Carotid Intima–Media Thickness and Improved Stroke Risk Assessment in Hypertensive Black Adults

Abstract

BACKGROUND

We aim to determine the added value of carotid intima–media thickness (cIMT) in stroke risk assessment for hypertensive Black adults.

METHODS

We examined 1,647 participants with hypertension without a history of cardiovascular (CV) disease, from the Jackson Heart Study. Cox regression analysis estimated hazard ratios (HRs) for incident stroke per standard deviation increase in cIMT and quartiles while adjusting for baseline variables. We then evaluated the predictive capacity of cIMT when added to the pool cohort equations (PCEs).

RESULTS

The mean age at baseline was 57 ± 10 years. Each standard deviation increase in cIMT (0.17 mm) was associated with approximately 30% higher risk of stroke (HR 1.27, 95% confidence interval: 1.08–1.49). Notably, cIMT proved valuable in identifying residual stroke risk among participants with well-controlled blood pressure, showing up to a 56% increase in the odds of stroke for each 0.17 mm increase in cIMT among those with systolic blood pressure <120 mm Hg. Additionally, the addition of cIMT to the PCE resulted in the reclassification of 58% of low to borderline risk participants with stroke to a higher-risk category and 28% without stroke to a lower-risk category, leading to a significant net reclassification improvement of 0.22 (0.10–0.30).

CONCLUSIONS

In this community-based cohort of middle-aged Black adults with hypertension and no history of CV disease at baseline, cIMT is significantly associated with incident stroke and enhances stroke risk stratification.

Stroke remains a major healthcare burden and a leading cause of death in the United States, disproportionately affecting Black adults with higher stroke prevalence and mortality rates compared with other racial groups.^1,2 Additionally, Black stroke survivors are more likely to face disability.^3–5 The increased prevalence of stroke in Black adults can be partly attributed to the high occurrence, greater severity, and earlier onset of hypertension, compounded by lower treatment and control rates.^6–9 Despite increased awareness, the incidence of hypertension-induced stroke in Black adults is rising.^10,11 This trend is further exacerbated by limited risk stratification strategies.

Current stroke-specific risk prediction models have shown reduced predictive accuracy in Black adults.¹² A retrospective cohort study involving over 62,000 participants found that all risk algorithms exhibited worse discrimination in Black adults, emphasizing the importance of exploring novel risk assessment tools to address this disparity.¹²

Carotid intima–medial thickness (cIMT) is a marker of vascular injury associated with incident stroke in the general population and Black adults.^13,14 However, the specific role of cIMT in stroke risk prediction among hypertensive Black adults remains uncertain. The pathogenesis of stroke in this population is notably complex, as it entails a multifaceted interplay of cardiovascular (CV) risk factors, genetic predispositions, and socio-determinants of health.^10,15–18 Furthermore, Black adults exhibit an increased prevalence of hypertension-induced small vessel strokes, and this distinct feature emphasizes the potential relevance of cIMT.¹⁹ cIMT measurement directly quantifies vascular damage secondary to hypertension and encapsulates a cumulative reflection of lifetime exposure to the other risk factors highlighted above.²⁰

Therefore, using the Jackson Heart Study (JHS), we explored the added value of cIMT in stroke risk assessment in Black adults with hypertension. First, we determined if there is any association between cIMT and incident stroke and evaluated its potential enhance risk prediction compared with the American College of Cardiology/American Heart Association pooled cohort equations (PCEs).

