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. Author manuscript; available in PMC: 2026 Jun 17.
Published in final edited form as: Am J Hypertens. 2026 Apr 1;39(4):547–553. doi: 10.1093/ajh/hpaf230

Association of Physical Activity with Aortic Stiffness in the Jackson Heart Study

Zakary Patrick 1,*, Elizabeth Heitman 2, Olivia Affuso 3, Benjamin Walker 4, Leroy L Cooper 5, Jennifer C Reneker 4
PMCID: PMC13017752  NIHMSID: NIHMS2140040  PMID: 41273767

Abstract

BACKGROUND:

Vascular aging, often defined in terms of arterial stiffness and impaired arterial hemodynamics, is an important factor associated with hypertension and CVD. Aortic stiffness, a more particular measure of arterial stiffness focusing on central hemodynamics (i.e., the aorta), is an independent predictor of hypertension and CVD risk. Higher levels of physical activity are associated with lower arterial stiffness in various White populations, for peripheral and central measures of stiffness, but further investigations into Black populations are warranted. We examined the association between physical activity and aortic stiffness among participants in the Jackson Heart Study (JHS).

METHODS:

We analyzed data from JHS participants who completed applanation tonometry assessment as part of an ancillary study (2012-2017). 1,226 Black adults (age 59.0 ± 10.0, 60.4% female) were included for analysis. Associations were assessed using multivariable linear regression models, adjusted for age and sex and then further adjusted for other demographic and CVD-related risk factors. Physical activity was measured via self-report, and aortic stiffness was measured by carotid-femoral pulse wave velocity (cfPWV) using applanation tonometry.

RESULTS:

Higher total physical activity was associated with lower cfPWV when controlling for risk factors associated with arterial and aortic stiffness (estimated B=−0.96; 95% CI −1.59 to −0.33). When considering American Heart Association physical activity recommendations (i.e., ideal activity vs not meeting recommendations), this relationship remained.

CONCLUSION:

Higher levels of physical activity were associated with lower levels of aortic stiffness in the Jackson Heart Study.

Keywords: aortic stiffness, arterial stiffness, Black Americans, hypertension, physical activity, blood pressure

Introduction

Cardiovascular disease (CVD) and its associated risk factors are leading contributors to global mortality.1 Hypertension disproportionately affects Black Americans, contributing to higher rates of CVD-related deaths from myocardial infarction, stroke, and end-stage renal disease in this population.2 Vascular aging, often defined in terms of arterial stiffness and impaired arterial hemodynamics, is an important factor associated with hypertension and CVD.3,4 Arterial stiffness, defined as high rigidity of the arterial wall, is associated with CVD later in the lifespan.5 Aortic stiffness is a more particular measure of arterial stiffness focusing on central hemodynamics (i.e., the aorta), and has been suggested to be an independent predictor of hypertension6 and CVD risk in the general population.7 The reference standard for assessment of aortic stiffness is carotid-femoral pulse wave velocity (cfPWV).8 Previous work has demonstrated that Black Americans have higher cfPWV than White Americans across the lifespan.9 The disproportionate hypertension rates among Black Americans may be due to disproportionally higher levels of aortic stiffness.10 Investigations into methods to reduce the risk of CVD and, ultimately, the onset of vascular aging in Black Americans are needed: physical activity and engagement in structured exercise have been of particular interest.

Physical activity has been well established to combat direct risk factors for CVD (i.e., physical inactivity and obesity11,12), warranting its inclusion in the American Heart Association’s (AHA) Life’s Simple 7 (LS7) guidelines for healthy Americans. (Life’s Essential Eight has since replaced the LS7 recommendations, expanding the original guidelines to include sleep. The physical activity recommendations referenced throughout the paper come from Life’s Simple 7). Physical activity, particularly moderate-to-vigorous physical activity, is associated with lower brachial-ankle pulse wave velocity measures in normal weight and overweight populations.13 A recent study of two small cohorts of healthy Black adults (cross-sectional, including a replication cohort) found that higher levels of physical activity were associated with lower levels of aortic stiffness in that sample.10 However, this association may not be generalizable to the broader population of Black Americans, who have the aforementioned high prevalence of hypertension and CVD.14 Further investigations into Black populations, regardless of present CVD risk factors and diagnoses, is warranted.

