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Hypertension. 2005;46:124-129
Published online before print June 6, 2005, doi: 10.1161/01.HYP.0000169972.96201.8e
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(Hypertension. 2005;46:124.)
© 2005 American Heart Association, Inc.


Original Articles

Left Ventricular Hypertrophy Is More Prevalent in Blacks Than Whites in the General Population

The Dallas Heart Study

Mark H. Drazner; Daniel L. Dries; Ronald M. Peshock; Richard S. Cooper; Chris Klassen; Farhana Kazi; DuWayne Willett; Ronald G. Victor

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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*Abstract
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Although recent studies have suggested that blacks compared with whites have an increased prevalence of left ventricular hypertrophy, it remains uncertain whether this is true despite adjustment for body composition (fat mass and fat-free mass) and when assessed by cardiac MRI in the general population. The Dallas Heart Study is a population-based study of Dallas County in which 1335 black and 858 white participants 30 to 67 years of age underwent detailed assessment including dual-energy x-ray absorptiometry scan to measure body composition and cardiac MRI. Left ventricular hypertrophy, whether defined by indexation to body surface area (P<0.001), fat-free mass (P=0.002), or height2.7 (P<0.001) was 2- to 3-fold more common in black versus white women. Similar results were seen when comparing black and white men (P<0.001 when left ventricular hypertrophy was indexed to body surface area or height2.7 and P=0.05 when indexed to fat-free mass). Ethnic disparities in left ventricular mass persisted in multivariable models despite adjustment for fat mass, fat-free mass, systolic blood pressure, age, gender, and measures of socioeconomic status. We conclude that blacks compared with whites have increased left ventricular mass and a 2- to 3-fold higher prevalence of left ventricular hypertrophy in the general population, as assessed by cardiac MRI. The ethnic differences in left ventricular mass are independent of differences in body composition.


Key Words: hypertrophy • ethnic groups • epidemiology • obesity


*    Introduction
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Major efforts are under way to reduce disparities in health outcomes between blacks and whites.1 Because left ventricular hypertrophy (LVH) is associated with adverse cardiovascular outcomes and overall mortality,2,3 it is important to know whether, to what extent, and why LVH is more prevalent among blacks compared with whites. Previous studies addressing these questions have had important limitations, including being based on highly selected cohorts that may not represent the general population,4 by relying on electrocardiography or echocardiography, which are not as accurate as cardiac MRI,5,6 and by not adequately adjusting for the disparities in socioeconomic status between blacks and whites, which may confound a potential association of ethnicity and LVH.7

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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*Methods
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For additional details regarding methods, please see http://www.hypertensionaha.org.

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 {chi}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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*Results
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There were many differences in baseline characteristics between black and white participants (Table 1). Compared with whites, blacks had higher systolic blood pressure, LV mass (crude and indexed), LV concentricity (LV mass/end-diastolic volume), more prevalent hypertension, and lower socioeconomic status as measured by income, perceived financial strain, and achievement of educational level beyond high school. Black compared with white women were younger but had a higher body mass index, fat-free mass, and fat mass and were more likely to have diabetes. Black men had a higher fat-free mass but lower fat mass than white men.


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TABLE 1. Baseline Characteristics*

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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Figure 1. Frequency distribution of LV mass indexed to BSA in black vs white women (A) and men (B). LV mass was measured by cardiac MRI.

Black women and men compared with whites had {approx}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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TABLE 2. Prevalence of LVH in Black and White Residents of Dallas County, Ages 30 to 65*



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Figure 2. Prevalence of LV hypertrophy, defined by indexation to BSA, fat-free mass (FFM), or height2.7 in black vs white participants of the Dallas Heart Study stratified by systolic blood pressure (SBP; A), body mass index (B), or age (C). LV hypertrophy was defined as BSA 89 g/m2 (women) and 112 g/m2 (men); FFM 3.7 g/kg, or height2.7 39 g/m2.7 (women) and 48 g/m2.7 (men). Subjects with self-reported hypertensive therapy were excluded in the analysis stratified by systolic blood pressure. {dagger}P=0.06; *P<0.05; **P<0.01; ***P<0.001.

