Search

The relation between serial high-sensitivity C-reactive protein (hsCRP) and long-term major cardiovascular events (MACEs; cardiovascular death, myocardial infarction, stroke, coronary revascularization, hospitalization for unstable angina) has not been explored in optimally-treated patients with atherosclerotic cardiovascular disease. We tested the hypothesis that longitudinal follow-up hsCRP (repeated measures over time) would associate with 30-month MACE rates. We performed a post hoc analysis of ACCELERATE (Assessment of Clinical Effects of Cholesteryl Ester Transfer Protein Inhibitor with Evacetrapib in Patients with High-Risk for Vascular Outcomes), involving optimally-treated patients with high-risk vascular disease, with available baseline and at least 1 follow-up hsCRP level. Using multivariable Cox proportional hazard models, we determined the association of longitudinal follow-up hsCRP with MACE at 30 months among 8,563 patients (aged 64.6 ± 9 years, 22% women). Patients with incident MACE (n = 961) had higher baseline hsCRP levels (1.77 vs 1.46 mg/L, plt;0.0001 for patients with and without MACE, respectively) and showed an upward trajectory during follow-up, whereas median hsCRP levels remainedlt;2 mg/L at all time points (1.83 vs 1.53 mg/L, 1.91 vs 1.53 mg/L, 1.76 vs 1.37 mg/L, at 3, 12, and 24 months, respectively). In a multivariable analysis, higher longitudinal hsCRP levels were independently associated with MACE (hazard ratio [95% confidence interval] per SD 1.19 [1.10 to 1.29], plt;0.001), the majority of its individual components and all-cause death. Multivariable models containing longitudinal hsCRP provided improved predictive ability of MACE over baseline hsCRP. In the setting of established medical therapies, longitudinal follow-up hsCRP was independently associated with long-term MACE. In conclusion, these findings suggest that longitudinal hsCRP represents a novel approach of residual cardiovascular risk even when on-treatment hsCRP levels remainlt;2 mg/L.

Objective To evaluate the relationship between hypertensive diseases in pregnancy and kidney function later in life. Methods We evaluated measured glomerular filtration rate (mGFR) using iothalamate urinary clearance in 725 women of the Genetic Epidemiology Network of Arteriopathy (GENOA) study. Women were classified by self-report as nulliparous (n=62), a history of normotensive pregnancies (n=544), a history of hypertensive pregnancies (n=102), or a history of pre-eclampsia (n=17). We compared adjusted associations among these four groups with mGFR using generalized estimating equations to account for familial clustering. Chronic kidney disease (CKD) was defined as mGFR of less than 60 mL/min per 1.73 m2 or urinary albumin-creatinine ratio (UACR) greater than or equal to 30 mg/g. Results Among women with kidney function measurements (mean age, 59±9 years, 52.9% African American), those with a history of hypertensive pregnancy had lower mGFR (–4.66 ml/min per 1.73 m2; 95% CI, -9.12 to -0.20) compared with women with a history of normotensive pregnancies. Compared with women with a history of normotensive pregnancies, women with a history of hypertensive pregnancy also had higher odds of mGFR less than 60 ml/min per 1.73 m2 (odds ratio, 2.09; 95% CI, 1.21 to 3.60). Additionally, women with a history of hypertensive pregnancy had greater odds for chronic kidney disease (odds ratio, 4.89; 95% CI, 1.55 to 15.44), after adjusting for age, race, education, smoking history, hypertension, body mass index, and diabetes. Conclusion A history of hypertension in pregnancy is an important prognostic risk factor for kidney disease. To our knowledge, this is the first and largest investigation showing the association between hypertensive diseases in pregnancy and subsequent kidney disease using mGFR in a large biracial cohort.

