Particulate matter <2.5 µm (PM2.5) and pulse wave velocities (PWV) in SPRINT (Systolic Blood Pressure [BP] Intervention Trial). A, Scatter plot of mean PM2.5 and change in PWV over 3 y. B, Unadjusted and adjusted association between PM2.5 with change in PWV at 3 y. Model 1: age, sex, Black race. Model 2: model 1+total cholesterol, baseline systolic and diastolic BP, Clinical/subclinical cardiovascular disease, baseline estimated glomerular filtration rate, smoking status, and randomization arm, body mass index, heart rate, and baseline PWV.Arterial stiffness is an established risk factor for cardiovascular disease,4 and has been proposed as a pathway linking pollution-triggered cardiovascular events. Although exposure to air pollutants has demonstrated changes in acute arterial stiffness, results from epidemiological studies with longer exposures have been mixed.1 Our analysis, from a randomized controlled trial that enrolled moderate to high-risk patients with hypertension, demonstrated a significant association between PM2.5 and PWV after controlling for baseline characteristics. Higher progression in PWV was seen in areas with PM2.5 levels above NAAQS, but the relationship between PM2.5 and ∆PWV continued to very low exposure levels. Importantly, intensive BP lowering did not modify this association. Prior studies involving exposure to a variety of pollutants including diesel exhaust have noted changes in arterial stiffness, through mechanisms that involve hemodynamic changes and alterations in nitric oxide signaling.1,5 The fact that BP lowering did not alter the association between PM2.5 and ΔPWV could suggest that the pathways that lead to arterial stiffness may involve nonhemodynamic pathways.This post hoc study has limitations and should be interpreted as hypothesis-generating including potential exposure misclassification, patient bias by virtue of enrolling in this ancillary study, and small cohort size. Nevertheless, the longitudinal structure of this study and the randomized design in a carefully performed trial lends unique aspects to these data.In conclusion, SPRINT participants who live in areas with higher ambient air pollution (PM2.5) levels experienced larger increase in PWV over 3 years, without a significant impact of intensive BP lowering. Our study findings provide a mechanistic basis for elevated cardiovascular risk at exposure levels well below NAAQS.Article InformationAcknowledgmentsThis article was prepared using SPRINT (Systolic Blood Pressure Intervention Trial) Research Materials obtained from the National Heart, Lung, and Blood Institute (NHLBI) Biologic Specimen and Data Repository Information Coordinating Center and does not necessarily reflect the opinions or views of SPRINT or the NHLBI.Sources of FundingThis study was partly funded by National Institutes of Health (NIH) grants (P50MD017351, R35ES031702, R01ES019616, 5R01HL141846).Disclosures None.FootnotesFor Sources of Funding and Disclosures, see page e145 & e146.Correspondence to: Sadeer Al-Kindi, University Hospitals Harrington Heart and Vascular Institute, Case Western Reserve University School of Medicine, 11100 Euclid Ave, Cleveland, OH 44106. Email sadeer.[email protected]orgCorrespondence to: Sanjay Rajagopalan, Cardiovascular Research Institute, University Hospitals Harrington Heart and Vascular Institute, Case Western Reserve University School of Medicine, 11100 Euclid Ave, Cleveland, OH 44106. Email sanjay.[email protected]orgReferences1. Rajagopalan S, Al-Kindi SG, Brook RD. Air pollution and cardiovascular disease: JACC state-of-the-art review.J Am Coll Cardiol. 2018; 72:2054–2070. doi: 10.1016/j.jacc.2018.07.099CrossrefMedlineGoogle Scholar2. Al-Kindi SG, Brook RD, Bhatt U, Brauer M, Cushman WC, Hanson HA, Kostis J, Lash JP, Paine R, Raphael KL, et al; SPRINT Research Group. The benefits of intensive versus standard blood pressure treatment according to fine particulate matter air pollution exposure: a post hoc analysis of SPRINT.Hypertension. 2021; 77:813–822. doi: 10.1161/HYPERTENSIONAHA.120.15923LinkGoogle Scholar3. Vlachopoulos C, Terentes-Printzios D, Laurent S, Nilsson PM, Protogerou AD, Aznaouridis K, Xaplanteris P, Koutagiar I, Tomiyama H, Yamashina A, et al. Association of estimated pulse wave velocity with survival: a secondary analysis of SPRINT.JAMA Netw Open. 2019; 2:e1912831. doi: 10.1001/jamanetworkopen.2019.12831CrossrefMedlineGoogle Scholar4. Mitchell GF, Hwang SJ, Vasan RS, Larson MG, Pencina MJ, Hamburg NM, Vita JA, Levy D, Benjamin EJ. Arterial stiffness and cardiovascular events: the Framingham Heart Study.Circulation. 