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(Hypertension. 2005;46:124.)
© 2005 American Heart Association, Inc.
Original Articles |
From the Heart Failure Research Unit (M.H.D., D.L.D.), Donald W. Reynolds Cardiovascular Clinical Research Center (M.H.D., D.L.D., R.G.V., R.M.P., C.K., F.K., D.W.), and Divisions of Cardiology (M.H.D., D.L.D., R.M.P., C.K., F.K., D.W.) and Hypertension (R.G.V.), Department of Internal Medicine University of Texas Southwestern Medical Center, Dallas; and the Department of Preventive Medicine and Epidemiology (R.S.C.), Loyola University, Maywood, Ill.
Reprint requests to Dr Mark Drazner, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9047. E-mail Mark.Drazner{at}utsouthwestern.edu
| Abstract |
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Key Words: hypertrophy ethnic groups epidemiology obesity
| Introduction |
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Another major limitation of previous studies comparing prevalent LVH in blacks and whites has been inadequate adjustment for body composition. Left ventricular (LV) mass is highly correlated with fat-free mass,8,9 yet fat-free mass has not been measured in previous large studies comparing the prevalence of LVH in blacks and whites.4,7,10 Further, these studies have not accounted for the potential impact of ethnic disparities in fat mass despite the increased rates of overweight and obesity among black women compared with their white counterparts.11
In part to overcome these limitations, we conducted the Dallas Heart Study, a random, population-based study of Dallas County.12 Participants underwent detailed phenotypic characterization including serial blood pressure measurements at home and in the clinic, ascertainment of socioeconomic status, cardiac MRI for measurement of LV mass, and assessment of body composition using dual-energy x-ray absorptiometry (DXA) scan. Herein we compare the prevalence of LVH in the 2 ethnic groups in the general population accounting for differences in body composition as well as traditional risk factors for LVH.
| Methods |
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Dallas Heart Study
The design and methodology of the Dallas Heart Study have been reported previously.12 In brief, we conducted a multistep probability sample of civilian, noninstitutionalized English- or Spanish-speaking Dallas County residents. Blacks were oversampled to ensure that they represented 50% of the final cohort. Eligible subjects were invited to participate in 3 stages of the project, including 2 home visits during which a survey was administered and blood and urine specimens were obtained and a third visit at the University of Texas at Southwestern Medical Center during which imaging studies were accomplished. In the present study, we restricted our analysis to those who had a cardiac MRI and self-identified themselves (see next section) as black (n=1335) or white (n=858). Eligible subjects who did versus did not complete the cardiac MRI had lower blood pressure and body mass index (see supplemental data, available online at http://www.hypertensionaha.org). Sampling weights reflecting the different probabilities of selection and sample attrition were constructed at each step so that inferences of our findings could be extrapolated back to the target population. Informed consent was obtained from all participants and the institutional review board of the University of Texas Southwestern Medical Center approved the study protocol.
Assignment of Race/Ethnicity
Subjects were asked in separate questions "Are you of Hispanic origin?" and "What is your primary racial or ethnic identity?" The following options were provided for the latter question: black/African American; white/Caucasian; American Indian, Alaska Native; Asian, Pacific Islander, East Indian; Other (Specify).
Blood Pressure
At each of the 3 visits (home visits 1 and 2 and visit 3 for imaging), 5 sets of blood pressure measurements were obtained using an automatic oscillometric device (Series 52 000; Welch Allyn) with an appropriately sized blood pressure cuff. This device has been validated against catheter measurement of arterial pressure.13 The blood pressure was considered the average of measurements 3 through 5 at each visit (total 9 readings).
Cardiac MRI
Details of the cardiac MRI protocol are available at http://www.hypertensionaha.org. In brief, we used short-axis, breath-hold, electrocardiographic-gated cine magnetic resonance images obtained from 2 comparable 1.5-T MRI systems (Philips Medical Systems). We manually traced the endocardial and epicardial borders of slices obtained from the apex to the base of the left ventricle to measure LV cavity and wall volume. Measurements from each slice were summed using the method of disks, and the papillary muscles were included in the myocardial mass. Interobserver difference for LV mass was 9.2±5 g (5.8±3.5%; n=15), intraobserver was 10.5±8.6 g (7.1±6.0%; n=8), and interscan variability was 4.9±10.9 g (2.9±7.5%; n=8).
Dual-Energy X-Ray Absorptiometry
DXA scans were performed using a dual-beam absorption energy unit (Delphi W unit; Hologic, Inc) bone densitometer in array mode.14,15 Oasis software (Hologic, Inc) was used to quantify body composition. Three quality controls were monitored routinely using a lumbar spine phantom 8362: bone mineral composition (g) with a coefficient of variation (CV) of 0.5%, bone mineral density (g/cm2) with a CV of 0.3%, and area (cm2) with a CV of 0.4%.
