Abstract
We calculated the prevalence of white coat hypertension (WCH) using out‐of‐clinic blood pressure (BP) in the daytime period; daytime and 24‐hour periods; and daytime, 24‐hour, and nighttime periods among 199 African Americans with clinic‐measured systolic/diastolic BP ≥140/90 mm Hg in the Jackson Heart Study. Left ventricular mass index (LVMI) was measured among participants with WCH and 374 participants with sustained normotension (ie, non‐hypertensive clinic, daytime, 24‐hour, and nighttime BP). The prevalence of WCH was 29.6%, 21.1%, and 10.6% using daytime BP; daytime and 24‐hour BP; and daytime, 24‐hour, and nighttime BP, respectively. Compared with sustained normotension, LVMI was higher when WCH was defined using daytime BP (adjusted mean difference [95% CI] 5.0 [−0.2, 10.1] g/m2), but not when defined using daytime and 24‐hour BP or daytime, 24‐hour, and nighttime BP (adjusted mean difference [95% CI] 3.9 [−1.9, 9.7] and 0.4 [−7.3,8.2] g/m2, respectively). Using only daytime BP overestimates the prevalence of WCH among African Americans.
Keywords: ambulatory blood pressure/home blood pressure monitor, clinical management of high blood pressure (HBP), hypertension in African Americans, hypertension—general, risk assessment
1. INTRODUCTION
White coat hypertension is defined by blood pressure (BP) in the hypertensive range when measured in a clinic setting, but not when measured out‐of‐clinic.1 Controversy persists regarding whether there is increased cardiovascular disease (CVD) risk associated with white coat hypertension compared with non‐hypertensive BP in and out‐of‐clinic.2, 3 Many guidelines and scientific statements recommend obtaining out‐of‐clinic BP measurements to rule out the presence of white coat hypertension before initiating antihypertensive medication.4, 5, 6 Several of these recommendations suggest using the mean of BP measurements during the daytime period or the entire 24‐hour ambulatory BP monitoring (ABPM) period to define non‐hypertensive out‐of‐clinic BP.5, 6 In addition to the daytime and 24‐hour periods, the 2013 European Society of Hypertension recommends using the mean BP during the nighttime period to rule out the presence of white coat hypertension.4 Nighttime hypertension is a well‐established risk factor for cardiovascular events, independent of daytime and clinic BP.7, 8
Prior studies in European and Asian cohorts have found that the prevalence of white coat hypertension is substantially lower when requiring BP to be in the normotensive range during all 3 periods (daytime, 24‐hour, and nighttime periods) compared with requiring BP to be in the normotensive range only during the daytime or 24‐hour periods.9, 10 The prevalence of nighttime hypertension is high among African Americans.7 For example, in the Jackson Heart Study (JHS), a community‐based cohort of African Americans, the prevalence of nighttime hypertension was 49% and 62% for participants not taking and taking antihypertensive medication, respectively.11
Furthermore, in the same cohort, 19.1% of African Americans without daytime hypertension and not taking antihypertensive medication, had nighttime hypertension.7 Therefore, if only daytime or 24‐hour BP are used to define normotensive out‐of‐clinic BP, many African Americans may be considered to have white coat hypertension despite having nighttime hypertension.
In this analysis, we calculated the prevalence of white coat hypertension among African Americans using 3 separate periods for evaluating out‐of‐clinic BP: (1) daytime; (2) daytime and 24‐hour; and (3) daytime, 24‐hour, and nighttime. Also, we compared left ventricular mass index (LVMI), a marker of cardiovascular end‐organ damage, for participants meeting each of these white coat hypertension definitions vs their counterparts having sustained normotension (ie, non‐hypertensive clinic, daytime, 24‐hour, and nighttime BP).
