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Hypertension. 2004;43:1160-1161
Published online before print May 3, 2004, doi: 10.1161/01.HYP.0000128740.68851.8a
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(Hypertension. 2004;43:1160.)
© 2004 American Heart Association, Inc.


Editorial Commentaries

Left Ventricular Hypertrophy Is More Common in Black than White Hypertensives: Is This News?

Mark H. Drazner

From the Heart Failure Research Unit, Donald W. Reynolds Cardiovascular Clinical Research Center, Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas.

Correspondence to Dr Mark Drazner, University of Texas Southwestern Medical Center, Dallas, TX 75390-9047. E-mail Mark.Drazner{at}utsouthwestern.edu

It is often stated that left ventricular hypertrophy (LVH) is more common in blacks than in whites.1,2 Given that hypertension and hypertensive complications such as stroke and end-stage renal disease are more common in blacks than whites,3 it would be surprising if LVH was also not more common in blacks. Why then is the study by Kizer4 in this issue of Hypertension newsworthy?

First, it is important to recognize that LVH is an important cardiovascular phenotype. It has been shown to be associated with an increased risk for a number of adverse clinical outcomes including heart failure, incident coronary artery disease, stroke, arrhythmia, and mortality.5 Thus, understanding whether ethnic disparities in LVH do exist has clear public health implications, especially as vigorous attempts are made to understand and eliminate the increased cardiovascular mortality endured by black men and women as compared with their white counterparts.

Next, it is important to critically assess the data which support the claim that LVH is known to be more common in blacks than whites. In 1998, Deveraux and colleagues in a meta-analysis of the 9 prior echocardiographic studies that addressed black-white disparities in LVH in hypertensives concluded that left ventricular wall thickness but not left ventricular mass was consistently increased in blacks as compared with whites.6 In addition, the individual studies on which the meta-analysis was based were often small convenience samples and thus were likely not to be representative of the general population.

Since then, several studies have again addressed the issue of ethnic disparity in LVH. For example, a study of 408 subjects recruited from a hypertension clinic found that LVH was more common in blacks (50%) than in whites (33%).7 In 687 children followed longitudinally with echocardiography, blacks had higher left ventricular mass than whites in early adulthood.8 In contrast, in 332 white and 112 black participants of the Hypertension Optimal Treatment study, there were no significant ethnic differences in left ventricular mass indexed to body surface area.9

Two other studies merit special attention. The Coronary Artery Disease Risk Development in Young Adults (CARDIA) Study, a National Heart, Lung, and Blood Institute–sponsored prospective epidemiological study of black and white young adults, found increased left ventricular mass in blacks as compared with whites in a cohort of approximately 4000 subjects.10 Additionally, the CARDIA year 10 follow-up study of 669 blacks and 949 whites found a higher prevalence of LVH among blacks than whites, but there were only {approx}30 total cases of LVH in both groups,11 which questions the strength of that conclusion. The Atherosclerosis Risk in Communities (ARIC) Study also recently reported their findings based on M-mode echocardiographic examinations of 1730 subjects performed in Jackson, Mississippi, between 1993 and 1996.12 LVH was extremely common in their cohort of middle-aged blacks, with estimates ranging in male hypertensives from 35% (LVH defined by indexation to body surface area) to 56% (LVH defined by indexation to height2.7). The comparable estimates of LVH prevalence were even higher in hypertensive women, ranging from 64% to 79%. However, because this study cohort was entirely black, it was not possible to determine whether there was an ethnic disparity in LVH in this community. Thus, despite increasingly suggestive data, the question as to whether LVH is more common in blacks than whites remains open.

The present study by Kizer and colleagues,4 an analysis of the Hypertension Genetic Epidemiology Network (HyperGEN) Study, is therefore of interest. In previous HyperGEN analyses, black race was reported to be associated with increased left ventricular mass and prevalent LVH13,14 but those studies focused on other risk factors for increased left ventricular mass and did not address the association of ethnicity and LVH in detail. In contrast, the present report now focuses directly on this issue. Kizer and colleagues find substantial differences between blacks and whites in cardiac structure including blacks having increased left ventricular mass, posterior and septal wall thickness, and relative wall thickness. The differences in left ventricular mass and relative wall thickness persisted in multivariable models that adjusted for important confounders. Although the crude prevalence of LVH in each ethnic group was not reported, the adjusted odds ratio for LVH associated with black race was 1.8 (LVH as defined by indexation to height2.7) to 2.5 (LVH as defined by indexation to body surface area). Additionally, the multivariable-adjusted left ventricular internal dimension was smaller in blacks than whites, confirming the predominance of concentric and not eccentric LVH, a pattern that would be expected if LVH was a consequence of hypertension. In total, these data provide important support to the contention that hypertensive blacks have increased left ventricular mass and more prevalent LVH than white hypertensives.