The comprehensive benefits of physical activity on arterial/aortic stiffness among Black Americans is understudied. Previous literature has reported that higher levels of physical activity were associated with improved arterial stiffness in various non-Black cohorts15,16 for peripheral and central measures of stiffness, respectively. Previous work in the Jackson Heart Study (JHS) has highlighted the significant associations of cfPWV and various CVD risk factors.17 Recent research highlighted the importance of domain-specific physical activity for CVD and other risk factors in the JHS cohort: greater engagement in physical activity, particularly moderate-to-vigorous physical activity, was associated with a lower risk of incident hypertension.18 The potential association of aortic stiffness with physical activity, a modifiable behavioral risk factor of CVD, has not been well elucidated in a predominantly Black cohort. Thus, emphasizing the importance of investigating the potential association of aortic stiffness with physical activity in the JHS. Additionally, subclinical microvascular measures are worthy of inclusion into such investigations, as their respective dysfunction is prevalent among the population of interest with CVD and has been associated with elevated aortic stiffness.14 Central pulse pressure is a distinct measure of stiffness separate from other peripheral measures; forward wave amplitude is a composite measure of proximal aortic stiffness and aortic flow, and characteristic impedance is a measure sensitive to changes in aortic cross-sectional area.19 It also remains unclear whether these measures may be sensitive, in a cross-sectional investigation, to associations with physical activity engagement.

Thus, we sought to evaluate the association between physical activity and aortic stiffness in this large, all Black American cohort. We hypothesized that higher levels of physical activity would be associated with lower aortic stiffness and subclinical central pressure pulsatility measures in this sample of Black Americans.

Methods

Our study followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guidelines.20 The procedure for requesting data from the JHS can be found at https://www.jacksonheartstudy.org/.

Study Design and Participants.

The JHS is a longitudinal investigation of genetic and environmental risk factors associated with the high burden of CVD among Black Americans in the Jackson, Mississippi metropolitan area. Details about the study design, recruitment approach, and methodology for the JHS have been reported elsewhere.21

We obtained de-identified data from the Jackson Heart Study under a data use agreement and approval from the study’s Publications and Presentations committee. We analyzed data from JHS Examination 3 participants who completed applanation tonometry assessment as part of a JHS ancillary study (2012-2017). Participants who had previously completed JHS Exam 3 (2009-2013) were invited to participate in the ancillary study. Participants included in the current analysis had complete data on the independent variable (physical activity), dependent variables (measures of aortic stiffness and pressure pulsatility), and all selected theory-driven covariables. The dependent variables, heart rate, and mean arterial pressure were assessed as part of the ancillary study, and all other variables were assessed previously at JHS Exam 3. The selection of participants and exclusion criteria are illustrated in Figure 1.

Figure 1.

Figure 1.

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Flow chart for determination of analytic sample.

Physical Activity Measures.

Physical activity was assessed via the JHS Physical Activity survey, a 30-item questionnaire including 4 domains: active living habits, work, home life, and sport/exercise activities. Response options range from 1 to 5 (reflecting frequency or length of time estimations, depending on the context of the question): 1 = “never” to 5 = “always” for frequency questions; for minute estimations, 1 = “less than 5 minutes” to 5 = “at least 45 minutes”. Items within each domain are summed and then divided by the number of domain items to generate a score ranging from 1 to 5, with lower scores representing lower physical activity. The total physical activity score ranges from 0 to 16 (i.e., a summation of scores across the four 1-5 scale domains and then shifted to a 0-16 scale). As a measure for self-reported physical activity, this survey has been externally validated and has been shown to be highly reliable as an instrument for assessment using accelerometry data.22 More information regarding the described indices can be found elsewhere.18

In addition to the total physical activity score variable, physical activity was assessed via the AHA physical activity guidelines’ classification, where ‘low’ constitutes 0 minutes/week of physical activity, ‘intermediate/moderate’ represents moderate-to-vigorous physical activity less than 150 minutes/week, and ‘ideal’ is greater than 150 moderate-to-vigorous physical activity minutes/week (minutes of physical activity engagement were calculated based on the top three activities participants engaged in and were assigned a time of engagement / intensity based on categorization of the respective activities).

Aortic Stiffness and Pressure Pulsatility Measures.