2. METHODS
2.1. Study population
The Jackson Heart Study (JHS) is a community‐based prospective cohort study designed to evaluate cardiovascular disease (CVD) risk among African Americans.12 The JHS enrolled 5306 non‐institutionalized African Americans, aged ≥20 years, between 2000 and 2004 from Jackson, Mississippi.12 The current analysis was restricted to 1015 JHS participants with echocardiography data who underwent ABPM, and had a complete ABPM recording (defined below). The analysis was further restricted to 199 participants with clinic‐measured systolic BP (SBP) ≥140 mm Hg or diastolic BP (DBP) ≥90 mm Hg and 374 participants with sustained normotension as defined below. The institutional review boards governing research in human subjects approved the JHS protocol and all participants provided written informed consent.
2.2. Data collection
At baseline, participants completed an in‐home interview and a clinic visit.13 During the baseline in‐home interview, trained staff administered questionnaires to collect self‐reported information on demographics, health behaviors (eg, alcohol use and current smoking), and previously diagnosed conditions, including diabetes and a history of CVD. Alcohol use was categorized as none, moderate (1 to 7 drinks per week for women and 1 to 14 drinks per week for men), or heavy (≥8 drinks per week for women or ≥15 drinks per week for men). Current smoking was defined by affirmative responses to the questions “Have you smoked more than 400 cigarettes in your lifetime?” and “Do you now smoke cigarettes?” During the clinic visit, blood pressure measurements, blood and urine collection, and a 2D echocardiogram were performed. Diabetes was defined by defined as a fasting (≥8 hours) serum glucose ≥126 mg/dL or hemoglobin A1c ≥6.5% or self‐reported use of insulin or oral hypoglycemic medications within 2 weeks prior to the study visit. A history of CVD was defined as a self‐reported prior stroke or myocardial infarction. Estimated glomerular filtration rate (eGFR) was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD‐EPI) equation.14 Albuminuria was defined as urinary albumin‐to‐creatinine ratio >30 mg/g. Antihypertensive medication use was defined by self‐report.
2.3. Echocardiography
Certified technicians, using standardized protocols, performed 2D transthoracic echocardiograms (Sonos‐4500, Philips Medical Systems).15 Echocardiograms were reviewed for clinical interpretation and analytical measurements by experienced cardiologists.15 Left ventricular mass (LVM), LVMI, and left ventricular hypertrophy (LVH) were derived according to the 2015 American Society of Echocardiography (ASE) recommendations.16 LVMI was calculated as LVM/body surface area. LVH was defined as increased LVMI ≥96 g/m2 in females and ≥116 g/m2 in males.16
2.4. BP measurement and categories
Clinic BP was measured following a standardized protocol. Participants were asked to avoid caffeine, eating, heavy physical activity, smoking, and alcohol intake for 12 hours prior to their clinic visit. Two BP measurements were obtained using an appropriately sized cuff, determined from an arm circumference measurement, and a random‐zero sphygmomanometer (Hawksley and Sons Ltd.).13, 17 Participants sat for at least 5 minutes in an upright position with their back and arms supported, feet flat on the floor, and legs uncrossed, after which trained staff conducted the two BP measurements in the right arm, separated by 1 minute. As previously described, the random‐zero BP measurements were calibrated to an oscillometric device using robust regression.18
Participants were fitted with an ABPM device (Spacelabs 90207) on their non‐dominant arm following the baseline clinic visit and ambulatory BP was recorded every 20 minutes. Data were processed and evaluated for quality with Medifacts International's Medicom software. Participants were considered to have a complete ABPM recording if they met the International Database of Ambulatory Blood Pressure Monitoring and Cardiovascular Outcomes (IDACO) criteria: ≥10 daytime (10:00 am to 8:00 pm) and ≥5 nighttime (midnight to 6:00 am) SBP and DBP measurements.19 Mean daytime and nighttime SBP and DBP were calculated by averaging the readings obtained between 10:00 am and 8:00 pm and between midnight and 6:00 am, respectively. Twenty‐four‐hour BP was defined using the average of all available readings obtained during the ABPM period.
