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The Journal of Clinical Hypertension logoLink to The Journal of Clinical Hypertension
. 2017 Feb 6;19(6):592–600. doi: 10.1111/jch.12974

Metabolic syndrome and masked hypertension among African Americans: The Jackson Heart Study

Lisandro D Colantonio 1, D Edmund Anstey 2, April P Carson 1, Gbenga Ogedegbe 3, Marwah Abdalla 2, Mario Sims 4, Daichi Shimbo 2, Paul Muntner 1,
PMCID: PMC5697142  NIHMSID: NIHMS838585  PMID: 28165190

Abstract

The metabolic syndrome is associated with higher ambulatory blood pressure. The authors studied the association of metabolic syndrome and masked hypertension (MHT) among African Americans with clinic‐measured systolic/diastolic blood pressure (SBP/DBP) <140/90 mm Hg in the Jackson Heart Study. MHT was defined as daytime, nighttime, or 24‐hour hypertension on ambulatory blood pressure monitoring. Among 359 participants not taking antihypertensive medication, the metabolic syndrome was associated with MHT (prevalence ratio, 1.38; 95% confidence interval, 1.10–1.74]). When metabolic syndrome components (clinic SBP/DBP 130–139/85–89 mm Hg, abdominal obesity, impaired glucose, low high‐density lipoprotein cholesterol, high triglycerides) were analyzed separately, only clinic SBP/DBP 130–139/85–89 mm Hg was associated with MHT (prevalence ratio, 1.90; 95% confidence interval, 1.56–2.32]). The metabolic syndrome was not associated with MHT among participants not taking antihypertensive medication with SBP/DBP 130–139/85–89 and <130/85 mm Hg, separately, or among participants taking antihypertensive medication (n=393). Ambulatory blood pressure monitoring screening for MHT among African Americans should be considered based on clinic BP, not metabolic syndrome.

1. INTRODUCTION

The metabolic syndrome (MetS) is characterized by high clinic blood pressure (BP), abdominal obesity, impaired fasting glucose, low high‐density lipoprotein (HDL) cholesterol, and high triglycerides.1 According to data from the National Health and Nutrition Examination Survey 2011–2012, 34.7% of US adults have MetS.2 Prior studies have demonstrated that there is a high prevalence of hypertension‐related end organ damage and a high risk for cardiovascular disease (CVD) events among adults with MetS.3, 4, 5, 6 However, a substantial proportion of adults with MetS do not have hypertension based on clinic BP.7, 8, 9

Masked hypertension (MHT), defined as having hypertension based on out‐of‐clinic BP measurements without hypertension based on clinic BP measurements, is associated with an increased risk for end organ damage and CVD events.10, 11, 12, 13 Several components of the MetS have been associated with a higher out‐of‐clinic BP vs clinic BP.14, 15 However, there are few data on the association between MetS and MHT. If the prevalence of MHT is higher among individuals with vs those without MetS, this may indicate a role for MetS to guide the indication of ambulatory BP monitoring (ABPM) for diagnosing MHT.

We examined the association between MetS and the prevalence of MHT in the Jackson Heart Study (JHS), a population‐based cohort study comprised exclusively of African Americans. We hypothesized that among JHS participants with clinic systolic BP <140 mm Hg and clinic diastolic BP <90 mm Hg, the prevalence of MHT would be higher among those with vs those without MetS. We also hypothesized that each MetS component would be associated with a higher prevalence of MHT.

2. METHODS

2.1. Study population

The JHS was designed to examine the etiology of CVD and related risk factors among African Americans.16 Overall, 5306 African American men and women 20 years and older were recruited between 2000 and 2004 from the Jackson, Mississippi, metropolitan area. All participants completed an in‐home interview and a clinic visit at baseline. A sample of JHS participants (n=1148) also completed ABPM at baseline.16 The current analysis was restricted to 1046 JHS participants with a complete ABPM recording at baseline defined using the International Database of Ambulatory Blood Pressure and Cardiovascular Disease criteria (ie, 10 or more daytime readings and five or more nighttime readings).17 Participants with clinic systolic BP ≥140 mm Hg or diastolic BP ≥90 mm Hg (n=202) cannot have MHT and, therefore, were excluded from the current analysis. Additionally, we excluded five participants with missing clinic systolic or diastolic BP values, 68 participants with missing data on variables used to define MetS (see below), and 19 participants with missing data on antihypertensive medication use. After these inclusion/exclusion criteria were applied, 359 JHS participants not taking antihypertensive medication and 393 taking antihypertensive medication were included in the current analysis.

The JHS protocol was approved by the institutional review boards governing research in human subjects at the University of Mississippi Medical Center, Jackson State University, and Tougaloo College. All JHS participants provided written informed consent at baseline. The current analysis of deidentified data was approved by the institutional review board at the University of Alabama at Birmingham.