Defining LVH
We identified a healthy normotensive subpopulation of the Dallas Heart Study that was not overweight (n=380), as detailed at http://www.hypertension.org, and defined gender-specific values of LVH as the 97.5% percentile: LV mass/body surface area (BSA) 89 g/m2 (women) and 112 g/m2 (men); LV mass/height2.7 39 g/m2.7 (women) and 48 g/m2.7 (men); and LV mass/fat-free mass 3.7 g/kg (men and women).
Definitions
Hypertension was defined as an average systolic blood pressure from the 3 visits of
140 mm Hg or an average diastolic blood pressure of
90 mm Hg or if the participant self-reported antihypertensive therapy at the baseline visit. Obesity was defined as body mass index >30 kg/m2.
Statistics
Analyses were performed with SUDAAN to account for the complex study design and sampling weights, thereby allowing extrapolation of inferences from our study cohort back to the general population of Dallas County, as described previously in detail.12 Continuous variables were expressed as mean (SEM) and categorical variables as percentages. Differences in baseline characteristics between blacks and whites were compared with t test and
2 where appropriate. Frequency distributions of LV mass dichotomized by ethnicity were constructed. Comparisons were made between blacks and whites in the overall cohort for the prevalence of LVH. Similar analyses stratified by body mass index, age, systolic blood pressure, gender, and hypertension status were also performed. Multivariable linear and logistic regression models were constructed to determine whether socioeconomic status as assessed by educational status (completion of high school) and family income <$16 000 in a year confounded the association of ethnicity and LV mass and LVH. Additional covariates in multivariable models included systolic blood pressure, age, gender, fat-free mass, and fat mass. All models were restricted to participants who did not report taking antihypertensive therapy, except in subgroup analysis of hypertensive participants. Self-reported duration of hypertension was incorporated in another model of hypertensive participants.
| Results |
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The distribution of LV mass indexed to BSA in women (Figure 1A) and men (Figure 1B) dichotomized by ethnicity demonstrates a shift to the right (ie, increased LV mass) in blacks compared with whites. A similar shift to the right was seen when comparing the distribution of unindexed LV mass between the 2 ethnic groups stratified by gender (data not shown).
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Black women and men compared with whites had
2- to 3-fold higher prevalence of LVH (Table 2) whether LVH was defined by indexation to BSA, height2.7, or fat-free mass, although the latter was of marginal significance in men. To assess the impact of potential confounders on the comparative prevalence of LVH, analyses stratified by systolic blood pressure, body mass index, and age were conducted. In analyses stratified by blood pressure in participants not on antihypertensive therapy (Figure 2A), blacks with systolic blood pressure <120 mm Hg (n=354) did not have an increased prevalence of LVH as defined by indexation to BSA compared with whites (n=356). Similarly, blacks compared with whites with systolic blood pressure <140 mm Hg (n=689 and n=759, respectively) did not have an increased prevalence of LVH when defined by indexation by fat-free mass. In contrast, when LVH was defined by indexation to height2.7, the ethnic disparities persisted even in normotensive participants. In analyses stratified by body mass index (Figure 2B), blacks compared with whites had increased prevalence of LVH irrespective of body mass index, although the contrast in the normal weight participants did not reach statistical significance when LVH was defined by indexation to fat-free mass (P=0.2). In analyses stratified by age (Figure 2C), ethnic disparities were present in each age category when LVH was defined by BSA or height2.7, but only in participants
40 years when LVH was defined by indexation to fat-free mass.
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In comparing LV mass in blacks and whites in unadjusted linear regression analysis, black ethnicity was associated with increased LV mass (Table 3). In multivariable linear regression models that adjusted for systolic blood pressure, fat-free mass, fat mass, and gender, black ethnicity was associated with an increase of
4 g of LV mass (model 1). This association persisted after adjustment for measures of socioeconomic status and diabetes mellitus (model 2; Table 3). In subgroup analysis using multivariable models with the same covariates as above (in model 1), black ethnicity remained associated with LV mass in hypertensive participants (n=974) but not in normotensive (n=1219) participants. Black ethnicity remained independently associated with LV mass among the hypertensive subjects either when self-reported duration of hypertension was added to the model (black ß-coefficient 12; P=0.002) or when hypertensive subjects on therapy were excluded (black ß-coefficient 12; P=0.03).