Among participants with clinic BP ≥140/90 mm Hg, white coat hypertension was defined using 3 separate definitions: (1) daytime BP < 135/85 mm Hg; (2) daytime BP < 135/85 mm Hg and 24‐hour BP < 130/80 mm Hg; or (3) daytime BP < 135/85 mm Hg, 24‐hour BP < 130/80 mm Hg and nighttime BP < 120/70 mm Hg. Sustained normotension was defined as clinic BP < 140/90 mm Hg, awake BP < 135/85 mm Hg, 24‐hour BP < 130/80 mm Hg, and nighttime BP < 120/70 mm Hg.
2.5. Statistical methods
We calculated the prevalence of white coat hypertension defined using out‐of‐clinic BP in the (1) daytime; (2) daytime and 24‐hour; and (3) daytime, 24‐hour, and nighttime periods among participants with clinic‐measured SBP ≥140 mm Hg or DBP ≥90 mm Hg. Participant characteristics were calculated for participants with sustained normotension and with each of the 3 definitions of white coat hypertension. The statistical significance of differences in characteristics between participants meeting each definition of white coat hypertension, separately, vs their counterparts with sustained normotension were calculated using t‐tests and chi‐square tests, as appropriate. Mean LVMI was calculated for participants meeting each of the white coat hypertension definitions and with sustained normotension. Differences in LVMI between participants with white coat hypertension, using each definition separately, and with sustained normotension were calculated using unadjusted and 3 multivariable‐adjusted linear regression models. Model 1 included adjustment for age and sex. Model 2 included adjustments for age, sex, diabetes, alcohol use, smoking status, eGFR < 60 mL/min/1.73 m2, and history of CVD. Model 3 included the variables in Model 2 and antihypertensive medication use. Statistical significance was defined by a two‐sided P‐value <.05. Multiple imputation using chained equations and 20 data sets was performed to account for missing data (n = 28). Analyses were conducted in STATA 13 (Stata Corp.).
3. RESULTS
Among participants with clinic SBP ≥140 mm Hg or DBP ≥90 mm Hg (n = 199), 59 (29.6%), 42 (21.1%), and 21 (10.6%) were categorized as having white coat hypertension when non‐hypertensive out‐of‐clinic BP was defined using the (1) daytime; (2) daytime and 24‐hour; and (3) daytime, 24‐hour, and nighttime periods, respectively (Figure 1). Of the 42 participants categorized as having white coat hypertension when non‐hypertensive out‐of‐clinic BP was defined using the daytime and 24‐hour periods, 21 (50%) had nighttime hypertension. Compared to participants with sustained normotension (n = 374), those with white coat hypertension by each definition were older and more likely to be taking antihypertensive medication (Table 1). Participants with white coat hypertension defined using only daytime BP had a higher prevalence of albuminuria compared to those with sustained normotension. The prevalence of albuminuria was not statistically significantly different between participants with white coat hypertension defined using daytime BP and 24‐hour BP or daytime BP, 24‐hour BP and nighttime BP compared to their counterparts with sustained normotension.
Figure 1.
Prevalence of white coat hypertension when out‐of‐clinic blood pressure was defined using the daytime; the daytime and 24‐h; and the daytime, 24‐h, and nighttime periods, separately. ABPM, Ambulatory blood pressure monitoring
Table 1.