2.2. Baseline assessment

Data collected through interviewer‐administered questionnaires at baseline included age, sex, education, cigarette smoking, physical activity, history of heart attack and diabetes, and use of antihypertensive medication. Participants who reported no moderate or vigorous physical activity were considered to be physically inactive.18

During the clinic visit, trained staff performed electrocardiography, measured participants' waist circumference, and conducted an inventory of all medications that participants took in the past 2 weeks. In addition, BP was measured two times by trained research staff members using a random‐zero sphygmomanometer (Hawksley and Sons Ltd., Lancing, UK) following a standardized protocol. The two BP measurements were averaged for all analyses. As previously described, BP measurements were calibrated using robust regression to an oscillometric device (Omron HEM‐907XL, Omron Healthcare Inc., Lake Forest, IL, USA).19 History of coronary heart disease (CHD) was defined by a self‐reported history of heart attack or evidence of a prior myocardial infarction on the study electrocardiogram. Use of statins, oral hypoglycemic medication, and insulin was defined based on the medication inventory.

As part of the clinic visit, blood samples were collected after participants had fasted for 8 hours or more. Serum glucose was measured using a glucose oxidase method on a Vitros 250 or 950, Ortho‐Clinical Diagnostics analyzer.20 Glycated hemoglobin was measured using a TOSOH high‐performance liquid chromatography system. Total and HDL cholesterol and triglycerides were measured using spectrophotometry on a Roche Cobas FARA analyzer. Diabetes was defined by a self‐reported history with current use of oral hypoglycemic medication or insulin, fasting serum glucose ≥126 mg/dL, or glycated hemoglobin ≥6.5%.

2.3. Metabolic syndrome

MetS was defined using the 2009 harmonized definition from the International Diabetes Federation; the National Heart, Lung, and Blood Institute; the American Heart Association; the World Heart Federation; the International Atherosclerosis Society; and the International Association for the Study of Obesity.1 Specifically, MetS was defined by having three or more of the following components:

  • Systolic BP 130 to 139 mm Hg or diastolic BP 85 to 89 mm Hg during the clinic visit, or self‐reported use of antihypertensive medication.

  • Abdominal obesity, defined as a waist circumference ≥88 cm among women and ≥102 cm among men.

  • Impaired glucose, defined by a fasting serum glucose ≥100 mg/dL or diabetes.

  • Low HDL cholesterol, defined as <50 mg/dL among women and <40 mg/dL among men.

  • High triglycerides, defined as ≥150 mg/dL.

2.4. Ambulatory BP monitoring

ABPM was performed following the clinic visit using a SpaceLabs 90207 device (Medifacts International Ltd, Rockville, MD, USA).16 The size of the cuff was selected after measuring the circumference of each participant's nondominant arm. Participants were instructed to wear the device for 24 hours while performing their daily activities. BP was recorded every 20 minutes.21 Using ambulatory BP measurements taken between 10 am and 8 pm, masked daytime hypertension was defined as a mean systolic BP ≥135 mm Hg or mean diastolic BP ≥85 mm Hg.22 Using BP measurements taken between midnight and 6 am, masked nighttime hypertension was defined as a mean systolic BP ≥120 mm Hg or mean diastolic BP ≥70 mm Hg. Using all BP measurements from ABPM, masked 24‐hour hypertension was defined as a mean systolic BP ≥130 mm Hg or mean diastolic BP ≥80 mm Hg. Any MHT was defined as having masked daytime, nighttime, or 24‐hour hypertension. For the current study, the term masked uncontrolled hypertension is used rather than MHT for participants taking antihypertensive medication.

2.5. Statistical analysis

Analyses were conducted among participants not taking and those taking antihypertensive medication, separately. We calculated the prevalence of MetS and each MetS component. Participant characteristics and the prevalence of any MHT were calculated among those with and without MetS, separately. We used Poisson regression models with robust variance and progressive adjustment for covariates to calculate prevalence ratios (PRs) and 95% confidence intervals (CIs) for any MHT associated with MetS.23, 24 The initial model (model 1) was unadjusted. A second model (model 2) included adjustment for age, sex, and education. The third model (model 3) included adjustment for age, sex, education, current smoking, physical inactivity, history of CHD, total cholesterol, and statin use. We also calculated the prevalence and PRs of any MHT associated with each component of the MetS, separately. In secondary analyses, we analyzed the association between MetS and each of its components with masked daytime, nighttime, and 24‐hour hypertension, separately. Also, among participants not taking antihypertensive medication, we analyzed the prevalence of any masked and masked daytime, nighttime, and 24‐hour hypertension, separately, associated with MetS stratified by clinic BP (systolic/diastolic BP 130–139 mm Hg/85–89 mm Hg and systolic/diastolic BP <130/85 mm Hg). All participants taking antihypertensive medication met the BP component of the MetS definition. Therefore, we did not conduct separate analyses on the association between MetS and MHT by clinic BP levels among participants taking antihypertensive medication.