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In unadjusted logistic regression analysis restricted to participants off antihypertensive therapy, black ethnicity was associated with LVH whether indexed to BSA or height2.7 (Table 3). The odds ratio for LVH when defined by indexation to fat-free mass was 1.7 (0.9 to 3.4; P=0.1). In multivariable logistic regression, which adjusted for body composition, black ethnicity was associated with a
2-fold increased relative risk of LVH whether defined by indexation to BSA or height2.7, although when indexed to BSA, this association did not achieve conventional threshold levels of statistical significance. In subgroup analysis, black ethnicity remained associated with LVH in those with hypertension, whereas this association was less robust in the normotensive participants.
| Discussion |
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Our criteria for LVH are lower than those reported previously by echocardiography,1822 possibly because cardiac MRI estimates of LV mass are lower than those obtained by echocardiography6,23,24 or because of the selection of the controls used to define LVH. In contrast, our criteria for LVH (indexed to BSA) are higher than those reported by the Framingham Heart Study using cardiac MRI,24 although their assessment of LV mass excluded the papillary muscles, whereas ours did not.
Given the relative insensitivity of electrocardiography for diagnosing LVH,25 it is worthwhile to focus on the available echocardiographic studies that compare the prevalence of LVH in blacks versus whites. In 1998, a meta-analysis of such studies reported that LV wall thickness but not LV mass was consistently increased in blacks when compared with whites. After that report, a number of large studies have readdressed this question, with most4,7,10 but not all26 reporting an increase in LV mass and prevalent LVH in blacks compared with whites. Also comparable to our findings (Table 2), LVH defined by indexation to height2.7 was alarmingly prevalent in middle-aged blacks in the Jackson cohort of the Atherosclerosis Risk in Communities Study (37% of men and 41% of women).27
Previous studies have demonstrated the importance of obesity as measured by body mass index as a risk factor for LVH when defined by indexation to height.2831 Because blacks have higher rates of overweight and obesity than whites,11 it was important to determine whether differences in body composition may account for the purported differences in prevalent LVH between the 2 ethnic groups. We find that black men and women compared with whites still have
2- to 3-fold increased prevalence of LVH as defined by indexation to fat-free mass (Table 2). Further, disparities in prevalent LVH largely persist despite adjustment for fat mass and fat-free mass in multivariable models (Table 3), demonstrating that differences in body composition between blacks and whites are not the sole explanation for ethnic disparities in LV mass. Nevertheless, given that height-indexed LVH has been demonstrated to convey prognostic information in blacks22 and that there is a marked association of obesity and height-indexed LVH (Figure 2B), the critical need to reduce obesity in blacks to improve cardiovascular outcomes is clear.
Several lines of data herein suggest that the ethnic disparities in LV mass are mediated in large part via differences in blood pressure. Blacks compared with whites had an increase in the ratio of LV mass to end-diastolic volume (concentricity; Table 1). This pattern of hypertrophy would be expected in response to a pressure load on the ventricle. Second, when the cohort was stratified by systolic blood pressure, the prevalence of LVH was similar in the 2 ethnic groups in subjects with systolic blood pressure <120 mm Hg when LVH was defined by indexation to BSA and in those subjects with systolic blood pressure <140 mm Hg when LVH was defined by indexation to fat-free mass (Figure 2A). Third, in multivariable regression analysis, the association of black ethnicity and LV mass and LVH was more robust in the hypertensive than in the nonhypertensive participants.
Limitations
Subjects who did not versus did undergo cardiac MRI were older and had a higher BMI and systolic blood pressure, highlighting the potential limitations of cardiac MRI in assessing a high-risk, obese population. However, because obesity is more common in black than white women, and obesity is associated with increased LV mass, the true ethnic disparity in LVH in the population is likely underestimated rather than overestimated by our study.
Perspectives
In the first population-based study using cardiac MRI, we found that blacks compared with whites have increased LV mass and
2- to 3-fold higher prevalence of LVH in Dallas County. Although blacks and whites have significant differences in fat mass and fat-free mass, we demonstrated for the first time that the ethnic disparities in LV mass persist despite adjustment for such measures of body composition. Given that ethnic disparities in prevalent LVH were dramatically reduced in those subjects with systolic blood pressure <120 mm Hg (LVH indexed to BSA) or <140 mm Hg (LVH indexed to fat-free mass), these epidemiological data emphasize the need in blacks to achieve target levels of blood pressure control and possibly lower blood pressure, raising the provocative concept of whether ethnic-specific criteria for initiation and target goal of antihypertensive therapy are appropriate. Such recommendations would require testing in prospective clinical trials. Nevertheless, these data emphasize that aggressive treatment of hypertensive heart disease in blacks is urgently needed to improve cardiovascular outcomes in this ethnic group.
| Acknowledgments |
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Received January 31, 2005; first decision February 23, 2005; accepted April 1, 2005.
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