Characteristics of the Jackson Heart Study participants with sustained normotension and 3 definitions of white coat hypertension
| Characteristics | Sustained normotension (n = 374) | White coat hypertension definition | P‐value* | P‐value** | P‐value*** | ||
|---|---|---|---|---|---|---|---|
| Daytime ABPM (n = 59) | Daytime and 24‐h ABPM (n = 42) | Daytime, 24‐h, and nighttime ABPM (n = 21) | |||||
| Age, years | 56.5 (11.3) | 63.0 (8.8) | 62.8 (9.7) | 63.0 (8.7) | <.001 | .001 | .009 |
| Female, n (%) | 83 (22.2) | 16 (27.1) | 12 (28.6) | 6 (28.6) | .40 | .35 | .50 |
| Clinical characteristics | |||||||
| History of CVD, n (%) | 30 (8.0) | 6 (10.2) | 3 (7.1) | 2 (9.5) | .58 | .84 | .81 |
| Diabetes, n (%) | 62 (16.7) | 13 (22.8) | 7 (17.1) | 2 (9.5) | .26 | .95 | .39 |
| eGFR <60 mL/min/1.73 m2, n (%) | 19 (5.1) | 5 (8.8) | 5 (12.2) | 2 (9.5) | .27 | .07 | .39 |
| Left ventricular hypertrophy, n (%) | 26 (7.0) | 6 (10.2) | 4 (9.5) | 1 (4.8) | .38 | .54 | .70 |
| Albuminuria, n (%) | 15 (5.1) | 7 (13.5) | 3 (8.3) | 1 (5.3) | .02 | .41 | .97 |
| Health behaviors | |||||||
| Current smoking, n (%) | 28 (7.5) | 3 (5.2) | 2 (4.9) | 1 (5.0) | .53 | .54 | .68 |
| Alcohol use, n (%) | |||||||
| Non‐drinker | 208 (57.0) | 42 (72.4) | 29 (70.7) | 13 (61.9) | .06 | .11 | .12 |
| Moderate drinker | 148 (40.5) | 14 (24.1) | 10 (24.4) | 6 (28.6) | |||
| Heavy drinker | 9 (2.5) | 2 (3.4) | 2 (4.9) | 2 (9.5) | |||
| Blood pressure measures | |||||||
| Clinic SBP, mm Hg | 118.6 (10.7) | 151.1 (12.8) | 151.8 (14.5) | 152.7 (18.3) | <.001 | <.001 | <.001 |
| Daytime SBP, mm Hg | 118.9 (7.6) | 125.7 (6.4) | 123.9 (6.2) | 120.7 (6.8) | <.001 | <.001 | .28 |
| Nighttime SBP, mm Hg | 107.7 (7.3) | 120.8 (10.7) | 116.7 (8.9) | 109.9 (6.3) | <.001 | <.001 | .18 |
| 24‐h SBP, mm Hg | 114.5 (6.9) | 124.4 (7.3) | 121.5 (6.3) | 116.8 (5.5) | <.001 | <.001 | .13 |
| Clinic DBP, mm Hg | 72.0 (6.9) | 80.4 (9.5) | 80.2 (9.9) | 82.0 (9.9) | <.001 | <.001 | <.001 |
| Daytime DBP, mm Hg | 72.5 (6.3) | 72.2 (6.9) | 71.1 (6.9) | 69.9 (6.1) | .67 | .17 | .06 |
| Nighttime DBP, mm Hg | 61.1 (5.2) | 65.8 (8.6) | 63.5 (8.0) | 60.1 (7.3) | <.001 | .008 | .42 |
| 24‐h DBP, mm Hg | 67.9 (5.3) | 70.1 (7.1) | 68.4 (6.9) | 66.6 (6.2) | .005 | .58 | .26 |
| Nocturnal hypertension | 0 (0.0) | 38 (64.4) | 21 (50.0) | 0 (0.0) | – | – | – |
| Antihypertensive medication use | 173 (47.3) | 39 (67.2) | 26 (63.4) | 14 (66.7) | .005 | .05 | .08 |
ABPM, Ambulatory blood pressure monitoring; CVD, Cardiovascular disease – history of stroke, myocardial infarction, or revascularization; DBP, Diastolic blood pressure; eGFR, Estimated glomerular filtration rate; SBP, Systolic blood pressure.
The numbers in the table are mean (standard deviation) or n (percentage).