Overall, three (0.4%), five (0.7%), and 53 (7.0%) JHS participants included in the analysis had missing data on education, smoking status, and statin use, respectively. We used multiple imputation to impute missing covariates and include these observations in regression models. Multiple imputation was conducted using chained equations to obtain 15 imputed datasets.25, 26 All analyses were performed in Stata 12 (Stata Corp, College Station, TX, USA).

3. RESULTS

3.1. Participants not taking antihypertensive medication (n=359)

Abdominal obesity was the component of the MetS with the highest prevalence (54.0%) among JHS participants not taking antihypertensive medication (Figure, top panel). Overall, 61 (17.0%) participants who were not taking antihypertensive medication had the MetS. The mean age of participants with and without the MetS was 56.0 and 54.1 years, respectively, and 68.9% and 64.4%, respectively, were women (Table 1). Participants with the MetS had higher total cholesterol and clinic and ambulatory BP compared with their counterparts without MetS. Education and the prevalence of current smoking, physical inactivity, history of CHD, and statin use were not different between participants with and without the MetS.

Figure 1.

Figure 1

Prevalence of metabolic syndrome component criteria among participants taking and not taking antihypertensive medication included in the analysis. BP indicates blood pressure; HDL, high‐density lipoprotein. aDefined as clinic systolic BP 130 to 139 mm Hg or diastolic BP 85 to 89 mm Hg among participants not taking antihypertensive medication, or as taking antihypertensive medication

Table 1.

Characteristics of Jackson Heart Study participants not taking antihypertensive medication included in the analysis (n=359)

Characteristics Without Metabolic Syndrome n=298 With Metabolic Syndrome n=61 P Value
Age, y 54.1 (0.65) 56.0 (1.43) .23
Women 64.4 68.9 .39
Less than high school education 12.5 19.7 .14
Current smoker 9.8 11.6 .67
Physical inactivity 43.6 45.9 .74
Total cholesterol, mg/dL 199.7 (2.25) 214.2 (5.19) .01
History of CHD 4.0 3.3 .78
Statin use 2.3 4.9 .27
Systolic BP, mm Hg
Clinic 118.9 (0.58) 125.6 (1.28) <.001
Daytime 124.3 (0.62) 127.8 (1.50) .02
Nighttime 114.1 (0.70) 119.1 (1.73) .004
24‐H 120.3 (0.62) 124.6 (1.50) .01
Diastolic BP, mm Hg
Clinic 72.9 (0.41) 74.9 (0.87) .05
Daytime 77.6 (0.48) 76.7 (0.98) .45
Nighttime 66.6 (0.49) 68.1 (1.10) .23
24‐H 73.2 (0.45) 73.4 (0.90) .90
Metabolic syndrome components
Clinic BP componenta 16.4 55.7 <.001
Abdominal obesity 46.3 91.8 <.001
Impaired glucose 12.8 50.8 <.001
Low HDL cholesterol 19.1 72.1 <.001
High triglycerides 5.4 62.3 <.001

Values are expressed as mean (standard error) or percentage. Results were obtained using multiple imputation for variables with missing data.

Abbreviations: CHD, coronary heart disease; HDL, high‐density lipoprotein.

a

Defined as clinic systolic blood pressure (BP) 130 to 139 mm Hg or diastolic BP 85 to 89 mm Hg among participants not taking antihypertensive medication.

The prevalence of any MHT was 62.3% (95% CI, 49.8%–74.8%) and 43.6% (95% CI, 38.0%–49.3%) among participants with and without the MetS, respectively (Table 2). After multivariable adjustment, the PR for any MHT associated with MetS was 1.38 (95% CI, 1.10–1.74). The prevalence of any MHT was 77.1% (95% CI, 67.9%–86.3%) among participants with clinic systolic BP 130 to 139 mm Hg or diastolic BP 85 to 89 mm Hg and 37.7% (95% CI, 31.9%–43.4%) among their counterparts with clinic systolic/diastolic BP <130/85 mm Hg. After multivariable adjustment, having a clinic systolic BP 130 to 139 mm Hg or diastolic BP 85 to 89 mm Hg was associated with a PR of 1.90 (95% CI, 1.56–2.32) for any MHT compared with having clinic systolic/diastolic BP <130/85 mm Hg. Abdominal obesity, impaired glucose, low HDL cholesterol and high triglycerides were not associated with having any MHT. MetS was also associated with a higher prevalence of masked nighttime hypertension, but not with masked daytime or 24‐hour hypertension (Tables S1S3). The prevalence of masked daytime, nighttime, and 24‐hour hypertension was higher among participants with clinic systolic BP 130 to 139 mm Hg or diastolic BP 85 to 89 mm Hg vs those with clinic systolic/diastolic BP <130/85 mm Hg. High triglycerides were also associated with a higher prevalence of masked nighttime hypertension, but not with masked daytime or 24‐hour hypertension. Abdominal obesity, impaired glucose, and low HDL cholesterol were not associated with masked daytime, nighttime, or 24‐hour hypertension. MetS was not associated with any MHT, or masked daytime, nighttime, or 24‐hour hypertension when participants with clinic systolic BP 130 to 139 mm Hg or diastolic BP 85 to 89 mm Hg and those with clinic systolic/diastolic BP <130/85 mm Hg were analyzed separately (Table 3).