METHODS

Study population

This retrospective study is reported after the strengthening of the reporting guidelines of observational studies in epidemiology (STROBE).²¹ The JHS is a prospective, community-based observational cohort designed to investigate the origin and natural history of CV disease in Black men and women. Study design, recruitment process, and data collection details have been published.^22,23 Briefly, 5,306 participants aged 35–84 years of age were enrolled from the tri-county area surrounding Jackson, Mississippi (Hinds, Rankin, and Madison). A baseline examination was conducted from 2000 to 2004, with 2 in-person follow-up examinations from 2005 to 2008 and 2009 to 2013. For the present study, we identified participants with available data on cIMT with prevalent hypertension at the baseline examination. Participants with a medical history of other CV diseases, stroke, prior cardiac procedures, carotid angioplasty, and missing data on cIMT were excluded (Supplementary Figure S1 online). The study protocol was approved by the University of Mississippi Medical Center Institutional Review Board, and the participants provided written informed consent.

cIMT assessment

Carotid artery images were obtained using a 7.5 MHz rectangular-array transducer and electrocardiography gated, B-mode, and spectral steered Doppler with an integrated ultrasound machine. A preliminary scan was first performed from the proximal common carotid artery through the bifurcation and distal 1 cm of the internal and external carotid arteries to determine the extent of stenotic regions, the longitudinal interrogation angle needed to identify the flow divider, and orientation of the internal and external carotid arteries. The scan protocol was then conducted in the longitudinal view focusing bilaterally on 3 segments: common carotid artery, bifurcation carotid artery, and internal carotid artery. The 3 segments were imaged from an angle that clearly showed the separation of the internal and external carotid arteries and the tip of the flow divider. Additional images were obtained bilaterally in the anterior, posterior, and lateral angles. Near and far wall boundaries for each segment were also obtained simultaneously. Mean and maximum values were obtained bilaterally for each segment, wall, and angle. Maximum likelihood estimates were calculated by adjusting for missing data in collecting, processing, and reading images according to standardized JHS protocol.²⁴ Maximum likelihood estimates of average right and left common carotid far wall intima–media thickness was used for this analysis.

Ascertainment of incident stroke

Incident stroke in the JHS cohort was ascertained through active and passive surveillance.^25,26 Trained interviewers conducted telephone interviews with the participants or next of kin to determine healthcare events such as diagnostics tests, hospitalizations, or death. Information on hospitalizations and death is transmitted to a medical record abstraction unit that reviews death certificates and hospital records to identify stroke events. A computer-generated diagnosis with review and adjudication by physicians completes the final classification of hospitalized and fatal stroke events. Stroke events were formally ascertained and adjudicated in JHS starting at baseline to 2016.

Clinical covariates

Baseline information was obtained through standardized JHS protocol. Certified technicians measured anthropometric data and vital signs. Blood pressure was measured twice using a random zero sphygmomanometer, and the average was used for analysis. Hypertension status was based on blood pressure ≥140/90 mm Hg or self-reported blood pressure lowering medication use.

Age, sex, medications use, education, and medical history were self-reported. Physical activity was defined according to the American Heart Association categorization as poor health (0 minute of moderate and vigorous activity), intermediate health (>0 minute but <150 minutes of moderate activity, >0 minute but <75 minutes of vigorous activity, or >0 minute but <150 minutes of combined moderate and vigorous activity), and ideal health (≥150 minutes of moderate activity, ≥75 minutes of vigorous activity, or ≥150 minutes of combined moderate and vigorous activity). Body mass index was determined as weight divided by the square of height in meters. Glucose and glycosylated hemoglobin concentrations were measured as previously described. Diabetes mellitus was defined as fasting glucose level ≥126 mg/dl, glycosylated hemoglobin ≥6.5%, or the use of diabetes medications. High-density lipoprotein cholesterol, low-density lipoprotein cholesterol, serum creatinine levels, and high-sensitivity C-reactive protein were assayed using standard techniques.^22–24,27 The estimated glomerular filtration rate was calculated using the Chronic Kidney Disease Epidemiology Collaboration equation.²⁸

Statistical analyses

The baseline characteristics of participants were categorized by 4 cIMT quartiles. Descriptive statistics were reported as frequencies with percentages for categorical variables, while numerical variables were expressed in means with standard deviations. We estimated survival free of stroke by categories of each cIMT quartile using the Kaplan–Meier method, and then we compared those categories using the log-rank test. This analysis was then stratified by sex. Multivariable Cox proportional hazards regression models to examine the associations of cIMT with incident stroke by modeling cIMT as a continuous variable and as quartiles. Proportionality assumption was tested for continuous cIMT and cIMT quartiles with P values of 0.3746 and 0.0586, respectively. In the clinical model (primary model) we adjusted for baseline clinical and demographic variables that were different in bivariate analysis using P < 0.2 as the cutoff. The demographic model (secondary model) adjusted for age, sex, and education status.