White coat hypertension was defined using 3 separate periods for evaluating out‐of‐clinic blood pressure on ABPM: (1) daytime, (2) daytime and 24‐h and (3) daytime, 24‐h, and nighttime. Sustained normotension defined as clinic, daytime, 24‐h, and nighttime blood pressure in the non‐hypertensive range. Non‐hypertensive out‐of‐clinic blood pressure on daytime ABPM defined as a mean blood pressure <135/85 mm Hg using measurements recorded between 10:00 am to 8:00 pm. Non‐hypertensive out‐of‐clinic blood pressure on 24‐h ABPM defined as mean of all blood pressure measurements <130/80 mm Hg. Non‐hypertensive out‐of‐clinic blood pressure on nighttime ABPM defined as a mean blood pressure <120/70 mm Hg using measurements recorded between midnight to 6:00 am. Left ventricular hypertrophy defined as increased left ventricular mass index ≥96 g/m2 in females and ≥116 g/m2 in males. Albuminuria defined as urinary albumin‐to‐creatinine ratio >30 mg/g.
*P‐values comparing non‐hypertensive daytime ABPM to sustained normotension.
**P‐value comparing non‐hypertensive daytime and non‐hypertensive 24‐h ABPM to sustained normotension.
***P‐value comparing non‐hypertensive daytime, 24‐h, and nighttime ABPM to sustained normotension.
LVMI was higher among participants with white coat hypertension defined using only daytime BP and daytime and 24‐hour BP compared to their counterparts with sustained normotension (Table 2). The difference in LVMI between participants with white coat hypertension defined using only daytime BP and sustained normotension remained statistically significant after adjustment for age and sex, and age, sex, body mass index and further adjustment for diabetes, alcohol use, smoking status, eGFR < 60 mL/min/1.73 m2, and history of CVD. After additional adjustment for antihypertensive medication use, LVMI was 5.0 (95% CI ‐0.2, 10.1) g/m2 higher among participants with white coat hypertension defined using daytime BP only compared with their counterparts with sustained normotension. In an unadjusted model, LVMI was higher among participants with white coat hypertension defined using the daytime and 24‐hour periods compared with sustained normotension. This difference was not statistically significant after multivariable adjustment. In unadjusted and multivariable‐adjusted models, mean LVMI was not statistically significantly different between participants with white coat hypertension defined using daytime, 24‐hour, and nighttime periods, and their counterparts with sustained normotension.
Table 2.
Mean and mean differences in left ventricular mass indexed to body surface area comparing participants with white coat hypertension, using 3 definitions, and sustained normotension
| Sustained normotension (n = 374) | White coat hypertension definition | P‐value* | P‐value** | P‐value*** | |||
|---|---|---|---|---|---|---|---|
| Daytime ABPM (n = 59) | Daytime and 24‐h ABPM (n = 42) | Daytime, 24‐h, and nighttime ABPM (n = 21) | |||||
| Mean difference (95% confidence interval) | |||||||
| Mean (SD) LVMI, g/m2 | 72.7 (17.9) | 80.6 (22.1) | 79.8 (20.5) | 76.0 (14.1) | |||
| Difference (95% CI) | |||||||
| Unadjusted | 0 (reference) | 7.9 (2.8, 13.0) | 7.1 (1.3, 12.9) | 3.3 (−4.5, 11.1) | .003 | .02 | .40 |
| Model 1 | 0 (reference) | 5.7 (0.6, 10.8) | 5.0 (−0.8, 10.8) | 1.2 (−6.5, 8.9) | .03 | .09 | .76 |
| Model 2 | 0 (reference) | 5.4 (0.3, 10.5) | 4.2 (−1.6, 10.0) | 0.9 (−6.9, 8.7) | .04 | .16 | .82 |
| Model 3 | 0 (reference) | 5.0 (−0.2, 10.1) | 3.9 (−1.9, 9.7) | 0.4 (−7.3, 8.2) | .06 | .19 | .91 |
ABPM, Ambulatory blood pressure monitoring; CI, confidence interval; LVMI, Left ventricular mass index is calculated as left ventricular mass/body surface area; SD, standard deviation.