Table 2.

Prevalence and prevalence ratios for any masked hypertension associated with metabolic syndrome and each component of the metabolic syndrome among participants not taking antihypertensive medication (n=359)

Prevalence (95% CI) Prevalence Ratios (95% CI)
Model 1 Model 2 Model 3
Metabolic syndrome
No, n=298 43.6 (38.0–49.3) 1 (reference) 1 (reference) 1 (reference)
Yes, n=61 62.3 (49.8–74.8) 1.43 (1.13–1.81) 1.41 (1.13–1.77) 1.38 (1.10–1.74)
Clinic BP componenta
No, n=276 37.7 (31.9–43.4) 1 (reference) 1 (reference) 1 (reference)
Yes, n=83 77.1 (67.9–86.3) 2.05 (1.69–2.48) 1.93 (1.58–2.35) 1.90 (1.56–2.32)
Abdominal obesity
No, n=165 49.1 (41.4–56.8) 1 (reference) 1 (reference) 1 (reference)
Yes, n=194 44.8 (37.8–51.9) 0.91 (0.73–1.14) 1.00 (0.80–1.26) 0.99 (0.79–1.24)
Impaired glucose
No, n=290 45.5 (39.8–51.3) 1 (reference) 1 (reference) 1 (reference)
Yes, n=69 52.2 (40.1–64.3) 1.15 (0.88–1.49) 0.96 (0.74–1.25) 0.94 (0.72–1.23)
Low HDL cholesterol
No, n=258 48.8 (42.7–55.0) 1 (reference) 1 (reference) 1 (reference)
Yes, n=101 41.6 (31.8–51.4) 0.85 (0.65–1.11) 0.92 (0.71–1.18) 0.92 (0.72–1.19)
High triglycerides
No, n=305 44.9 (39.3–50.5) 1 (reference) 1 (reference) 1 (reference)
Yes, n=54 57.4 (43.8–71.0) 1.28 (0.98–1.66) 1.26 (0.98–1.62) 1.23 (0.95–1.59)

Results were obtained using multiple imputation for variables with missing data.

Abbreviations: CI, confidence interval; HDL, high‐density lipoprotein.

a

Defined as clinic systolic blood pressure (BP) 130 to 139 mm Hg or diastolic BP 85 to 89 mm Hg among participants not taking antihypertensive medication.

Model 1 is unadjusted.

Model 2 adjusts for age, sex, and education.

Model 3 adjusts for variables in model 2 plus current smoker, physical inactivity, history of coronary heart disease, total cholesterol, and statin use.

Table 3.

Prevalence and prevalence ratios for any masked and masked daytime, nighttime, and 24‐hour hypertension associated with MetS among participants not taking antihypertensive medication according to clinic blood pressure levels (n=359)

Prevalence (95% CI) Prevalence Ratios (95% CI)
Model 1 Model 2 Model 3
SBP 130 to 139 mm Hg or DBP 85 to 89 mm Hga
Any masked hypertension prevalence
Without MetS 75.5 (63.0–88.0) 1 (reference) 1 (reference) 1 (reference)
With MetS 79.4 (65.1–93.8) 1.05 (0.83–1.33) 1.08 (0.85–1.38) 1.13 (0.88–1.45)
Masked daytime hypertension prevalence
Without MetS 65.3 (51.5–79.1) 1 (reference) 1 (reference) 1 (reference)
With MetS 47.1 (29.3–64.8) 0.72 (0.48–1.09) 0.75 (0.50–1.13) 0.75 (0.49–1.13)
Masked nighttime hypertension prevalence
Without MetS 63.3 (49.3–77.3) 1 (reference) 1 (reference) 1 (reference)
With MetS 73.5 (57.9–89.2) 1.16 (0.86–1.56) 1.22 (0.91–1.64) 1.30 (0.97–1.75)
Masked 24‐h hypertension prevalence
Without MetS 63.3 (49.3–77.3) 1 (reference) 1 (reference) 1 (reference)
With MetS 52.9 (35.2–70.7) 0.84 (0.57–1.23) 0.89 (0.61–1.30) 0.89 (0.61–1.31)
SBP <130 mm Hg and DBP <85 mm Hgb
Any masked hypertension prevalence
Without MetS 37.3 (31.3–43.4) 1 (reference) 1 (reference) 1 (reference)
With MetS 40.7 (20.9–60.6) 1.09 (0.67–1.77) 1.13 (0.72–1.79) 1.11 (0.71–1.73)
Masked daytime hypertension prevalence
Without MetS 16.9 (12.2–21.6) 1 (reference) 1 (reference) 1 (reference)
With MetS 7.4 (0.0–18.0) 0.44 (0.11–1.72) 0.48 (0.12–1.89) 0.48 (0.12–1.90)
Masked nighttime hypertension prevalence
Without MetS 35.7 (29.7–41.7) 1 (reference) 1 (reference) 1 (reference)
With MetS 40.7 (20.9–60.6) 1.14 (0.70–1.85) 1.17 (0.74–1.84) 1.15 (0.74–1.79)
Masked 24‐h hypertension prevalence
Without MetS 22.1 (16.9–27.3) 1 (reference) 1 (reference) 1 (reference)
With MetS 22.2 (5.4–39.0) 1.01 (0.48–2.12) 1.02 (0.49–2.11) 1.01 (0.48–2.13)

Results were obtained using multiple imputation for variables with missing data.