The performance of cIMT to PCE was evaluated using time-dependent receiver operative characteristics curve analyses. The discriminative value of the models (cIMT only, PCE only, and cIMT + PCE) was expressed with Harrell’s C-index. In addition, to determine the added value of cIMT to PCE, cross-tabulation of risk categories for the models with and without cIMT was performed for participants with and without ischemic stroke, and the net reclassification improvement was calculated as previously described²⁹ at the current treatment threshold of 7.5%.

A separate mediation analysis that included participants with and without hypertension at baseline using the same methodology described above and SAS CAUSALMED procedure to determine if cIMT mediates the longitudinal association between hypertension and incident stroke.³⁰ SAS 9.4 was used for data management and analysis. P value <0.05 was considered statistically significant.

RESULTS

Baseline characteristics

A total of 1,647 participants with hypertension and cIMT measurements without a history of other CV diseases from the JHS baseline examination were identified. Baseline characteristics per cIMT quartiles (and related length in mm) are presented in Table 1. Participants in the third (0.73–0.84 mm) and fourth (>0.84 mm) quartiles were more likely to be older, male, and had less than high school education. Participants in these groups were also more likely to have diabetes mellitus, higher mean systolic blood pressure (SBP), and low-density lipoprotein cholesterol, while the estimated glomerular filtration rate was lower.

Table 1.

Characteristics at baseline of Black adults with hypertension by carotid intima–media thickness

Carotid intima–media thickness quartiles
Characteristics	Quartile 1 <0.63 mm	Quartile 2 0.63–0.72 mm	Quartile 3 0.73–0.84 mm	Quartile 4 >0.84 mm
Age, mean (SD), y	50.99 (10.4)	56.22 (9.55)	58.19 (9.85)	62.57 (9.17)
Sex, n (%)
Female	322 (78.35)	321 (77.91)	282 (68.45)	238 (57.77)
Male	89 (21.65)	91 (22.09)	130 (31.55)	174 (42.23)
Education, n (%)
Less than high school	35 (8.56)	63 (15.33)	84 (20.49)	103 (25.06)
High school graduate	74 (18.09)	89 (21.65)	103 (25.12)	96 (23.36)
Vocational/traditional school or college	300 (73.35)	259 (63.02)	223 (54.39)	212 (51.58)
AHA physical activity, n (%)
Poor	188 (45.74)	189 (45.87)	213 (51.82)	227 (55.10)
Intermediate	147 (35.77)	142 (34.47)	132 (32.12)	118 (28.64)
Ideal	76 (18.49)	81 (19.66)	66 (16.06)	67 (16.26)
Comorbidities
Alcohol use, %	188 (46.08)	161 (39.08)	173 (42.09)	150 (36.41)
Tobacco use, %	38 (9.29)	32 (7.80)	41 (10.17)	41 (9.95)
Diabetes mellitus, %	91 (22.30)	93 (22.91)	123 (29.85)	144 (35.12)
Body mass index, kg m−2, mean (SD)	33.52 (7.81)	33.46 (7.59)	32.46 (6.52)	32.34 (6.42)
eGFR, mean (SD)	97.41 (19.98)	93.54 (18.17)	91.59 (19.55)	88.62 (17.96)
Systolic blood pressure, mean (SD)	129.19 (16.17)	130.88 (15.67)	132.78 (16.33)	136.4 (17.55)
Diastolic blood pressure, mean (SD)	78.73 (9.02)	77.94 (8.74)	77.47 (9.3)	77.05 (9.31)
Antihypertensive, %	349 (84.91)	363 (88.32)	353 (85.89)	366 (89.05)
Self-reported antihypertensive, %	322 (79.12)	340 (83.33)	328 (80.79)	344 (84.73)
HDL-cholesterol, mg/dl	53	53	53	51
LDL-cholesterol, mg/dl	122	125	128	140
Statin, %	52 (12.68)	60 (14.67)	76 (18.49)	78 (19.02)
hsCRP, mean (SD)	0.58 (0.74)	0.58 (0.74)	0.64 (1.94)	0.49 (0.67)
Incident stroke per 1,000 follow-up years	2.9	5.3	5.8	10.8
Median years to stroke (minimum–maximum)	14.29 (0.88–16.12)	14.07 (0.14–16.19)	14.27 (0.11–16.26)	14.02 (0.05–16.25)