White coat hypertension was defined using 3 separate periods for evaluating out‐of‐clinic blood pressure on ABPM: (1) daytime; (2) daytime and 24‐h; and (3) daytime, 24‐h, and nighttime. Sustained normotension defined as clinic, daytime, 24‐h, and nighttime blood pressure in the non‐hypertensive range. Non‐hypertensive out‐of‐clinic blood pressure on daytime ABPM defined as a mean blood pressure <135/85 mm Hg using measurements recorded between 10:00 am to 8:00 pm. Non‐hypertensive out‐of‐clinic blood pressure on 24‐h ABPM defined as mean of all blood pressure measurements <130/80 mm Hg. Non‐hypertensive out‐of‐clinic blood pressure on nighttime ABPM defined as a mean blood pressure <120/70 mm Hg using measurements recorded between midnight to 6:00 am.
Model 1 includes adjustment for age, sex, and body mass index.
Model 2 includes adjustment for variables in Model 1 and diabetes, alcohol use, smoking status, estimated glomerular filtration <60 mL/min/1.73 m2, and history of cardiovascular disease.
Model 3 includes adjustment for variables in Models 1 and 2 and antihypertensive medication use.
*P‐values comparing non‐hypertensive daytime ABPM to sustained normotension.
**P‐value comparing non‐hypertensive daytime and non‐hypertensive 24‐h ABPM to sustained normotension.
***P‐value comparing non‐hypertensive daytime, 24‐h, and nighttime ABPM to sustained normotension.
4. DISCUSSION
In the current study, the prevalence of white coat hypertension was substantially higher when 24‐hour or nighttime BP was not included in the definition of out‐of‐clinic BP. Overall, including nighttime BP in the definition of white coat hypertension resulted in a 10 to 20 percentage point lower prevalence of white coat hypertension. Also, participants with white coat hypertension defined using daytime BP only had a higher LVMI than those with sustained normotension. In contrast, participants with white coat hypertension defined using daytime, 24‐hour, and nighttime BP had a similar LVMI compared to those with sustained normotension.
The current findings extend results from a clinical registry of patients in Spain9 and the IDACO cohort10 to African Americans. In the analysis from the Spanish ABPM registry, the prevalence of white coat hypertension was 10 to 20 percentage points lower when defined using daytime, 24‐hour, and nighttime BP vs daytime BP only or 24‐hour BP only.9 Also, compared to their counterparts with sustained normotension, the prevalence of LVH, albuminuria, and a history of CVD was higher among patients with white coat hypertension defined using daytime BP or 24‐hour BP. In contrast, there were no differences in these outcomes when comparing patients with sustained normotension vs those with white coat hypertension defined by having BP in the normotensive range during the daytime, 24‐hour, and nighttime periods. Similar findings were present in an analysis of IDACO. Specifically, white coat hypertension defined using daytime BP and daytime and 24‐hour BP was associated with a higher risk of CVD events when compared to sustained normotension.10 However, CVD risk was similar among participants with white coat hypertension defined using daytime, 24‐hour, and nighttime BP and their counterparts with sustained normotension. In the current study, 50% of participants who met criteria for non‐hypertensive out‐of‐clinic BP according to the daytime and 24‐hour periods, had nighttime hypertension. As a result, the prevalence of white coat hypertension was substantially lower (10.6%) when including daytime, 24‐hour, and nighttime BP in the definition of out‐of‐clinic hypertension as compared to using the daytime BP and daytime and 24‐hour BP. The prevalence of white coat hypertension in the current study was also lower as compared with the Spanish ABPM registry (26.1%) and IDACO (21.0%). This difference may reflect the higher prevalence of nighttime hypertension among African Americans compared with Europeans and Asians.7
The United States Preventive Services Task Force5 and the American College of Cardiology/American Heart Association BP guideline6 recommend measuring out‐of‐clinic BP to confirm the diagnosis of hypertension before initiating antihypertensive medication.5 The current study demonstrates the importance of including 24‐hour and nighttime BP levels when conducting ABPM to assess white coat hypertension in African Americans. Although home BP monitoring (HBPM) is recommended for out‐of‐clinic BP assessment when ABPM is not available, few HBPM devices currently available in the United States can measure BP during sleep. Therefore, ABPM may be preferable over HBPM to rule‐out white coat hypertension in African Americans.