Aortic stiffness and pressure pulsatility were assessed via arterial tonometry with Doppler ultrasound and subsequent wave separation analysis as previously described.23 We included four measures in these analyses: cfPWV, central pulse pressure (pressure pulsatility), forward wave amplitude, and characteristic impedance. These reflect distinct but related central measures for aortic stiffness. Central pulse pressure is defined as the difference between the carotid systolic and diastolic blood pressures. Forward pressure wave amplitude is defined as the difference between pressure at the foot and at the peak of the forward pressure waveform. Characteristic impedance is thought to be associated with age-related aortic stiffening. Data was obtained via arterial tonometry, using a custom tonometer, with simultaneous electrocardiography from brachial, radial, femoral, and carotid arteries. Auscultatory brachial systolic and diastolic blood pressures were obtained from the right arm using a computer-controlled device at the time of tonometry. cfPWV was calculated as the ratio of the adjusted transit distance and the pulse transit time difference between carotid and femoral sites. Further explanations of data acquisition procedures have been previously described.19

Clinical Evaluation of Covariates.

Prevalent CVD was defined as a history of myocardial infarction, coronary heart disease, heart failure, or stroke. We calculated the cholesterol ratio as the ratio of total to high-density lipoprotein cholesterol from a fasting blood test. We defined the presence of diabetes as fasting serum glucose ≥126 mg/dL, use of diabetes medications within 2 weeks of the clinic visit, or prior physician-diagnosed diabetes. Height (meters) and weight (kilograms) were assessed during the examination, and we calculated body mass index as the ratio of body weight and the square of height. Age, sex, hypertension status (defined as blood pressure ≧ 140/90 mmHg (per JNC 7) or use of blood pressure lowering medication) were assessed via a questionnaire. Heart rate (beats per minute) and mean arterial pressure (mmHg) were assessed during tonometry.

Statistical Analysis.

Sample characteristics for the included sample were tabulated. For the primary analysis, we assessed the association between measures of physical activity (continuous total physical activity score and categorical AHA physical activity category) and measures of aortic stiffness and pressure pulsatility (cfPWV, central pulse pressure, forward wave amplitude, and characteristic impedance). We inverted cfPWV to limit heteroscedasticity then multiplied it by −1000 to convert units to ms/m and rectify directionality of associations with aortic stiffness. To account for non-constant error variance (heteroskedasticity), heteroskedasticity-consistent (Huber–White sandwich) standard errors were used in all multivariable ordinary least squares (OLS) linear regression models (models adhered to other regression assumptions). We assessed associations using simple (unadjusted) and multivariable linear regression models, minimally adjusted for age and sex and then further adjusted for age, sex, body mass index, heart rate, cholesterol ratio, diabetes, hypertension, mean arterial pressure, and self-reported CVD in expanded models. For significant associations between continuous physical activity and hemodynamic variables, we generated scatterplots with a fitted regression curves to help visualize correlations. For the follow up analyses investigating AHA physical activity categorization, estimated marginal means were calculated and represented (i.e., as bar graphs) for each physical activity category across the central hemodynamic variables.

All analyses were performed with R-Studio (v 4.3) using the lm_robust and emmeans packages. Two-tailed P<0.05 was considered significant.

Results

The final number of eligible participants included for analysis was 1,226. Participants’ reported demographic characteristics, physical activity behavior, and hemodynamic variables are shown in Table 1, with these data stratified by physical activity category in Table 2. The participants were older, more likely to be female, more likely to report a current hypertension diagnosis, and overwhelmingly did not meet AHA physical activity recommendations.

Table 1.

Demographic, Behavioral, and Central Hemodynamic Characteristics of eligible participants from JHS Exam 3 (2009-2013).

Variable Value*
Age, years 59.0±10.0
Female, N (%) 740 (60.4)
BMI, kg/m2 31.1±6.1
MAP, mm Hg 99.3±11.6
Medical history
 Prevalent CVD, N (%) 55 (4.5)
 Prevalent diabetes, N (%) 311 (25.4)
 Prevalent hypertension, N (%) 857 (69.9)
Ratio of total to HDL cholesterol, unitless 3.6±1.1
Jackson Heart Study physical activity questionnaire
Total physical activity score 6.2±2.3
AHA physical activity category, N (%)
 Low 438 (35.7)
 Moderate 419 (34.2)
 Ideal 369 (30.1)
Carotid-femoral pulse wave velocity, m/s 10.4±3.8
Negative inverse carotid-femoral pulse wave velocity, ms/m −106.6±31.1
Central pulse pressure, mm Hg 62.9±18.9
Characteristic impedance, dyne·s/cm5 253.5±99.5
Forward wave amplitude, mm Hg 51.0±14.5
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BMI, Body mass index; MAP, Mean arterial pressure; CVD, cardiovascular disease; HDL, high-density lipoprotein; AHA, American Heart Association.