Abbreviations: CI, confidence interval; DBP, diastolic blood pressure; SBP, systolic blood pressure.

a

Analyses include 34 participants with metabolic syndrome (MetS) and 49 participants without MetS.

b

Analyses include 27 participants with MetS and 249 participants without MetS.

Model 1 is unadjusted.

Model 2 adjusts for age, sex, and education.

Model 3 adjusts for variables in model 2 plus current smoker, physical inactivity, history of coronary heart disease, total cholesterol, and statin use.

3.2. Participants taking antihypertensive medication (n=393)

All participants taking antihypertensive medication met the clinic BP component of the MetS (Figure, bottom panel). Abdominal obesity was the second most prevalent component of the MetS after clinic BP among JHS participants taking antihypertensive medication. Overall, 223 (56.7%) participants taking antihypertensive medication had MetS. Participants with MetS were more likely to be women and have a history of CHD compared with their counterparts without MetS (Table S4). Participants with and without MetS had similar clinic and ambulatory BP.

The prevalence of any masked uncontrolled hypertension was 59.6% (95% CI, 53.2%–66.1%) and 58.2% (95% CI, 50.7%–65.7%) among participants taking antihypertensive medication with and without MetS, respectively (Table S5). MetS was not associated with any masked uncontrolled hypertension after multivariable adjustment. In addition, MetS was not associated with masked daytime, nighttime, or 24‐hour uncontrolled hypertension (Tables S6S8). Having impaired glucose was associated with a higher prevalence of masked nighttime uncontrolled hypertension (crude and multivariable adjusted PR, 1.25 [95% CI, 1.04–1.51] and 1.19 [95% CI, 0.98–1.43], respectively) but not masked daytime or 24‐hour uncontrolled hypertension. Abdominal obesity, low HDL cholesterol, and high triglycerides were not associated with any masked or masked daytime, nighttime, or 24‐hour uncontrolled hypertension.

4. DISCUSSION

In the current study of African Americans not taking antihypertensive medication with clinic‐measured systolic BP <140 mm Hg and diastolic BP <90 mm Hg, the prevalence of MHT was higher among participants with vs without MetS. When each component of the MetS was analyzed separately, only clinic BP was associated with MHT. MetS was not associated with MHT when the analysis was stratified by clinic BP. Among African Americans taking antihypertensive medication, MetS was not associated with any type of masked uncontrolled hypertension. These results indicate that the MetS does not provide additional predictive information to identify individuals with MHT beyond that obtained from clinic BP.

The MetS has been associated with higher ambulatory BP in some, but not all, prior studies.27, 28, 29, 30, 31 For example, in the population‐based Pressioni Arteriose Monitorate E Loro Associazioni (PAMELA) study,29 the mean 24‐hour ambulatory systolic/diastolic BP among participants with and without MetS was 126.3/77.0 mm Hg and 119.0/73.9 mm Hg, respectively. Most studies reporting an association between MetS and higher ambulatory BP did not control for differences in clinic BP. Further, few studies have investigated whether the MetS is associated with a higher prevalence of MHT. The current analyses expand on prior studies by showing that African Americans not taking antihypertensive medication who have MetS have a higher prevalence of MHT compared with their counterparts without MetS. This association appears to be primarily explained by higher clinic BP among persons with MetS.

Results from the current analysis are consistent with prior studies showing that the prevalence of MHT increases with higher clinic BP.32, 33, 34, 35 In the Masked Hypertension Study,36 there was a graded increase in the prevalence of MHT with higher levels of clinic systolic and diastolic BP among 813 participants (6.5% African Americans) not taking antihypertensive medication. In that study, the prevalence of MHT was 0% among participants with clinic systolic BP <100 mm Hg and clinic diastolic BP <70 mm Hg, and 51.7% among participants with clinic systolic BP 130 to 139 mm Hg or diastolic BP 85 to 89 mm Hg.

The current analysis suggests that MetS components other than clinic BP do not contribute to the association between MetS and MHT among African Americans not taking antihypertensive medication. Prior studies have reported that several components of the MetS may be associated with MHT.32 For example, Hanninen and colleagues14 and Asayama and colleagues15 have reported that waist circumference is higher among adults with MHT vs their counterparts with sustained normotension (defined as not having hypertension based on clinic or out‐of‐clinic BP measurements) in studies conducted in Finland and Japan, respectively.14, 15 In addition, mean triglycerides were higher among participants with MHT vs their counterparts with sustained normotension in the PAMELA study.10 However, these studies did not adjust for potential confounders including clinic BP.