This study has several strengths. The JHS enrolled a community‐based sample of African Americans and is one of the largest samples of ABPM conducted among African Americans. Also, both ABPM and clinic BP were conducted following standardized protocols. There are also several potential limitations to the current analysis. JHS participants only underwent one ABPM session, and it is possible that the results would differ if ABPM were repeated. There was a small sample size for some definitions of white coat hypertension. Due to the small sample size, we were unable to conduct the analyses for participants taking and not taking antihypertensive medications separately. Finally, the prevalence of LVH was low among participants included in the current analysis. However, the prevalence of LVH in JHS was similar to findings from prior studies evaluating individuals with white coat hypertension and sustained normotension.9, 20, 21 It is possible that the differences in LVMI would be larger in cohorts with a higher prevalence of LVH.
In conclusion, these data demonstrate the importance of using mean BP during the daytime, 24‐hour, and nighttime periods when evaluating the presence of white coat hypertension. Relying only on daytime BP measurements will overestimate the prevalence of white coat hypertension and underestimate its cardiovascular risk among African Americans. Strategies that do not include assessment of BP during the 24‐hour and nighttime periods may potentially leave many African Americans under‐treated and at increased CVD risk.
CONFLICT OF INTEREST
PM received an institutional grant from Amgen Inc. unrelated to the topic of the current manuscript. There are no other potential conflicts of interest.
ACKNOWLEDGMENTS
The authors wish to thank the staffs and participants of the JHS.
Anstey DE, Colantonio LD, Yano Y, Booth JN III, Muntner P. The importance of using 24‐hour and nighttime blood pressure for the identification of white coat hypertension: Data from the Jackson Heart Study. J Clin Hypertens. 2018;20:1176‐1182. 10.1111/jch.13330
Funding information
The Jackson Heart Study is supported and conducted in collaboration with Jackson State University (HHSN268201300049C and HHSN268201300050C); University of Mississippi Medical Center (HHSN268201300046C and HHSN268201300047C); and Touglaoo College (HHSN268201300048C) contracts from the National Heart, Lung, and Blood Institute (NHLBI) and the National Center on Minority Health and Health Disparities (NCMHD) at the National Institute of Health (NIH). This analysis was supported by grant 2R01 HL117323 from the National Heart, Lung, and Blood Institute and grant 15SFRN2390002 from the American Heart Association. DEA receives support through 2T32HL007854‐21.