*

All values are mean±standard deviation or number, N (%)

Table 2.

Demographic, Behavioral, and Central Hemodynamic Characteristics of eligible participants stratified by physical activity categorization.

Variable AHA Physical Activity Category
Low Moderate Ideal
Age, years 60.7±10.2 58.0±9.8 58.2±9.9
Female, N (%) 244 (51.1) 290 (69.2) 206 (55.8)
BMI, kg/m2 31.8±6.9 31.2±6.0 30.1±9.9
MAP, mm Hg 100.0±12.3 99.2±11.4 98.6±11.1
Medical history
 Prevalent CVD, N (%) 31 (7.1) 17 (4.1) 7 (1.9)
 Prevalent diabetes, N (%) 126 (28.8) 97 (23.2) 88 (23.8)
 Prevalent hypertension, N (%) 329 (75.1) 293 (69.9) 235 (63.7)
Ratio of total to HDL cholesterol, unitless 3.7±1.1 3.6±1.1 3.5±1.0
Carotid-femoral pulse wave velocity, m/s 11.1±4.2 10.0±3.5 9.9±3.6
Negative inverse carotid-femoral pulse wave velocity, ms/m −100.5±30.4 −109.8±31.2 −110.4±30.7
Central pulse pressure, mm Hg 64.4±19.8 63.4±19.1 60.8±17.3
Characteristic impedance, dyne·s/cm5 258.3±102.0 256.1±101.3 245.0±94.1
Forward wave amplitude, mm Hg 52.2±15.2 50.8±14.5 49.8±13.5
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BMI, Body mass index; MAP, Mean arterial pressure; CVD, cardiovascular disease; HDL, high-density lipoprotein; AHA, American Heart Association.

*

All values are mean±standard deviation or number, N (%)

Negative Inverse cfPWV and Physical Activity.

Higher total physical activity score was associated with less aortic stiffness as assessed by negative inverse cfPWV (estimated B = −2.38; 95% CI: −3.16 to −0.1.60; p < 0.01; R2 = 0.03) and in the model adjusted for age and sex (B = −1.33; 95% CI: −2,00, −0.65; p < 0.01; R2 = 0.27) (Table 3). Importantly, when controlling for risk factors associated with arterial and aortic stiffness, such as hypertension and mean arterial pressure, the significant inverse association between physical activity and negative inverse cfPWV remained (B = −0.96; 95% CI: −1.59 to −0.33; p < 0.01; R2 = 0.41) (Figure 2). Total physical activity score was not associated with central pulse pressure, characteristic impedance, or forward wave amplitude in expanded models.

Table 3.

Central Hemodynamic Variables and Total Physical Activity Score.

Hemodynamic variables Unadjusted
Est. B (95% CI)
p value, R2 		Age-sex adjusted
Est. B (95% CI)
p value, R2 		Expanded
Est. B (95% CI)
p value, R2
Aortic Stiffness* −2.38 (−3.16, −1.60)
p < 0.01
R2 = 0.03		 −1.33 (−2.00, −0.65)
p < 0.01
R2 = 0.27		 −0.96 (−1.59, −0.33)
p < 0.01
R2 = 0.40
Central pulse pressure −0.57 (−1.05, −0.09)
p = 0.02
R2 < 0.01		 −0.05 (−0.52, 0.41)
p = 0.82
R2 = 0.15		 −0.16 (−0.53, 0.22)
p = 0.41
R2 = 0.45
Forward wave amplitude −0.50 (−0.86, −0.13)
p < 0.01
R2 < 0.01		 −0.14 (−0.49, 0.21)
p = 0.44
R2 = 0.14		 −0.09 (−0.40, 0.23)
p = 0.59
R2 = 0.34
Characteristic Impedance −2.95 (−5.37, −0.52)
p = 0.02
R2 < 0.01		 −0.5 (−2.81, 1.80)
p = 0.67
R2 = 0.12		 −0.10 (−2.35, 2.16)
p = 0.93
R2 = 0.21
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Notes: Minimally adjusted models control for age and sex. Multivariable adjusted models additionally control for BMI, cholesterol ratio, diabetes, hypertension, mean arterial pressure, cardiovascular disease history, and heart rate.