Quartile 1: 0–25th percentile, quartile 2: 26–50th percentile, quartile 3: 51–75th percentile, and quartile 4: 75–99th percentile. Categorical variables are expressed in percentage. Numerical variables are expressed in mean with standard deviation. Abbreviations: AHA, American Heart Association; eGFR, estimate glomerular filtration rate; HDL, high-density lipoprotein; hsCRP, highly sensitive C-reactive protein; LDL, low-density lipoprotein.

Hypertension, cIMT, and incident stroke

During a median (interquartile interval) follow-up of 14.2 (0.05–16.26) years, 138 of 1,647 participants (8.4%) developed incident stroke. Of the participants with stroke, 58 (42%; 58/138) had cIMT in the fourth quartile (>0.84 mm) at baseline. The overall incident stroke rate was 6.13 per 1,000 follow-up years. The incident stroke rates were highest among participants with cIMT in the fourth quartile (>0.84 mm) with 10.81 cases per 1,000 follow-up years and lowest with cIMT in the first quartile (<0.63 mm) with 2.93 cases per 1,000 follow-up years. Incident stroke rates were 5.3 and 5.8 per 1,000 follow-up years among participants with cIMT in the second (0.63–0.72 mm) and third quartiles (0.73–0.84 mm), respectively.

In the Kaplan–Meier survival estimates, survival free of stroke was worse in participants in the cIMT in the fourth quartile (>0.84 mm) compared with the other quartiles (Figure 1). Across all cIMT quartiles, there was no significant difference in survival free estimates of stroke by sex (Supplementary Figure S2 online).

Figure 1.

Primary outcome of stroke. Shown are the Kaplan–Meier estimates of the survival free of stroke per carotid intima–media thickness quartiles over the median 14 years follow-up period of Black adults with hypertension in the Jackson Heart Study cohort. Q1 represents quartile 1: 0–25th percentile (<0.63 mm), quartile 2: 26–50th percentile (0.63–0.72 mm), quartile 3: 51–75th percentile (0.73–0.84 mm), and quartile 4: 75–99th percentile (>0.84 mm).

We compared incident stroke rates by mean SBP and cIMT quartiles and mean diastolic blood pressure (DBP) and cIMT quartiles (Supplementary Table S1 online, Figure 2). The incident rates of stroke steadily increased as the mean SBP and cIMT quartile increased. For example, participants with combined mean SBP (<120 mm Hg) and cIMT (<0.63 mm) in the first quartiles had 0.0 incident rates of stroke per 1,000 follow-up years, compared with 13.55 per 1,000 follow-up years among participants with mean SBP (>143 mm Hg) and cIMT (>0.84 mm) in the fourth quartiles. Also, participants with mean SBP in the first quartile (<120 mm Hg) but cIMT in the fourth quartile (>0.84 mm) had increased incident rates of stroke with 7.32 cases per 1,000 follow-up years. The linear relationship described above was less pronounced with DBP. However, participants with mean DBP (<70 mm Hg) and cIMT (<0.63 mm) in the first quartiles had 2.3 incident rates of stroke per 1,000 follow-up years, compared with 14.02 per 1,000 follow-up years among participants with mean DBP and cIMT in the third quartiles.