2010; 121:505–511. doi: 10.1161/CIRCULATIONAHA.109.886655LinkGoogle Scholar5. Langrish JP, Unosson J, Bosson J, Barath S, Muala A, Blackwell S, Söderberg S, Pourazar J, Megson IL, Treweeke A, et al. Altered nitric oxide bioavailability contributes to diesel exhaust inhalation-induced cardiovascular dysfunction in man.J Am Heart Assoc. 2013; 2:e004309. doi: 10.1161/JAHA.112.004309LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails December 2022Vol 79, Issue 12 Advertisement Article InformationMetrics © 2022 American Heart Association, Inc.https://doi.org/10.1161/HYPERTENSIONAHA.122.19779PMID: 36176038 Originally publishedSeptember 29, 2022 Keywordsriskblood pressureair pollutionhypertensionparticulate matterPDF download Advertisement SubjectsHypertensionRisk Factors

Background Cardiovascular risk factor control is challenging, especially in disadvantaged populations. However, few statewide efforts exist to tackle this challenge. Therefore, our objective is to describe the formation of a unique statewide cardiovascular health collaborative so others may learn from this approach. Methodology With funding from the Ohio Department of Medicaid’s Ohio Medicaid Technical Assistance and Policy Program, we used a collective impact model to link the seven medical schools in Ohio, primary care clinics across the state, the Ohio Department of Medicaid, and Ohio’s Medicaid Managed Care Plans in a statewide health improvement collaborative for expanding primary care capacity to improve cardiovascular health in Ohio. Results Initial dissemination activities for primary care teams included a virtual case-based learning series focused on hypertension and social determinants of health, website resources, a monthly newsletter with clinical tips, webinars, and in-person conferences. The collaborative is aligned with a separately funded hypertension quality improvement project for paired implementation. Conclusions The collective impact model is a useful framework for developing a statewide collaborative focused on the dissemination and implementation of evidence-based best practices for cardiovascular health improvement and disparity reduction. Statewide collaboratives bringing payers, clinicians, and academic partners together have the potential to substantially impact cardiovascular health.

Background Peripheral artery disease (PAD) increases the risk of cardiovascular events and limb events including amputations. PAD is twice as prevalent in Black compared with non‐Hispanic White individuals, especially among men. Screening for PAD using the ankle–brachial index in community settings, such as the barbershop, could lead to earlier diagnosis and treatment. Methods and Results A pilot study was conducted at 2 barbershops in Cleveland, OH from June to December 2020 to assess the feasibility of screening for PAD in the barbershop setting and the effect of an educational intervention on PAD awareness. After screening with both automated and Doppler ankle–brachial index, PAD was identified in 5/31 (16.1%) of participants. Baseline systolic blood pressure, low‐density lipoprotein cholesterol, and random blood glucose were higher in participants who screened positive for PAD (P<0.001). PAD awareness was low overall. There was a significant improvement in PAD awareness assessment scores obtained at the initial and exit visits (9.93±4.23 to 12.50±4.41, P=0.004). An association was found between PAD awareness at baseline and highest education level achieved: compared with those with some college/associate's degree or higher, non–high school graduates scored lower on PAD awareness (P=0.022), as did those who only had a high school diploma or tests of General Educational Development (P=0.049). Conclusions In a pilot study, barbershop‐based screening for PAD among Black men revealed a higher than expected PAD prevalence and low PAD awareness. An educational video was effective at increasing PAD awareness. Ankle–brachial index screening and educational outreach in the barbershop may be a feasible and effective tool to diagnose PAD and reduce PAD disparities among Black men at highest risk.