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 {approx}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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TABLE 3. Association of Black Ethnicity With LV Mass and LVH in Multivariable Models

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 {approx}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
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
The Dallas Heart Study is the first population-based study using cardiac MRI as well as detailed assessment of body composition to compare LV mass and prevalent LVH in blacks and whites. The major findings of this study are that blacks compared with whites in Dallas County have increased LV mass and 2- to 3-fold higher prevalence of LVH. These differences largely persisted after adjusting for traditional risk factors of increased LV mass as well as for body composition (fat-free mass and fat mass) in multivariable analysis and were particularly robust in the subgroup of participants with hypertension. Because blacks do not appear to have an increased coronary atherosclerotic burden compared with whites in this population,16 the disparities in LV mass and LVH are likely to explain a large part of the increased cardiovascular mortality17 endured by blacks.

Our criteria for LVH are lower than those reported previously by echocardiography,18–22 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.28–31 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 {approx}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 {approx}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
 
The Dallas Heart Study is funded by a center grant from the Donald W. Reynolds Foundation. M.H.D. was the recipient of a Doris Duke clinical scientist development award from the Doris Duke Charitable Foundation (New York, NY).

Received January 31, 2005; first decision February 23, 2005; accepted April 1, 2005.


*    References
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up arrowAbstract
up arrowIntroduction
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up arrowResults
up arrowDiscussion
*References
 
1. Department of Health and Human Services. Healthy People 2010: Understanding and Improving Health. 2nd ed. Washington DC: Government Printing Office; 2000.

2. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med. 1990; 322: 1561–1566.[Abstract]

3. Drazner MH, Rame JE, Marino EK, Gottdiener JS, Kitzman DW, Gardin JM, Manolio TA, Dries DL, Siscovick DS. Increased left ventricular mass is a risk factor for the development of a depressed left ventricular ejection fraction within five years: the Cardiovascular Health Study. J Am Coll Cardiol. 2004; 43: 2207–2215.[Abstract/Free Full Text]

4. Kizer JR, Arnett DK, Bella JN, Paranicas M, Rao DC, Province MA, Oberman A, Kitzman DW, Hopkins PN, Liu JE, Devereux RB. Differences in left ventricular structure between black and white hypertensive adults: the Hypertension Genetic Epidemiology Network Study. Hypertension. 2004; 43: 1182–1188.[Abstract/Free Full Text]

5. Grothues F, Smith GC, Moon JC, Bellenger NG, Collins P, Klein HU, Pennell DJ. Comparison of interstudy reproducibility of cardiovascular magnetic resonance with two-dimensional echocardiography in normal subjects and in patients with heart failure or left ventricular hypertrophy. Am J Cardiol. 2002; 90: 29–34.[CrossRef][Medline] [Order article via Infotrieve]

6. Bottini PB, Carr AA, Prisant LM, Flickinger FW, Allison JD, Gottdiener JS. Magnetic resonance imaging compared to echocardiography to assess left ventricular mass in the hypertensive patient. Am J Hypertens. 1995; 8: 221–228.[CrossRef][Medline] [Order article via Infotrieve]

7. Rodriguez CJ, Sciacca RR, Diez-Roux AV, Boden-Albala B, Sacco RL, Homma S, DiTullio MR. Relation between socioeconomic status, race-ethnicity, and left ventricular mass: the Northern Manhattan Study. Hypertension. 2004; 43: 775–779.[Abstract/Free Full Text]

8. Bella JN, Devereux RB, Roman MJ, O’Grady MJ, Welty TK, Lee ET, Fabsitz RR, Howard BV. Relations of left ventricular mass to fat-free and adipose body mass: the strong heart study. The Strong Heart Study Investigators. Circulation. 1998; 98: 2538–2544.[Abstract/Free Full Text]