Figure 2.

Primary outcome of stroke by blood pressure and carotid intima–media thickness quartiles. Shown are the 14 years cumulative incidence rates of stroke per 1,000 follow-up years by mean systolic blood pressure and carotid intima–media thickness quartiles (top panel) and mean diastolic blood pressure and carotid intima–media thickness quartiles (bottom panel) and associated risk of stroke per standard deviation increase in carotid intima–media thickness quartiles. Q1 represents quartile 1: 0–25th percentile (<0.63 mm), quartile 2: 26–50th percentile (0.63–0.72 mm), quartile 3: 51–75th percentile (0.73–0.84 mm), and quartile 4: 75–99th percentile (>0.84 mm). Abbreviations: aOR, adjusted odds ratio; cIMT, carotid intima–media thickness.

Multivariable adjusted analyses

In multivariable adjusted analysis modeling cIMT as a continuous variable, each standard deviation (0.17 mm) increase in cIMT was associated with a corresponding increase in the risk of stroke (Table 2). The risk of incident stroke increased by 30% in the primary model (hazard ratio [HR] 1.27, 95% confidence interval [CI]: 1.08–1.49) and secondary model (HR 1.30, 95% CI: 1.13–1.50). In the stratified analyses by blood pressure and cIMT quartiles, the association between cIMT and incident stroke remained significant for participants with SBP <120 and >143 mm Hg. Per unit standard deviation increase in cIMT, the odds of incident stroke increased by 56% and 25%, respectively. For DBP between 71 and 83 mm Hg, each unit standard deviation increases in cIMT results in a 25% increase in the odds of stroke (Supplementary Table S1 online and Figure 2).

Table 2.

Association of carotid intima–media thickness with incident stroke among Black adults with hypertension

	aOR (95% CI)	P value	Harrell’s C (95% CI)
Continuous cIMT
Demographic model	1.30 (1.13–1.50)	0.0003	0.69 (0.65–0.73)
Clinical model	1.27 (1.06–1.47)	0.0075	0.75 (0.71–0.81)
cIMT quartiles
Demographic model
Quartile 2 (0.63–0.72 mm)	1.33 (0.73–2.44)	0.3491	–
Quartile 3 (0.73–0.84 mm)	1.25 (0.68–2.29)	0.4647	–
Quartile 4 (>0.84 mm)	1.89 (1.06–3.38)	0.031	–
Clinical model
Quartile 2 (0.63–0.72 mm)	1.62 (0.80–3.27)	0.1763	–
Quartile 3 (0.73–0.84 mm)	1.48 (0.74–2.96)	0.2701	–
Quartile 4 (>0.84 mm)	2.04 (1.02–4.07)	0.0445	–

Adjusted odds for incident stroke per standard deviation increase in carotid intima–media thickness and by carotid intima–media thickness quartiles. Values are expressed in adjusted odds ratio and 95% confidence interval. Clinical model: adjusted for age, sex, educational status, physical activity alcohol use, diabetes mellitus, estimated glomerular filtration rate, high-density lipoprotein and low-density lipoprotein cholesterol, systolic and diastolic blood pressures, and statin use. Demographic model: adjusted for age, sex, and educational status. Abbreviations: aOR, adjusted odds ratio; CI, confidence interval; cIMT, carotid intima–media thickness.

For multivariable adjusted analysis per cIMT quartiles (Table 2), compared with the first quartile of cIMT, cIMT in the fourth quartile and above was associated with more than 2-fold increase in the risk of stroke in the primary model (HR 2.04, 95% CI: 1.02–4.07).

cIMT compared with the American College of Cardiology/American Heart Association PCE

In the time-dependent receiver operative characteristics curve analyses, cIMT was superior to the PCE in predicting incident stroke throughout the follow-up period. The predictive value cIMT was highest during the initial follow-up period compared with the PCE (Supplementary Figure S3 online).