Diabetes has been reported to be associated with masked uncontrolled hypertension among individuals taking antihypertensive medication.37, 38 After multivariable adjustment including clinic BP, the odds ratios for masked 24‐hour uncontrolled hypertension associated with diabetes among 14 840 patients taking antihypertensive medication in the Spanish Society of Hypertension ABPM Registry37 was 1.25 (95% CI, 1.14–1.37). Bromfield and colleagues38 also reported diabetes to be associated with a higher prevalence of masked daytime and isolated nocturnal uncontrolled hypertension among African Americans taking antihypertensive medication in the JHS. In the present analysis, the prevalence of masked nighttime uncontrolled hypertension was higher among African Americans taking antihypertensive medication with, vs those without, impaired glucose. However, having impaired glucose was not associated with a higher prevalence of masked daytime or 24‐hour uncontrolled hypertension. Taken together, results from the current and prior studies suggest that diabetes but not impaired glucose may play a role in the identification of populations to be screened with ABPM for masked uncontrolled hypertension.

African Americans have a higher prevalence and incidence of hypertension and an increased risk for CVD and chronic kidney disease compared with whites.39, 40, 41, 42, 43 In addition, MHT is associated with increased incidence of clinic hypertension, a higher prevalence of hypertension‐related end organ damage, and CVD events among African Americans.19, 44, 45 Identifying African Americans with MHT and masked uncontrolled hypertension can be useful for CVD risk stratification and for implementing intervention strategies to reduce the incidence of clinic hypertension and CVD in this population. Results from the current analysis indicate that clinic BP but not the MetS could be used to identify African Americans not taking antihypertensive medication with a higher probability of having MHT.

5. Study Strengths and Limitations

The present analysis has several strengths. The JHS enrolled a large population‐based cohort of African Americans. To date, there have been few published data on ABPM phenotypes in African Americans. Data on clinic BP and ABPM were collected by trained staff following standardized protocols. In addition, several MHT phenotypes were analyzed, including masked daytime, nighttime, and 24‐hour hypertension. The prevalence of masked daytime, nighttime, and 24‐hour hypertension differs substantially among African Americans.44 Studying only one of these phenotypes may result in misclassification and potential bias. The current analysis also has known and potential limitations. Only a sample of JHS participants completed the ABPM. Also, clinic and ambulatory BP measurements were performed on a single occasion, which may lead to potential misclassification of MetS and MHT. Only African Americans living in Mississippi were enrolled in the JHS. Therefore, results from the current analysis may not be generalizable to other racial groups or to African Americans living in other US regions.

6. CONCLUSIONS

Among African Americans not taking antihypertensive medication, those with the MetS have a higher prevalence of MHT compared with their counterparts without the MetS. This association was primarily explained by higher clinic BP among those with the MetS. Also, the MetS was not associated with masked uncontrolled hypertension among participants taking antihypertensive medication. The current study suggests that clinic BP but not MetS could be used to guide who to refer for ABPM to identify MHT.

CONFLICT OF INTEREST

Dr Daichi Shimbo is a consultant for Abbott Vascular and Novartis Pharmaceuticals Corporation. Dr Paul Muntner receives grant support from Amgen Inc. Drs Lisandro D. Colantonio, D. Edmund Anstey, April P. Carson, Gbenga Ogedegbe, Marwah Abdalla, and Mario Sims have no conflicts of interest to declare.

Supporting information

 

ACKNOWLEDGEMENTS

The JHS is supported and conducted in collaboration with Jackson State University (HHSN268201300049C and HHSN268201300050C), Tougaloo College (HHSN268201300048C), and the University of Mississippi Medical Center (HHSN268201300046C and HHSN268201300047C) contracts from the National Heart, Lung, and Blood Institute and the National Institute for Minority Health and Health Disparities. The authors also wish to thank the staffs and participants of the JHS. 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 US Department of Health and Human Services.

Colantonio LD, Anstey DE, Carson AP, et al. Metabolic syndrome and masked hypertension among African Americans: The Jackson Heart Study. J Clin Hypertens. 2017;19:592–600. 10.1111/jch.12974