High blood pressure (BP) based on measurements obtained in the office setting has been associated with the presence and level of coronary artery calcification (CAC)—a measure of subclinical atherosclerosis. We studied the association between out-of-office BP and CAC among 557 participants who underwent 24-hour ambulatory BP monitoring at visit 1 in 2000–2004 and a computed tomography scan at visit 2 in 2005–2008 as part of the JHS (Jackson Heart Study)—a community-based cohort of African American adults. Mean awake, asleep, and 24-hour BP were calculated for each participant. Among participants included in this analysis, 279 (50%) had any CAC defined by an Agatston score >0. After multivariable adjustment including office systolic BP (SBP), the prevalence ratios for any CAC comparing the highest versus the lowest quartiles of SBP on ambulatory BP monitoring were 1.08 (95% CI, 0.84–1.39) for awake SBP, 1.32 (95% CI, 1.01–1.74) for asleep SBP, and 1.19 (95% CI, 0.91–1.55) for 24-hour SBP. After multivariable adjustment including office diastolic BP, the prevalence ratios for any CAC comparing the highest versus the lowest quartiles of awake, asleep, and 24-hour diastolic BP were 1.27 (95% CI, 1.02–1.59), 1.29 (95% CI, 1.02–1.64), and 1.25 (95% CI, 0.99–1.59), respectively. The current results suggest that higher asleep SBP and higher awake and asleep diastolic BP may be risk factors for subclinical atherosclerosis and underscore the potential role of ambulatory BP monitoring in identifying individuals at high risk for coronary artery disease.

Objective To examine associations between physical activity (PA), inflammation, coronary artery calcification (CAC), and incident coronary heart disease (CHD) in African Americans. Methods Among Jackson Heart Study participants without prevalent CHD at baseline (n=4295), we examined the relationships between PA and high-sensitivity C-reactive protein, the presence of CAC (Agatston score ≥100), and incident CHD. Based on the American Heart Association’s Life’s Simple 7 metrics, participants were classified as having poor, intermediate, or ideal PA. Results After adjustment for possible confounding factors, ideal PA was associated with lower high-sensitivity C-reactive protein levels (β, −0.15; 95% CI, −0.15 to −0.002) and a lower prevalence of CAC (odds ratio, 0.70; 95% CI, 0.51-0.96) compared with poor PA. During a median of 12.8 years of follow-up, there were 164 incident CHD events (3.3/1000 person-years). Ideal PA was associated with a lower rate of incident CHD compared with poor PA (hazard ratio, 0.55; 95% CI, 0.31-0.98). Conclusion In a large community-based African American cohort, ideal PA was associated with lower inflammation levels, a lower prevalence of CAC, and a lower rate of incident CHD. These findings suggest that promotion of ideal PA may be an important way to reduce the risk of subclinical and future clinical CHD in African Americans.

There is no clear consensus on a lower cutoff value for normal left ventricular ejection fraction (EF) and the prognostic implications of low normal EF (LNEF) are poorly understood, particularly in Blacks. Therefore, we investigated the association of LNEF and incident heart failure (HF) in a community-based cohort of Blacks. We studied 3,669 participants (mean age 54 years, 63% women) of the Jackson Heart Study without prevalent HF or coronary heart disease (CHD). Participants were divided into three groups: (1) Reduced EF (

Background Hypertensive diseases in pregnancy have been associated with altered cardiac structure and function, yet these associations have not been systematically investigated in larger populations including African Americans. We evaluated the relationships between hypertensive diseases in pregnancy with cardiac structure and function later in life in the Genetic Epidemiology Network of Arteriopathy (GENOA) study. Methods We investigated 1013 African American women sibships with echocardiographic measurements from the GENOA study (Phase II, 2000-05; Jackson, MS). Women were classified as self-reported nulliparous (n = 61), a history of normotensive pregnancies (n = 780), a history of a hypertensive pregnancies (n = 152), or a history of preeclampsia (n = 20). We compared adjusted associations among these 4 groups with echocardiographic measurements of cardiac structure and function using generalized estimating equations, accounting for familial clustering. Results Among 1013 women with echocardiographic data (mean age 62 ± 9.5 years), women with a history of hypertensive pregnancy had lower left ventricular ejection fraction (LVEF) (P = 0.043) compared to nulliparous women and higher left atrial systolic dimension (LASD) compared to women with a history of normotensive pregnancies (P = 0.010), After adjusting for cardiovascular risk factors. There were no statistically significant differences in other echocardiographic parameters among these groups. Conclusions A history of hypertension in pregnancy is associated with lower LVEF later in life, compared to nulliparous women and higher LASD compared to women with a history of normotensive pregnancies. However, given the multiple comparisons considered, this finding should be interpreted cautiously and requires further study.