When cIMT was added to the PCE, 32% of the participants were reclassified (Table 3). At a risk threshold of 7.5%, 45 of 101 (45%) events were correctly reclassified to a higher-risk category, and 4 of 101 (4%) events were incorrectly moved to the lower-risk category. For the nonevents, 81 of 1,332 (6%) were correctly moved to a lower-risk category, and 331 of 1,332 (25%) were incorrectly moved to a higher-risk category. As a result, the calculated net reclassification improvement indicated that the added value of cIMT was significant, 0.22 (0.10–0.30).

Table 3.

Net reclassification improvement of Black adults with hypertension

PCE risk threshold	PCE + cIMT risk threshold
	<7.5%	≥7.5%	% Reclassified	Improved classification
Events
<7.5%	44	45	51	+
≥7.5%	4	8	33	−
Nonevents
<7.5%	862	331	28	+
≥7.5%	81	58	58	−

Numbers reclassified according to a 7.5% risk threshold with the addition of carotid intima–media thickness (cIMT) to the pool cohort equations (PCEs). Events represent incident stroke. % Reclassified represents the percentage of participants reclassified with the addition of carotid intima–media thickness to the PCEs in each category. Rows corresponding to an improved classification with the PCE + cIMT model are denoted by a plus sign and a deterioration of the classification by a minus sign. Categorial net reclassification improvement (NRI) was calculated using the percentage of correct movement across categories for those with and without events. NRI = P(up|event) − P(down|event) + P(down|nonevent) − P(up|nonevent).

Mediation analyses

Adjusted for baseline demographics, an estimated 19% of the longitudinal association of hypertension with incident stroke was mediated through increased cIMT (natural indirect effect; Wald 95% CI: 0.00328–0.009013, P < 0.0001) (Supplementary Table S2 and Supplementary Figure S4 online). However, the mediation effects of increased cIMT were attenuated after adding clinical variables, including diabetes mellitus, estimated glomerular filtration rate, body mass index, and high- and low-density lipoprotein.

DISCUSSION

In this study, we investigated the role of cIMT in stroke risk stratification among Black adults with hypertension. Higher baseline cIMT was associated with an increased risk of incident stroke during a median follow-up of 14.2 years. Each 0.17 mm increase in cIMT was linked to approximately 30% higher risk of stroke. Participants in the fourth quartile of cIMT (>0.84 mm) had more than a 2-fold higher risk of stroke compared with those in the first quartile (<0.63 mm). The association between cIMT and stroke risk remained significant regardless of SBP and DBP, such that even among those with controlled blood pressure (SBP <120 mm Hg), each 0.17 mm increase in cIMT was associated with up to a 56% increase in the odds of stroke. Additionally, cIMT outperformed the PCE in predicting stroke risk, and its inclusion in the assessment led to 32% of participants being reclassified, with a significant net reclassification improvement.

Prior research on the association between cIMT and stroke in hypertensive patients has primarily focused on predominantly white populations.^31,32 For instance, a meta-analysis utilizing the USE-IMT data reported an approximately 20% higher risk of stroke per 0.16 mm increase in cIMT.³¹ Similarly, in our study, we also observed a significant increase in stroke risk associated with deviations in cIMT, with the most pronounced effects seen for values greater than 0.84 mm.

Achieving optimal blood pressure control remains crucial for reducing stroke risk in Black adults with hypertension.^33,34 However, recent studies have shown that even with controlled blood pressure, particularly when multiple antihypertensive medications are needed, there may still be an increased risk of stroke.³⁵ Our study yielded similar results, revealing that participants considered at low to intermediate risk due to well-controlled SBP (<120 mm Hg) had higher stroke risk if they had elevated cIMT. This suggests that hypertension treatment may not completely reverse the vascular damage caused by hypertension, and cIMT assessment could be valuable in identifying residual risk among Black adults with well-managed hypertension. These findings also emphasize the significance of primordial prevention (preventing the development of hypertension) and early treatment of hypertension in primary prevention to mitigate vascular damage and reduce the risk of stroke.