*

Negative Inverse cfPWV

Figure 2.

Figure 2.

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Scatterplot depicting the association of physical activity score and negative inverse carotid-femoral pulse wave velocity. The curve represents a locally estimated scatterplot smoothing (LOESS) line, and the shaded gray area indicates the 95% confidence interval for the fitted values.

Negative Inverse cfPWV and Physical Activity Category.

Regarding the utilization of the physical activity categorization based on AHA recommendations, participants with poor physical activity levels had lower negative inverse cfPWV compared to those with ideal activity levels (B = −1.87; 95% CI: −3.53 to −0.20; p = 0.03; R2 = 0.41). These results suggest that meeting AHA guidelines is associated with less aortic stiffness.

Discussion

We assessed associations of physical activity with measures of aortic stiffness and pressure pulsatility measures with measures of physical activity in a large cohort of Black Americans in the Jackson Heart Study. Our results suggest that higher levels of physical activity are associated with lower aortic stiffness, as measured by cfPWV, independent of traditional CVD risk factors. Importantly, we observed this association for both physical activity variables: the total physical activity score as calculated from the four indices of the JHS physical activity survey, as well as a physical activity category determination based on AHA guidelines. These results, and strength of association, are in line with previous investigations into physical activity and aortic stiffness.13,16

The primary finding reported in this cross-sectional analysis aligns with previous work investigating this relationship in Black adults;10 more particularly, this work broadens the scope of research investigating the associations between subclinical vascular measures and physical activity in a Black population. Our work expands on the previous investigation into physical activity and aortic stiffness in Black adults, such that we observed a significant association between reported total physical activity levels and aortic stiffness, measured by cfPWV.10 The primary outcome expands upon the previous understanding of this association in a disproportionately burdened population by including participants who, at the time of Exam 3, had current CVD diagnoses and associated risk factors.10,14 Furthermore, regarding the classification of engagement in physical activity based on AHA recommendations, we also observed a similar association with aortic stiffness: individuals who were classified as intermediate and ideal had lower aortic stiffness compared to those who were classified in the poor physical activity category.

It is well-established that physical activity has acute and long-lasting health benefits, both physically24,25 and cognitively.26,27 However, adherence to physical activity recommendations from major organizations like the American Heart Association and American College of Sports Medicine remains inadequate for most of the U.S. population. The significant inverse association found in this analysis underscores the importance of maintaining appropriate levels of physical activity, yet only ~30% of the reported sample met the ideal recommendation for physical activity. Chronic physical activity engagement is suggestive of attenuating the arterial stiffening that occurs with aging, potentially through mechanisms of maintaining and supporting microvascular endothelial function.28 Previous work has also linked physical activity with improved endothelial function and nitric oxide bioavailability, 29 enhanced baroreflex and lower sympathetic tone,30 reduced collagen cross linking mechanisms and fibrosis,31 and enhanced insulin signaling and reduced oxidative stress.32 Notably, when using this negative inverse of cfPWV, and when back-transformed, the observed effect herein corresponds to roughly a 1 m/s lower cfPWV in the more active participants. This magnitude, while modest, is within the range considered clinically meaningful in prior work.33 Thus, we believe our findings underscore the importance of promoting and maintaining appropriate levels of physical activity across the lifespan. As continued research further elucidates the benefits of physical activity, these important research questions related to central arterial health can inform healthcare policy and equip professionals who care for burdened populations. As higher cfPWV predicts incident hypertension, adequate physical activity may prevent hypertension via lower aortic stiffness, ultimately preventing CVD risk.34

We did not observe a similar inverse association with physical activity and the other subclinical vascular measures (i.e., forward wave amplitude, central pulse pressure, and characteristic impedance) we examined. It is important to note that, although the unadjusted models for each of these measures did demonstrate a similar inverse association, this association did not persist with the inclusion of the theory-driven covariates. A recent systematic review demonstrated that some of the benefits of physical activity and CVD events may be mediated by an inverse association between physical activity and subclinical CVD measures.35 Though we did not observe any partial associations across the models utilized herein, future work should still seek to investigate the associations between physical activity and subclinical microvascular measures, especially in Black populations.