REFERENCES

  • 1. Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120:1640–1645. [DOI] [PubMed] [Google Scholar]
  • 2. Aguilar M, Bhuket T, Torres S, Liu B, Wong RJ. Prevalence of the metabolic syndrome in the United States, 2003‐2012. JAMA. 2015;313:1973–1974. [DOI] [PubMed] [Google Scholar]
  • 3. Chen J, Muntner P, Hamm LL, et al. The metabolic syndrome and chronic kidney disease in U.S. adults. Ann Intern Med. 2004;140:167–174. [DOI] [PubMed] [Google Scholar]
  • 4. Ferrara LA, Cardoni O, Mancini M, Zanchetti A. Metabolic syndrome and left ventricular hypertrophy in a general population. Results from the Gubbio Study. J Hum Hypertens. 2007;21:795–801. [DOI] [PubMed] [Google Scholar]
  • 5. McNeill AM, Rosamond WD, Girman CJ, et al. Prevalence of coronary heart disease and carotid arterial thickening in patients with the metabolic syndrome (The ARIC Study). Am J Cardiol. 2004;94:1249–1254. [DOI] [PubMed] [Google Scholar]
  • 6. McNeill AM, Rosamond WD, Girman CJ, et al. The metabolic syndrome and 11‐year risk of incident cardiovascular disease in the atherosclerosis risk in communities study. Diabetes Care. 2005;28:385–390. [DOI] [PubMed] [Google Scholar]
  • 7. Beltran‐Sanchez H, Harhay MO, Harhay MM, McElligott S. Prevalence and trends of metabolic syndrome in the adult U.S. population, 1999‐2010. J Am Coll Cardiol. 2013;62:697–703. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8. Sattar N, Gaw A, Scherbakova O, et al. Metabolic syndrome with and without C‐reactive protein as a predictor of coronary heart disease and diabetes in the West of Scotland Coronary Prevention Study. Circulation. 2003;108:414–419. [DOI] [PubMed] [Google Scholar]
  • 9. Suzuki T, Voeks J, Zakai NA, et al. Metabolic syndrome, C‐reactive protein, and mortality in U.S. Blacks and Whites: the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study. Diabetes Care. 2014;37:2284–2290. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10. Mancia G, Bombelli M, Facchetti R, et al. Long‐term risk of sustained hypertension in white‐coat or masked hypertension. Hypertension. 2009;54:226–232. [DOI] [PubMed] [Google Scholar]
  • 11. Cuspidi C, Sala C, Tadic M, Rescaldani M, Grassi G, Mancia G. Untreated masked hypertension and subclinical cardiac damage: a systematic review and meta‐analysis. Am J Hypertens. 2015;28:806–813. [DOI] [PubMed] [Google Scholar]
  • 12. Stergiou GS, Asayama K, Thijs L, et al. Prognosis of white‐coat and masked hypertension: international database of home blood pressure in relation to cardiovascular outcome. Hypertension. 2014;63:675–682. [DOI] [PubMed] [Google Scholar]
  • 13. Pierdomenico SD, Lapenna D, Bucci A, et al. Cardiovascular outcome in treated hypertensive patients with responder, masked, false resistant, and true resistant hypertension. Am J Hypertens. 2005;18:1422–1428. [DOI] [PubMed] [Google Scholar]
  • 14. Hanninen MR, Niiranen TJ, Puukka PJ, Jula AM. Metabolic risk factors and masked hypertension in the general population: the Finn‐Home study. J Hum Hypertens. 2014;28:421–426. [DOI] [PubMed] [Google Scholar]
  • 15. Asayama K, Sato A, Ohkubo T, et al. The association between masked hypertension and waist circumference as an obesity‐related anthropometric index for metabolic syndrome: the Ohasama study. Hypertens Res. 2009;32:438–443. [DOI] [PubMed] [Google Scholar]
  • 16. 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:S6‐4‐17. [PubMed] [Google Scholar]
  • 17. 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]
  • 18. Dubbert PM, Carithers T, Ainsworth BE, Taylor HA Jr, Wilson G, Wyatt SB. Physical activity assessment methods in the Jackson Heart Study. Ethn Dis. 2005;15:S6‐56‐61. [PubMed] [Google Scholar]
  • 19. 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]
  • 20. 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]
  • 21. Jackson Heart Study Protocol, Manual 4, Blood Pressure, Visit 1 (Version 1.0). Jackson MS: Jackson Heart Study Coordinating Center; 2001. [Cited: November 19, 2016]. Available in: https://www.jacksonheartstudy.org/Portals/0/pdf/manuals1/Blood_pressure_manual4_02-18-2001(1).pdf.
  • 22. Pickering TG, White WB. When and how to use self (home) and ambulatory blood pressure monitoring. J Am Soc Hypertens. 2008;2:119–124. [DOI] [PubMed] [Google Scholar]
  • 23. Axelson O, Fredriksson M, Ekberg K. Use of the prevalence ratio v the prevalence odds ratio as a measure of risk in cross sectional studies. Occup Environ Med. 1994;51:574. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 24. Coutinho LM, Scazufca M, Menezes PR. Methods for estimating prevalence ratios in cross‐sectional studies. Rev Saude Publica. 2008;42:992–998. [PubMed] [Google Scholar]
  • 25. White IR, Royston P, Wood AM. Multiple imputation using chained equations: issues and guidance for practice. Stat Med. 2011;30:377–399. [DOI] [PubMed] [Google Scholar]