As illustrated in this study, cIMT displayed superior predictive performance compared with the PCE in predicting incident stroke among Black adults with hypertension and identified low and borderline risk patients who may benefit from more aggressive therapy. The enhanced predictive ability of cIMT can be attributed, in part, to the prevalence of strokes associated with hypertensive small vessel diseases which would be dominant in this specific cohort.^19,36 As a result, cIMT, primarily reflecting the impact of hypertension on arterial walls, displayed a heightened predictive capacity.³⁷ Moreover, cIMT exhibited modest net reclassification benefits in intermediate-risk hypertensive patients.³¹ There is evidence to suggest that antihypertensive therapies capable of limiting cIMT progression may be linked to a reduced risk of stroke.³⁸

It is essential to emphasize that cIMT is distinct from atherosclerosis and provides limited incremental value when incorporated into conventional risk assessment tools such as Framingham’s risk score for assessing atherosclerotic risk.^13,37,39,40 Additionally, cIMT has a narrow dynamic range (~0.5 to 1.5 mm), making it less appreciated.^41,42 Future research should explore alternative measures, such as vessel wall volume, particularly in individuals without plaque, with modern automated methods.^43–46

Approximately 19% of the association between hypertension and incident stroke was mediated through increased cIMT. However, its impact is somewhat attenuated when considering other clinical factors contributing to the overall risk of incident stroke. This underscores the complex and multifactorial nature of stroke risk in individuals with hypertension. Therefore, the integration of various risk factors, including cIMT, along with clinical variables, holds promise for enhancing risk assessment and aiding in the development of personalized prevention and management strategies to effectively mitigate stroke risk.

Unfortunately, over the past 2 decades, persistent racial and ethnic disparities have existed in stroke risk prevention and burden in the United States. More stroke awareness, improved access to care, a team-based approach, and novel interventions are urgently needed.^47,48

To our knowledge, this is the first study to investigate the relationship between cIMT and incident stroke among Black adults with hypertension. Other main strengths of our study include a long follow-up period and standardized methods for stroke ascertainment and cIMT measurements. Findings from this study must also be interpreted, keeping the following limitations in mind. The study has limited generalizability as it focuses on Black adults. The JHS cohort also recruited participants from a single metropolitan area in the southeastern United States who might have unique social and environmental risk factors. Also, a limited number of stroke events were observed, which could have affected the power of the study.

Among Black adults with hypertension, without another CV disease, cIMT is associated with incident stroke, with participants in the highest cIMT quartile (>0.84 mm) demonstrating a 2-fold higher risk of stroke compared with those in the lowest quartile (<0.63 mm). This association remained significant regardless of blood pressure levels, suggesting that cIMT assessment provides valuable prognostic information beyond traditional blood pressure measurements for stroke risk stratification. Furthermore, adding cIMT to the PCE allowed for identifying low and borderline risk participants who may benefit from statin therapy. These findings highlight the significance of cIMT as a valuable tool in stroke risk assessment for Black adults with hypertension, complementing traditional risk factors and facilitating the development of personalized preventive strategies.

FUNDING

The Jackson Heart Study (JHS) is supported and conducted in collaboration with Jackson State University (HHSN268201800013I), Tougaloo College (HHSN268201800014I), the Mississippi State Department of Health (HHSN268201800015I), and the University of Mississippi Medical Center (HHSN268201800010I, HHSN268201800011I, and HHSN268201800012I) contracts from the National Heart, Lung, and Blood Institute (NHLBI) and the National Institute for Minority Health and Health Disparities (NIMHD). The authors also wish to thank the staffs and participants of the JHS. Dr Benjamin is supported by R01HL092577, 1R01AG066914, and HHSN26818HV00006R.

CONFLICT OF INTEREST

Unrelated to this work, Dr Michos reports advisory boards with AstraZeneca, Amgen, Bayer, Boehringer Ingelheim, Esperion, Novartis, Novo Nordisk, and Pfizer. The remaining authors have nothing to disclose.

DISCLAIMER

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.