9. Whalley GA, Gamble GD, Doughty RN, Culpan A, Plank L, MacMahon S, Sharpe N. Left ventricular mass correlates with fat-free mass but not fat mass in adults. J Hypertens. 1999; 17: 569–574.[CrossRef][Medline] [Order article via Infotrieve]

10. Lorber R, Gidding SS, Daviglus ML, Colangelo LA, Liu K, Gardin JM. Influence of systolic blood pressure and body mass index on left ventricular structure in healthy African-American and white young adults: the CARDIA study. J Am Coll Cardiol. 2003; 41: 955–960.[Abstract/Free Full Text]

11. American Heart Association. Statistical Fact Sheet—Populations. African Americans and Cardiovascular Diseases. 2003; 1–8.

12. Victor RG, Haley RW, Willett DL, Peshock RM, Vaeth PC, Leonard D, Basit M, Cooper RS, Iannacchione VG, Visscher WA, Staab JM, Hobbs HH. The Dallas Heart Study: a population-based probability sample for the multidisciplinary study of ethnic differences in cardiovascular health. Am J Cardiol. 2004; 93: 1473–1480.[CrossRef][Medline] [Order article via Infotrieve]

13. O’Brien E, Mee F, Atkins N, O’Malley K. Inaccuracy of seven popular sphygmomanometers for home measurement of blood pressure. J Hypertens. 1990; 8: 621–634.[CrossRef][Medline] [Order article via Infotrieve]

14. Kelly TL, Berger N, Richardson TL. DXA body composition: theory and practice. Appl Radiat Isot. 1998; 49: 511–513.[CrossRef][Medline] [Order article via Infotrieve]

15. Salamone LM, Fuerst T, Visser M, Kern M, Lang T, Dockrell M, Cauley JA, Nevitt M, Tylavsky F, Lohman TG. Measurement of fat mass using DEXA: a validation study in elderly adults. J Appl Physiol. 2000; 89: 345–352.[Abstract/Free Full Text]

16. Jain T, Peshock R, McGuire DK, Willett D, Yu Z, Vega GL, Guerra R, Hobbs HH, Grundy SM. African Americans and Caucasians have a similar prevalence of coronary calcium in the Dallas Heart Study. J Am Coll Cardiol. 2004; 44: 1011–1017.[Abstract/Free Full Text]

17. NCHS. Health, United States, 2003 with Chartbook on Trends in the Health of Americans (Table 36). National Center for Health Statistics. Available at: http://www.cdc.gov/nchs/data/hus/tables/2003/03hus036.pdf. Accessed July 6, 2004.

18. Wachtell K, Bella JN, Liebson PR, Gerdts E, Dahlof B, Aalto T, Roman MJ, Papademetriou V, Ibsen H, Rokkedal J, Devereux RB. Impact of different partition values on prevalences of left ventricular hypertrophy and concentric geometry in a large hypertensive population: the LIFE Study. Hypertension. 2000; 35: 6–12.[Abstract/Free Full Text]

19. Palmieri V, de Simone G, Arnett DK, Bella JN, Kitzman DW, Oberman A, Hopkins PN, Province MA, Devereux RB. Relation of various degrees of body mass index in patients with systemic hypertension to left ventricular mass, cardiac output, and peripheral resistance (The Hypertension Genetic Epidemiology Network Study). Am J Cardiol. 2001; 88: 1163–1168.[CrossRef][Medline] [Order article via Infotrieve]

20. Liao Y, Cooper RS, Durazo-Arvizu R, Mensah GA, Ghali JK. Prediction of mortality risk by different methods of indexation for left ventricular mass. J Am Coll Cardiol. 1997; 29: 641–647.[Abstract]