Objectives: Ambulatory blood pressure (BP) monitoring (ABPM) parameters beyond mean BP may be useful for identifying individuals at high risk for cardiovascular end-organ damage. We examined the association between ABPM parameters, including 24-hour BP load, peak BP, peak increase in BP, and mean BP with left ventricular hypertrophy (LVH). Methods: Data were pooled from five US-based studies in which participants underwent ABPM for 24 hours (n=2,892). We defined systolic BP (SBP) load as the weighted average of the percent awake SBP readings ≥ 130 mm Hg and asleep SBP readings ≥ 110 mm Hg; peak SBP as the weighted average of awake and asleep 90 th percentile of SBP; peak increase as the difference between the peak SBP and mean SBP. These parameters were then categorized into quartiles. LVH was assessed by 2D-echocardiography. Analyses were stratified by mean 24-hour BP < 130/80 and ≥ 130/80 mm Hg. Results: Among participants with mean 24-hour BP < 130/80 mm Hg, the prevalence of LVH increased from the lowest to the highest quartile for SBP load, peak SBP, peak increase in SBP, and mean SBP ( Table ). The adjusted prevalence ratio (PR) for the association of the highest versus the lowest quartile with LVH was 1.82 (95%CI: 1.08-3.05) for SBP load, 2.00 (95%CI: 1.18-3.38) for peak SBP, 1.38 (95%CI: 0.85-2.23) for peak increase in SBP, and 1.51 (95%CI: 0.98-2.32) for mean SBP. Among participants with mean 24-hour BP ≥ 130/80 mm Hg, the prevalence of LVH increased for all ABPM parameters from the lowest to the highest quartile. The multivariable-adjusted PR for the association of the highest versus the lowest quartile with LVH was 1.39 (95%CI: 0.98-1.97) for SBP load, 1.66 (95%CI: 1.09-2.53) for peak SBP, 1.08 (95%CI: 0.76-1.53) for peak increase in SBP, and 1.88 (95%CI: 1.24-2.83) for mean SBP. Conclusion: The 24-hour SBP load and peak SBP were associated with a higher prevalence of LVH when mean 24-hour BP was < 130/80 mm Hg. The 24-hour peak SBP and mean SBP were associated with a higher prevalence of LVH when mean 24-hour BP was ≥ 130/80 mm Hg.

In observational studies, a lower serum vitamin DAmong 5306 Black Americans in the Jackson Heart Study cohort, we investigated the relationships between serum vitamin DIn this community-based Black American cohort, lower serum vitamin D

Background: Cigarette smoking has been associated with incident heart failure (HF), however the relationships with HF phenotypes have not been adequately investigated, particularly in African Americans. Methods and Results: Among 4129 African Americans participants in the Jackson Heart Study without a history of HF or coronary heart disease (CHD) at baseline, we investigated the relationships between baseline smoking status, smoking intensity (number of cigarettes/day) among current smokers, and smoking burden (pack years) among ever smokers and incident HF hospitalization. HF phenotypes were categorized either as HF with reduced ejection fraction (HFrEF: EF Conclusion: In this large community-based African American cohort, cigarette smoking (smoking status, smoking intensity, and smoking burden) was significantly associated with incident HFpEF, but not with HFrEF. Smoking cessation in African Americans who smoke may reduce risk for HFpEF in this high-risk population.