REFERENCES
- 1. Shimbo D, Abdalla M, Falzon L, Townsend RR, Muntner P. Role of ambulatory and home blood pressure monitoring in clinical practice: a narrative review. Ann Intern Med. 2015;163:691‐700. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2. Muntner P, Booth JN 3rd, Shimbo D, Schwartz JE. Is white‐coat hypertension associated with increased cardiovascular and mortality risk? J Hypertens. 2016;34:1655‐1658. [DOI] [PubMed] [Google Scholar]
- 3. Briasoulis A, Androulakis E, Palla M, Papageorgiou N, Tousoulis D. White‐coat hypertension and cardiovascular events: a meta‐analysis. J Hypertens. 2016;34:593‐599. [DOI] [PubMed] [Google Scholar]
- 4. Mancia G, Fagard R, Narkiewicz K, et al. 2013 ESH/ESC guidelines for the management of arterial hypertension: the Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Eur Heart J. 2013;34:2159‐2219. [DOI] [PubMed] [Google Scholar]
- 5. Siu AL, U.S. Preventive Services Task Force . Screening for high blood pressure in adults: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2015;163:778‐786. [DOI] [PubMed] [Google Scholar]
- 6. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2017;71:1269‐1324. [DOI] [PubMed] [Google Scholar]
- 7. Ogedegbe G, Spruill TM, Sarpong DF, et al. Correlates of isolated nocturnal hypertension and target organ damage in a population‐based cohort of African Americans: the Jackson Heart Study. Am J Hypertens. 2013;26:1011‐1016. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8. Yano Y, Kario K. Nocturnal blood pressure and cardiovascular disease: a review of recent advances. Hypertens Res. 2012;35:695‐701. [DOI] [PubMed] [Google Scholar]
- 9. de la Sierra A, Vinyoles E, Banegas JR, et al. Prevalence and clinical characteristics of white‐coat hypertension based on different definition criteria in untreated and treated patients. J Hypertens. 2017;35:2388‐2394. [DOI] [PubMed] [Google Scholar]
- 10. Asayama K, Thijs L, Li Y, et al. Setting thresholds to varying blood pressure monitoring intervals differentially affects risk estimates associated with white‐coat and masked hypertension in the population. Hypertension. 2014;64:935‐942. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11. Thomas SJ, Booth JN 3rd, Bromfield SG, et al. Clinic and ambulatory blood pressure in a population‐based sample of African Americans: the Jackson Heart Study. J Am Soc Hypertens. 2017;11(204–212):e205. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12. Taylor HA Jr. The Jackson Heart Study: an overview. Ethn Dis 2005;15(4 Suppl 6):S6‐1‐3. [PubMed] [Google Scholar]
- 13. Taylor HA Jr, Wilson JG, Jones DW, et al. Toward resolution of cardiovascular health disparities in African Americans: design and methods of the Jackson Heart Study. Ethn Dis. 2005;15(4 Suppl 6):S6‐4‐17. [PubMed] [Google Scholar]
- 14. Levey AS, Stevens LA, Schmid CH, et al. A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009;150:604‐612. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15. Carpenter MA, Crow R, Steffes M, et al. Laboratory, reading center, and coordinating center data management methods in the Jackson Heart Study. Am J Med Sci. 2004;328:131‐144. [DOI] [PubMed] [Google Scholar]
- 16. Lang RM, Badano LP, Mor‐Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the american society of echocardiography and the European association of cardiovascular imaging. J Am Soc Echocardiogr. 2015;28(1–39):e14. [DOI] [PubMed] [Google Scholar]
- 17. Barker MH, Erlanger J, Meakins J, et al. Standard method for taking and recording blood pressure readings. J Am Med Assoc. 1939;113:294‐297. [Google Scholar]
- 18. Abdalla M, Booth JN 3rd, Seals SR, et al. Masked hypertension and incident clinic hypertension among blacks in the Jackson Heart Study. Hypertension. 2016;68:220‐226. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19. Thijs L, Hansen TW, Kikuya M, et al. The International Database of Ambulatory Blood Pressure in relation to Cardiovascular Outcome (IDACO): protocol and research perspectives. Blood Press Monit. 2007;12:255‐262. [DOI] [PubMed] [Google Scholar]
- 20. Sega R, Trocino G, Lanzarotti A, et al. Alterations of cardiac structure in patients with isolated office, ambulatory, or home hypertension: data from the general population (Pressione Arteriose Monitorate E Loro Associazioni [PAMELA] Study). Circulation. 2001;104:1385‐1392. [DOI] [PubMed] [Google Scholar]
- 21. Cavallini MC, Roman MJ, Pickering TG, Schwartz JE, Pini R, Devereux RB. Is white coat hypertension associated with arterial disease or left ventricular hypertrophy? Hypertension. 1995;26:413‐419. [DOI] [PubMed] [Google Scholar]