21. de Simone G, Devereux RB, Daniels SR, Koren MJ, Meyer RA, Laragh JH. Effect of growth on variability of left ventricular mass: assessment of allometric signals in adults and children and their capacity to predict cardiovascular risk. J Am Coll Cardiol. 1995; 25: 1056–1062.[Abstract]

22. Nunez E, Arnett DK, Benjamin EJ, Liebson PR, Skelton TN, Taylor H, Andrew M. Optimal threshold value for left ventricular hypertrophy in blacks: the Atherosclerosis Risk in Communities Study. Hypertension. 2005; 45: 58–63.[Abstract/Free Full Text]

23. Missouris CG, Forbat SM, Singer DR, Markandu ND, Underwood R, MacGregor GA. Echocardiography overestimates left ventricular mass: a comparative study with magnetic resonance imaging in patients with hypertension. J Hypertens. 1996; 14: 1005–1010.[Medline] [Order article via Infotrieve]

24. Salton CJ, Chuang ML, O’Donnell CJ, Kupka MJ, Larson MG, Kissinger KV, Edelman RR, Levy D, Manning WJ. Gender differences and normal left ventricular anatomy in an adult population free of hypertension. A cardiovascular magnetic resonance study of the Framingham Heart Study Offspring cohort. J Am Coll Cardiol. 2002; 39: 1055–1060.[Abstract/Free Full Text]

25. Reichek N, Devereux RB. Left ventricular hypertrophy: relationship of anatomic, echocardiographic and electrocardiographic findings. Circulation. 1981; 63: 1391–1398.[Abstract/Free Full Text]

26. Rautaharju PM, Park LP, Gottdiener JS, Siscovick D, Boineau R, Smith V, Powe NR. Race- and sex-specific ECG models for left ventricular mass in older populations. Factors influencing overestimation of left ventricular hypertrophy prevalence by ECG criteria in African-Americans. J Electrocardiol. 2000; 33: 205–218.[CrossRef][Medline] [Order article via Infotrieve]

27. Skelton TN, Andrew ME, Arnett DK, Burchfiel CM, Garrison RJ, Samdarshi TE, Taylor HA, Hutchinson RG. Echocardiographic left ventricular mass in African-Americans: the Jackson cohort of the Atherosclerosis Risk in Communities Study. Echocardiography. 2003; 20: 111–120.[CrossRef][Medline] [Order article via Infotrieve]

28. de Simone G, Palmieri V, Bella JN, Celentano A, Hong Y, Oberman A, Kitzman DW, Hopkins PN, Arnett DK, Devereux RB. Association of left ventricular hypertrophy with metabolic risk factors: the HyperGEN Study. J Hypertens. 2002; 20: 323–331.[CrossRef][Medline] [Order article via Infotrieve]

29. Lauer MS, Anderson KM, Levy D. Separate and joint influences of obesity and mild hypertension on left ventricular mass and geometry: the Framingham Heart Study. J Am Coll Cardiol. 1992; 19: 130–134.[Abstract]

30. Gottdiener JS, Reda DJ, Materson BJ, Massie BM, Notargiacomo A, Hamburger RJ, Williams DW, Henderson WG. Importance of obesity, race and age to the cardiac structural and functional effects of hypertension. The Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents. J Am Coll Cardiol. 1994; 24: 1492–1498.[Abstract]

31. Fox E, Taylor H, Andrew M, Han H, Mohamed E, Garrison R, Skelton T. Body mass index and blood pressure influences on left ventricular mass and geometry in African Americans: The Atherosclerotic Risk in Communities (ARIC) Study. Hypertension. 2004; 44: 55–60.[Abstract/Free Full Text]