Introduction: Black Americans experience a heightened risk of heart failure (HF) and develop HF at earlier ages than other racial/ethnic groups. Limited data exist regarding the prevalence and prognostic relevance of ACC/AHA HF stages among Black Americans. We aimed to quantify the distribution and prognostic relevance of ACC/AHA HF stages among Black Americans in mid- and late-life. Methods: We classified 4,763 Black participants in the community-based Jackson Heart Study who underwent echocardiography at study Exam 1 (2000-2004) by HF stage as follows: Stage A: presence of clinical HF risk factors (prevalent cardiovascular disease, hypertension, diabetes, obesity, metabolic syndrome, or chronic kidney disease) in the absence of structural heart disease; Stage B: structural heart disease (LVEF Results: Mean age was 55.3 ± 12.7 years and 64% were women. No clinical risk factors or cardiac structural or functional abnormalities (Stage 0) were present in 13% of participants. Stage A was present in 59%, Stage B was present in 26%, and prevalent HF (Stage C) was present in 3%. Over a median of 12.8 [IQR 11.8-13.5] years follow up, 332 participants developed HF and 1,060 participants died. Compared to those free of risk factors or structural remodeling (Stage 0), a more advanced HF stage was associated with greater risk of incident HF, and the composite of HF or death (Figure). Conclusions: In this large community-based cohort of Black Americans, HF risk factors (Stage A) and/or asymptomatic structural heart disease (Stage B) was present in 85% of participants. Stage A and Stage B were each associated with heightened risk of HF hospitalization.

Introduction: Heart failure (HF) disproportionately burdens Black Americans. The contributions of impairments in cardiovascular (CV) and non-cardiovascular (non-CV) function to incident HF with reduced (HFrEF) and preserved (HFpEF) ejection fraction in this group remain unclear. Methods: Among 4,356 Black participants in the Jackson Heart Study (JHS) free of prevalent HF at visit 1 (2000-2004), multivariable Cox proportional hazard models were employed to assess the associations of measures of CV and non-CV organ function with incident HF, HFpEF, and HFrEF over a median follow-up of 13 years. Systems considered included: CV: left ventricular (LV) structure (mass index; LVMI), LV systolic function (LVEF), LV diastolic function (left atrial diameter; LAD), systemic arterial function (pulse pressure; PP); Non-CV: pulmonary function (percent predicted FEV1; ppFEV1), renal function (eGFR), body composition (waist circumference), and dysglycemia (hemoglobin A1c; HbA1c). Model covariates included age, sex, hypertension, diabetes, smoking status, and coronary disease history. Results: Average age was 54±13 years and 64% were women. Over median 13 (IQR 12-14) years follow-up, incident HF occurred in 315 participants (152 HFpEF, 134 HFrEF, 29 unknown LVEF). In multivariable models incorporating measures reflecting each organ system, significant predictors of incident HFpEF included greater LAD, higher PP, lower ppFEV1, lower eGFR, larger waist circumference, and higher HbA1c (Figure). Predictors of incident HFrEF included greater LVMI, lower LVEF, and lower eGFR. eGFR was the only independent predictor of both HFpEF and HFrEF. Conclusion: Subclinical impairments in CV and non-CV organ function differentially associate with risk of incident HFpEF and HFrEF among Black Americans. These findings support partially distinct mechanisms underlying HFrEF and HFpEF, and a greater contribution of multisystem non-cardiac impairments to HFpEF in particular.