There are some caveats to the conclusions of this study. First, there is a concern regarding the generalizability of its findings given the patient population studied. Specifically, HyperGEN used a sib-pair design that required 2 or more siblings to have hypertension of onset by the age of 60. If such criteria identified hypertensives uniquely susceptible to LVH and had this unintended effect disproportionately in blacks, then the estimate of the comparative prevalence of LVH in blacks to whites in this study may be biased as compared with the general population. It is also difficult to discern how often LVH was present in both members of the black sibships and the white sibships, data which may have provided insights into the potential bias introduced by the study design. Although the investigators adjusted for relatedness using statistical methodology, it is not clear whether this approach is sufficiently robust to yield estimates that are reflective of the general hypertensive population. Another concern is whether adequate adjustment for socioeconomic status was performed. The single measure adjusted for in multivariable models was attainment of at least 4 years of college, which may not be sufficient to address differences between the 2 ethnic groups at the lower end of the socioeconomic spectrum.

Despite these concerns, the study by Kizer et al contributes important information as to whether LVH is more common in black than white hypertensives. In this particular case, it appears that a widely held perception based on limited data will in the end prove correct. Two recently completed studies that performed cardiac MRI in large numbers of blacks and whites, the Dallas Heart Study15 and the Multi-Ethnic Study of Atherosclerosis,16 should provide additional data to answer this important question in the near future.

Acknowledgments

M.H.D. received support from the Donald W. Reynolds Cardiovascular Clinical Research Center, Dallas, Texas, and was the recipient of a Clinical Scientist Development Award from the Doris Duke Charitable Foundation.

Footnotes

The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.

References

1. Lenfant C. Report of the NHLBI working group on research in coronary heart disease in blacks. Circulation. 1994; 90: 1613–1623.[Free Full Text]

2. Yancy CW, Strong M. The natural history, epidemiology, and prognosis of heart failure in African Americans. Congest Heart Fail. 2004; 10: 15–18.[Medline] [Order article via Infotrieve]

3. American Heart Association. Statistical fact sheet-populations. African Americans and Cardiovascular Diseases. 2003: 1–8.

4. Kizer J, 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 (HyperGEN) study. Hypertension. 2004; 43: 1182–1188.[Abstract/Free Full Text]

5. Levy D. Left ventricular hypertrophy risk. In: Izzo J, Black, HR, eds. Hypertension Primer. Third ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2003: 243–246.

6. Devereux RB, Okin PM, Roman MJ. Pre-clinical cardiovascular disease and surrogate end-points in hypertension: does race influence target organ damage independent of blood pressure? Ethn Dis. 1998; 8: 138–148.[Medline] [Order article via Infotrieve]

7. Chapman JN, Mayet J, Chang CL, Foale RA, Thom SA, Poulter NR. Ethnic differences in the identification of left ventricular hypertrophy in the hypertensive patient. Am J Hypertens. 1999; 12: 437–442.[CrossRef][Medline] [Order article via Infotrieve]

8. Dekkers C, Treiber FA, Kapuku G, Van Den Oord EJ, Snieder H. Growth of left ventricular mass in African American and European American youth. Hypertension. 2002; 39: 943–951.[Abstract/Free Full Text]

9. Zabalgoitia M, Ur Rahman SN, Haley WE, Oneschuk L, Yunis C, Lucas C, Yarows S, Krause L, Amerena J. Impact of ethnicity on left ventricular mass and relative wall thickness in essential hypertension. Am J Cardiol. 1998; 81: 412–417.[CrossRef][Medline] [Order article via Infotrieve]

10. Gardin JM, Wagenknecht LE, Anton-Culver H, Flack J, Gidding S, Kurosaki T, Wong ND, Manolio TA. Relationship of cardiovascular risk factors to echocardiographic left ventricular mass in healthy young black and white adult men and women. The CARDIA study. Circulation. 1995; 92: 380–387.[Abstract/Free Full Text]

11. 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]

12. 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]

13. al’Absi M, Devereux RB, Lewis CE, Kitzman DW, Rao DC, Hopkins P, Markovitz J, Arnett DK. Blood pressure responses to acute stress and left ventricular mass (The Hypertension Genetic Epidemiology Network Study). Am J Cardiol. 2002; 89: 536–540.[CrossRef][Medline] [Order article via Infotrieve]

14. 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]

15. Victor R, Haley, RW, Willett, D, Peshock, R, Vaeth, P, Leonard, D, Basit, M, Cooper, R, Iannacchione, VG, Visscher, W, Staab, J, Hobbs, HH. A population-based probability sample for the multidisciplinary study of ethnic disparities in cardiovascular disease: Recruitment and validation in the Dallas Heart Study. Am J Cardiol. In press.

16. Bild DE, Bluemke DA, Burke GL, Detrano R, Diez Roux AV, Folsom AR, Greenland P, Jacob DR, Jr., Kronmal R, Liu K, Nelson JC, O’Leary D, Saad MF, Shea S, Szklo M, Tracy RP. Multi-ethnic study of atherosclerosis: objectives and design. Am J Epidemiol. 2002; 156: 871–881.[Abstract/Free Full Text]




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Left Ventricular Hypertrophy in Blacks and Whites: Different Genes or Different Exposure?
Hypertension, July 1, 2005; 46(1): 23 - 24.
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