Beyond the benefits of exercise for aortic and arterial stiffness and delaying or preventing the onset of CVD risk factors like obesity and hypertension, emerging research has explored the association of arterial stiffness and cognitive functioning. Most notably, higher levels of pulse wave velocity may be associated with cognitive decline in older adults.36 As the main conduits for blood flow to the brain, stiffening of the arteries may lead to downstream inefficiency of cerebral circulation and changes in cognition. Thus, stiffening has been associated with increased risk of dementia.37 Greater understanding of the relation between modifiable behavioral risk factors, such as physical inactivity, and aortic stiffness emphasizes the importance of practical strategies in mitigating dementia and other cognitive impairments later in the lifespan. Thus, future investigations into this population, and relationship, are warranted.

Overall, it remains paramount that future work continues to investigate disproportionate health disparities experienced by Black Americans. Especially with a great number of studies reporting higher rates of hypertension, CVD risk factors, and—pertinent to this paper—central arterial stiffness among Black adults,9,10,14 the mechanisms that cause these health disparities should remain critical for such investigations. Previous reporting in the literature has demonstrated that neighborhood characteristics, such as social cohesion, are associated with aortic stiffness in Black adults;38 moreover, socioeconomic status has also been reported to be associated with racial disparities in health.39 Future research within the Jackson Heart Study may help elucidate these issues further.

This study’s results have specific limitations. The reported findings come from cross-sectional data and causal relations cannot be inferred. Furthermore, the dependent variables were collected separately as part of an ancillary study (i.e., all outcome variables were assessed at a clinical callback visit that occurred during the Exam 3 cycle), while the covariates and exposure assessments were collected as part of the JHS Exam 3. Thus, these measurements did not completely align temporally. The physical activity variables used as the exposure variable in all statistical models were taken from self-reported measures. Although these measures have been validated and determined to be reliable, they may be subject to recall and social desirability bias, which can limit the strength of the findings. Furthermore, although we included expanded models with moderate R2 values, not all variables could be accounted for within the available data (i.e., appropriate data on smoking status and specific antihypertension medications, which might account for some additional unexplained variance within the utilized models, were not available for analysis). Nonetheless, this study contains various strengths that deserve to be acknowledged. As the largest longitudinal, observational study of CVD risk among Black Americans in the United States,19 the JHS offered an unparalleled opportunity to examine the association of central hemodynamic measures and physical activity in a U.S. Black cohort with cardiovascular risk factors. The current sample is over 3 times larger than the previously largest investigation; moreover, the present sample included participants who had known CVD and CVD-associated risk factors, which was a novel inclusion when evaluating this association. Thus, the current paper further expands upon the current understanding of subclinical vascular measures and physical activity and warrants further work within the population of Black Americans.

Conclusion

The results presented here demonstrated an inverse association between physical activity and aortic stiffness, with this association persisting when considering appropriate physical activity recommendations / categorizations. Future work in this area should include longitudinal investigations into the association between aortic stiffness and physical activity in this population, and, additionally, investigate the effects of acute exercise interventions (i.e., short term training studies) in lowering/mitigating vascular aging, respectively.

Acknowledgements

This manuscript has been reviewed by JHS for scientific content.

The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services.

Funding

The Jackson Heart Study is supported by Contracts HHSN268201800010I, HHSN268201800011I, HHSN268201800012I, HHSN268201800013I, HHSN268201800014I, HHSN268201800015I from the National Heart, Lung, and Blood Institute (NHLBI) with additional support from the National Institute on Minority Health and Health Disparities (NIMHD).

Footnotes

Conflict of interest: None

Conflicts of Interest

None declared.

Data Availability Statement

Jackson Heart Study data may be requested from the Biologic Specimen and Data Repository Information Coordinating Center (BioLINCC) repository and the database of Genotypes and Phenotypes (dbGaP). Additionally, investigators with a manuscript proposal or ancillary study proposal that has been approved by study committees may request data directly from the Jackson Heart Study Coordinating Center.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

Jackson Heart Study data may be requested from the Biologic Specimen and Data Repository Information Coordinating Center (BioLINCC) repository and the database of Genotypes and Phenotypes (dbGaP). Additionally, investigators with a manuscript proposal or ancillary study proposal that has been approved by study committees may request data directly from the Jackson Heart Study Coordinating Center.

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