Background High-sensitivity C-reactive protein (hsCRP) predicts major cardiovascular events (MACE) in patients with chronic atherosclerotic cardiovascular disease. The relationship between serial longitudinal hsCRP assessment and long-term MACE has not been explored. Purpose We tested the hypothesis that longitudinal follow-up hsCRP levels (repeated measures over time) would associate with 30-month MACE (cardiovascular death, myocardial infarction, cerebrovascular accident, coronary revascularization or hospitalization for unstable angina) rates. Methods We performed a post-hoc analysis of the ACCELERATE trial of optimally-treated patients with high-risk vascular disease and evaluated data from patients with available baseline and at least one follow-up hsCRP level measured at 3, 12, and 24 months. Those with a MACE event occurring before 3 months were omitted. Using multivariable Cox proportional hazard models, we determined the association of longitudinal follow-up hsCRP levels with MACE, its components, and all-cause mortality at 30-months, adjusting for age, race, sex, region, smoking status, body mass index, diabetes, baseline hsCRP, low density lipoprotein-cholesterol, high-density lipoprotein cholesterol, systolic blood pressure, statin use, and treatment group. Results Among 8,563 patients, mean age was 64.6±9.3 years and 22.2% were women. Median baseline hsCRP was 1.49 (0.74, 3.3) mg/L. Median time-weighted average follow-up hsCRP was 1.80 (0.88, 3.9) mg/L and mean time-weighted average follow-up LDL-C was 71.7±28.0 mg/dL. At 30 months, there was a significant stepwise relationship between cumulative MACE and increasing tertiles of last prior hsCRP value before an event or censoring (KM estimates for tertiles 1–3, respectively: 8.9 vs. 12.4 vs. 15.6%, p Conclusions In the setting of established medical therapies, longitudinal follow-up hsCRP is significantly associated with an increased risk of long-term MACE, myocardial infarction, stroke, cardiovascular mortality, coronary revascularization, and all-cause death. Longitudinal follow-up hsCRP may thus represent a novel marker of residual cardiovascular risk, supporting further work exploring the potential diagnostic and therapeutic implications of these findings. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): Iryna Dykun was supported by the German Research Foundation

The use of LiDAR (Light Detection And Ranging) in archaeological prospection is not a new phenomenon; its capacity to enhance fieldwork processes is well proven. Use of the technology makes it poss...

Aim Remnant cholesterol has been proposed to promote atherosclerotic cardiovascular disease independent of low-density lipoprotein cholesterol, yet the underlying mechanisms are not well understood. We aimed to study the association of remnant cholesterol with coronary atheroma progression and clinical events. Methods We analyzed data from 5754 patients with coronary artery disease undergoing serial intravascular ultrasonography who were enrolled in 10 trials examining various medical therapies. Remnant cholesterol was calculated as (non-high-density lipoprotein cholesterol – low-density lipoprotein cholesterol (estimated using the Hopkins–Martin equation)). Changes in percentage atheroma volume and 2-year major adverse cardiovascular events were compared across various levels of remnant cholesterol, and multivariable models were used to assess the independent relationship of remnant cholesterol with changes in percentage atheroma volume. Results The mean age was 58.1 ± 9.2 years, 28% were women and 96% received a statin. Percentage atheroma volume progression (changes in percentage atheroma volume > 0) occurred in a linear fashion at on-treatment remnant cholesterol levels of 25 mg/dL or greater. The highest on-treatment remnant cholesterol quartile demonstrated greater percentage atheroma volume progression (+0.53 ± 0.26 vs. –0.15 ± 0.25%, P Conclusions In statin-treated patients with atherosclerotic cardiovascular disease, remnant cholesterol was associated with coronary atheroma progression regardless of conventional lipid parameters, C-reactive protein or clinical risk factors. Higher remnant cholesterol levels also correlated with higher major adverse cardiovascular events. These data support further investigations into remnant cholesterol-lowering interventions in statin-treated patients harboring residual atherosclerotic cardiovascular disease risk.