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G. E. Peterson, T. de Backer, A. Gabriel, V. Ilic, T. Vagaonescu, L. J. Appel, G. Contreras, C. Kendrick, S. Rostand, R. A. Phillips, et al.
Prevalence and Correlates of Left Ventricular Hypertrophy in the African American Study of Kidney Disease Cohort Study
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S. K. Mehta, J. E. Rame, A. Khera, S. A. Murphy, R. M. Canham, R. M. Peshock, J. A. de Lemos, and M. H. Drazner
Left Ventricular Hypertrophy, Subclinical Atherosclerosis, and Inflammation
Hypertension, June 1, 2007; 49(6): 1385 - 1391.
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T. Omland, M. H. Drazner, T. Ueland, M. Abedin, S. A. Murphy, P. Aukrust, and J. A. de Lemos
Plasma Osteoprotegerin Levels in the General Population: Relation to Indices of Left Ventricular Structure and Function
Hypertension, June 1, 2007; 49(6): 1392 - 1398.
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J. E. Rame, M. H. Drazner, W. Post, R. Peshock, J. Lima, R. S. Cooper, and D. L. Dries
Corin I555(P568) Allele Is Associated With Enhanced Cardiac Hypertrophic Response to Increased Systemic Afterload
Hypertension, April 1, 2007; 49(4): 857 - 864.
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J Am Coll CardiolHome page
R. M. Canham, S. R. Das, D. Leonard, S. M. Abdullah, S. K. Mehta, A. K. Chung, J.-L. Li, R. G. Victor, R. J. Auchus, and M. H. Drazner
{alpha}2cDel322-325 and {beta}1Arg389 Adrenergic Polymorphisms Are Not Associated With Reduced Left Ventricular Ejection Fraction or Increased Left Ventricular Volume
J. Am. Coll. Cardiol., January 16, 2007; 49(2): 274 - 276.
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A. Y. Chang, S. M. Abdullah, T. Jain, H. G. Stanek, S. R. Das, D. K. McGuire, R. J. Auchus, and J. A. de Lemos
Associations Among Androgens, Estrogens, and Natriuretic Peptides in Young Women: Observations From the Dallas Heart Study
J. Am. Coll. Cardiol., January 2, 2007; 49(1): 109 - 116.
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J.-L. Li, R. M. Canham, W. Vongpatanasin, D. Leonard, R. J. Auchus, and R. G. Victor
Do Allelic Variants in {alpha}2A and {alpha}2C Adrenergic Receptors Predispose to Hypertension in Blacks?
Hypertension, June 1, 2006; 47(6): 1140 - 1146.
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T. W. Wallace, S. M. Abdullah, M. H. Drazner, S. R. Das, A. Khera, D. K. McGuire, F. Wians, M. S. Sabatine, D. A. Morrow, and J. A. de Lemos
Prevalence and Determinants of Troponin T Elevation in the General Population
Circulation, April 25, 2006; 113(16): 1958 - 1965.
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A. K. Chung, S. R. Das, D. Leonard, R. M. Peshock, F. Kazi, S. M. Abdullah, R. M. Canham, B. D. Levine, and M. H. Drazner
Women Have Higher Left Ventricular Ejection Fractions Than Men Independent of Differences in Left Ventricular Volume: The Dallas Heart Study
Circulation, March 28, 2006; 113(12): 1597 - 1604.
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S. R. Das, M. H. Drazner, D. L. Dries, G. L. Vega, H. G. Stanek, S. M. Abdullah, R. M. Canham, A. K. Chung, D. Leonard, F. H. Wians Jr, et al.
Impact of Body Mass and Body Composition on Circulating Levels of Natriuretic Peptides: Results From the Dallas Heart Study
Circulation, October 4, 2005; 112(14): 2163 - 2168.
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M. H. Drazner
The Transition From Hypertrophy to Failure: How Certain Are We?
Circulation, August 16, 2005; 112(7): 936 - 938.
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G. de Simone
Left Ventricular Hypertrophy in Blacks and Whites: Different Genes or Different Exposure?
Hypertension, July 1, 2005; 46(1): 23 - 24.
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