  • 26. Sterne JA, White IR, Carlin JB, et al. Multiple imputation for missing data in epidemiological and clinical research: potential and pitfalls. BMJ. 2009;338:b2393. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27. Pierdomenico SD, Cuccurullo F. Ambulatory blood pressure monitoring in type 2 diabetes and metabolic syndrome: a review. Blood Press Monit. 2010;15:1–7. [DOI] [PubMed] [Google Scholar]
  • 28. Schillaci G, Pirro M, Vaudo G, et al. Prognostic value of the metabolic syndrome in essential hypertension. J Am Coll Cardiol. 2004;43:1817–1822. [DOI] [PubMed] [Google Scholar]
  • 29. Mancia G, Bombelli M, Corrao G, et al. Metabolic syndrome in the Pressioni Arteriose Monitorate E Loro Associazioni (PAMELA) study: daily life blood pressure, cardiac damage, and prognosis. Hypertension. 2007;49:40–47. [DOI] [PubMed] [Google Scholar]
  • 30. Pierdomenico SD, Lapenna D, Di Tommaso R, et al. Prognostic relevance of metabolic syndrome in hypertensive patients at low‐to‐medium risk. Am J Hypertens. 2007;20:1291–1296. [DOI] [PubMed] [Google Scholar]
  • 31. Leoncini G, Ratto E, Viazzi F, et al. Metabolic syndrome and ambulatory arterial stiffness index in non‐diabetic patients with primary hypertension. J Hum Hypertens. 2007;21:802–807. [DOI] [PubMed] [Google Scholar]
  • 32. Sheppard JP, Fletcher B, Gill P, Martin U, Roberts N, McManus RJ. Predictors of the home‐clinic blood pressure difference: a systematic review and meta‐analysis. Am J Hypertens. 2016;29:614–625. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 33. Redmond N, Booth JN 3rd, Tanner RM, et al. Prevalence of masked hypertension and its association with subclinical cardiovascular disease in African Americans: results from the Jackson Heart Study. J Am Heart Assoc. 2016;5:e002284. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 34. Viera AJ, Lin FC, Tuttle LA, et al. Levels of office blood pressure and their operating characteristics for detecting masked hypertension based on ambulatory blood pressure monitoring. Am J Hypertens. 2015;28:42–49. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 35. Booth JN 3rd, Muntner P, Diaz KM, et al. Evaluation of criteria to detect masked hypertension. J Clin Hypertens (Greenwich). 2016;18:1086–1094. doi: 10.1111/jch.12830 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 36. Shimbo D, Newman JD, Schwartz JE. Masked hypertension and prehypertension: diagnostic overlap and interrelationships with left ventricular mass: the Masked Hypertension Study. Am J Hypertens. 2012;25:664–671. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 37. Banegas JR, Ruilope LM, de la Sierra A, et al. High prevalence of masked uncontrolled hypertension in people with treated h ypertension. Eur Heart J. 2014;35:3304–3312. [DOI] [PubMed] [Google Scholar]
  • 38. Bromfield SG, Shimbo D, Bertoni AG, Sims M, Carson AP, Muntner P. Ambulatory blood pressure monitoring phenotypes among individuals with and without diabetes taking antihypertensive medication: the Jackson Heart Study. J Hum Hypertens. 2016;30:731–736. doi: 10.1038/jhh.2016.1027. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 39. Nwankwo T, Yoon SS, Burt V, Gu Q. Hypertension among adults in the United States: national health and nutrition examination survey, 2011‐2012. NCHS Data Brief. 2013;(133):1–8. [PubMed] [Google Scholar]
  • 40. Carson AP, Howard G, Burke GL, Shea S, Levitan EB, Muntner P. Ethnic differences in hypertension incidence among middle‐aged and older adults: the multi‐ethnic study of atherosclerosis. Hypertension. 2011;57:1101–1107. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 41. Howard VJ, Kleindorfer DO, Judd SE, et al. Disparities in stroke incidence contributing to disparities in stroke mortality. Ann Neurol. 2011;69:619–627. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 42. Movahed MR, John J, Hashemzadeh M, Jamal MM, Hashemzadeh M. Trends in the age adjusted mortality from acute ST segment elevation myocardial infarction in the United States (1988‐2004) based on race, gender, infarct location and comorbidities. Am J Cardiol. 2009;104:1030–1034. [DOI] [PubMed] [Google Scholar]
  • 43. United States Renal Data System . Incidence, Prevalence, Patient Characteristics, and Treatment Modalities. 2015 USRDS annual data report: Epidemiology of Kidney Disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2015.
  • 44. Booth JN 3rd, Diaz KM, Seals SR, et al. Masked hypertension and cardiovascular disease events in a prospective cohort of blacks: the Jackson Heart Study. Hypertension. 2016;68:501–510. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 45. Diaz KM, Veerabhadrappa P, Brown MD, Whited MC, Dubbert PM, Hickson DA. Prevalence, determinants, and clinical significance of masked hypertension in a population‐based sample of African Americans: the Jackson Heart Study. Am J Hypertens. 2015;28:900–908. [DOI] [PMC free article] [PubMed] [Google Scholar]

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