Recent mapping for the Tooele 30' x 60' quadrangle geologic map revealed more information about interesting exposures of red beds cropping out in an 11-mile (18-km) swath along the northwestern flank of the Cedar Mountains (Clark and others, 2017, 2019 in review). They are unusual because such rocks are seldom preserved in northwestern Utah, an area known for thick thrust sheets of Paleozoic marine carbonate and sandstone. These rocks were first mapped by Robert Maurer for his Ph.D. dissertation on the geology of the Cedar Mountains (Maurer, 1970). He called them North Horn (?) Formation and noted the presence of fresh-water snails (Gyraulus sp.) that a paleontologist said were probably of late Paleocene or Eocene age. The North Horn Formation is considered Late Cretaceous (Maastrichtian age) to Paleocene or Eocene (~70 to 60 Ma) in age. However, recent detrital zircon analysis from sandstone in the unit suggest a much older age, with the youngest grains (maximum depositional age) of 117 Ma, or Early Cretaceous, Aptian (UGS and O’Sullivan, 2017). Two samples of gray mudstone taken for fossil pollen in the unit did not produce any usable material. Inspection of these rocks by Don DeBlieux (Utah Geological Survey paleontologist) revealed no bone or other biological material at this location.

In 2017, the American College of Cardiology/American Heart Association (ACC/AHA) and the American College of Physicians/American Academy of Family Physicians (ACP/AAFP) published blood pressure guidelines. Adults recommended antihypertensive medication initiation or intensification by the ACP/AAFP guideline receive the same recommendation from the ACC/AHA guideline. However, many adults ≥60 years old are recommended to initiate or intensify antihypertensive medication by the ACC/AHA but not the ACP/AAFP guideline. We compared atherosclerotic cardiovascular disease event rates according to antihypertensive treatment recommendations in the ACC/AHA and ACP/AAFP guidelines among adults ≥60 years old with systolic blood pressure ≥130 mm Hg or diastolic blood pressure ≥80 mm Hg in the REGARDS study (Reasons for Geographic and Racial Differences in Stroke) and the JHS (Jackson Heart Study). Among 4311 participants not taking antihypertensive medication at baseline, 11.4%, 61.2%, and 27.4% were recommended antihypertensive medication initiation by neither guideline, the ACC/AHA but not the ACP/AAFP guideline, and both guidelines, respectively. Atherosclerotic cardiovascular disease event rates (95% CI) for these groups were 3.4 (1.6–5.2), 18.0 (16.1–19.8), and 25.3 (21.9–28.6) per 1000 person-years, respectively. Among 7281 participants taking antihypertensive medication at baseline, 57.9% and 42.1% were recommended antihypertensive medication intensification by the ACC/AHA but not the ACP/AAFP guideline and both guidelines, respectively. Atherosclerotic cardiovascular disease event rates (95% CI) for these groups were 18.2 (16.7–19.7) and 33.0 (30.5–35.4) per 1000 person-years, respectively. In conclusion, adults recommended initiation or intensification of antihypertensive medication by the ACC/AHA but not the ACP/AAFP guideline have high atherosclerotic cardiovascular disease risk that may be reduced through treatment initiation or intensification.

ImportanceSparse data exist regarding the contributions of subclinical impairments in cardiovascular and noncardiovascular function to incident heart failure (HF) with reduced ejection fraction (HFrEF) and preserved ejection fraction (HFpEF) among Black US residents, limiting understanding of the etiology of HF subtypes.ObjectivesTo identify subclinical cardiovascular and noncardiovascular risk factors associated with HFrEF and HFpEF in Black US residents.Design, Setting, and ParticipantsThis cohort study used cross-sectional and time-to-event analysis with data from the community-based Jackson Heart Study (JHS), a longitudinal cohort study with baseline data collected from 2000 to 2004 (visit 1) and 10-year follow-up for incident HF. Black US residents from the Jackson, Mississippi, metropolitan area enrolled in JHS; those with prevalent HF, with moderate or greater aortic or mitral valve diseases on visit 1, who died before 2005, and who had missing HF status on follow-up were excluded. The analysis included 4361 participants and was performed between June 2020 to August 2021.ExposuresQuantitative measures of cardiovascular (left ventricular mass index [LVMI], left ventricular ejection fraction [LVEF], left atrial [LA] diameter, and pulse pressure) and noncardiovascular (percent predicted forced expiration volume in 1 second [FEV1 (percent predicted)], estimated glomerular filtration rate (eGFR), waist circumference, and hemoglobin A1c [HbA1c] level) organ function.Main Outcomes and MeasuresIncident HF, HFrEF, and HFpEF over 10-year follow-up.ResultsThe 4361 participants had a mean (SD) age of 54 (13); 2776 (64%) were women; and there were 163 HFpEF and 146 HFrEF events. In multivariable models incorporating measures reflecting each organ system, factors associated with incident HFpEF included greater LA diameter (hazard ratio [HR], 1.23; 95% CI, 1.03-1.47; P = .02), higher pulse pressure (HR, 1.23; 95% CI, 1.05-1.44; P = .009), lower FEV1 (percent predicted) (HR, 1.22; 95% CI, 1.04-1.43; P = .02), lower eGFR (HR, 1.43; 95% CI, 1.19-1.72; P 1c level (HR, 1.25; 95% CI, 1.07-1.45; P = .005), and higher waist circumference (HR, 1.41; 95% CI, 1.18-1.69; P P = .005), lower LVEF (HR, 1.65; 95% CI, 1.42-1.91; P 1 (percent predicted) (HR, 1.19; 95% CI, 1.00-1.42; P = .047), and lower eGFR (HR, 1.27; 95% CI, 1.04-1.55; P = .02).Conclusions and RelevanceIn this community-based cohort study of Black US residents, subclinical impairments in cardiovascular and noncardiovascular organ function were differentially associated with risk of incident HFpEF and HFrEF.

Background Visceral adipose tissue (VAT) is associated with incident heart failure (HF) and HF with preserved ejection fraction, yet it is unknown how pericardial and abdominal adiposity affect HF and mortality risks in Black individuals. We examined the associations of pericardial adipose tissue (PAT), VAT, and subcutaneous adipose tissue (SAT) with incident HF hospitalization and all‐cause mortality in a large community cohort of Black participants. Methods and Results Among the 2882 Jackson Heart Study Exam 2 participants without prevalent HF who underwent body computed tomography, we used Cox proportional hazards models to examine associations between computed tomography–derived regional adiposity and incident HF hospitalization and all‐cause mortality. Fully adjusted models included demographics and cardiovascular disease risk factors. Median follow‐up was 10.6 years among participants with available VAT (n=2844), SAT (n=2843), and PAT (n=1386). Fully adjusted hazard ratios (95% CIs) of distinct computed tomography–derived adiposity measures (PAT per 10 cm 3 , VAT or SAT per 100 cm 3 ) were as follows: for incident HF, PAT 1.08 (95% CI, 1.02–1.14) and VAT 1.04 (95% CI, 1.01–1.08); for HF with preserved ejection fraction, PAT 1.13 (95% CI, 1.04–1.21) and VAT 1.07 (95% CI, 1.01–1.13); for mortality, PAT 1.07 (95% CI, 1.03–1.12) and VAT 1.01 (95% CI, 0.98–1.04). SAT was not associated with either outcome. Conclusions High PAT and VAT, but not SAT, were associated with incident HF and HF with preserved ejection fraction, and only PAT was associated with mortality in the fully adjusted models in a longitudinal community cohort of Black participants. Future studies may help understand whether changes in regional adiposity improves HF, particularly HF with preserved ejection fraction, risk predictions. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT00005485.

High blood pressure (BP) is the leading cause of worldwide cardiovascular disease morbidity and mortality. Patients and clinicians dealing with hypertension have benefited from the evidence of event-based randomized controlled clinical trials. One result from those trials has been the development of evidence-based guidelines. The commitment to using evidence from these event-based randomized trials has been a cornerstone in the development of guideline treatment recommendations. However, in some situations, evidence from event-based trials is not available to guideline writers or clinicians for assistance in treatment decision making. Such is the case for the management of many patients with stage 1 hypertension. The purpose of this scientific statement is to provide information complementary to the 2017 Hypertension Clinical Practice Guidelines for the patient with untreated stage 1 hypertension (systolic BP/diastolic BP, 130–139/80–89 mm Hg) with a 10-year risk for atherosclerotic cardiovascular disease