An Update on Hypertension among African-Americans

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US Cardiology, 2007;4(1):81-4


Hypertension is a major contributor to the global disease burden and is one of the leading preventable causes of premature death worldwide.1 In the US, a disproportionate burden of hypertension and its associated complications—including coronary heart disease, heart failure, stroke, and end-stage renal disease and cardiovascular disease mortality—affect African-Americans (also referred to as US blacks).2 This excess burden of hypertension among African-Americans has been recognized since early in the 1900s and explains a substantial portion of health disparities in this population.3–5 The goal of this review is to provide an update of the current research on hypertension in African-Americans through a brief description of the epidemiology, pathophysiology, and management of hypertension.


The rates of hypertension in various populations of African ancestry have geographical variances related to high sodium intake, low potassium intake, obesity, and inactivity. As such, African-Americans have one of the highest rates of hypertension worldwide—much higher than other populations of African origin.6 Compared with white Americans, hypertension is not only more prevalent in this population, it is also observed at an earlier age, has greater severity, and is accompanied by a disproportionate level of target organ damage (1.8-fold higher rate of stroke, 4.2-fold higher rate of end-stage renal disease, 1.7-fold higher rate of heart failure, 1.5-fold higher rate of coronary heart disease mortality).2
Hypertension represents a risk across the lifespan. Perhaps the most alarming epidemiological data regarding hypertension among African- Americans come from studies of children and adolescents. Data from the Bogalusa Heart Study, a bi-racial cohort study conducted in the state of Louisiana including approximately 3,500 school-age children, demonstrate that beginning at age 10, African-American children had significantly higher blood pressure (BP) values than did white children.7,8 Data from other studies confirm that elevated blood pressure begins as early as pre-adolescence and children who remain in the highest 90th blood pressure percentile are more likely to evolve toward permanent hypertension or early target organ damage in young adulthood.9–11


  1. Kearney PM, Whelton M, Reynolds K, et al., Lancet, 2005;365: 217–23.
  2. Rosamond W, Flegal K, Friday G, et al., Circulation, 2007;115: e69–171.
  3. Casper ML BE, Williams GI Jr, Centers for Disease Control and Prevention, 2003.
  4. Adams J, Am J Med Sci, 1932;184:342–350.
  5. Hertz RP, Unger AN, Cornell JA, Saunders E, Arch Intern Med, 2005;165:2098–2104.
  6. Cooper R, Rotimi C, Ataman S, et al., Am J Public Health, 1997;87:160–68.
  7. Berenson GS, Voors AW,Webber LS, et al., Metabolism, 1979;28:1218–28.
  8. Gidding SS, Bao W, Srinivasan SR, Berenson GS, J Pediatr, 1995;127:868–74.
  9. Muntner P, He J, Cutler JA, et al., JAMA, 2004;291:2107–13.
  10. Sinaiko AR, Donahue RP, Jacobs DR, Jr, Prineas RJ, Circulation, 1999;99:1471–6.
  11. Bao W, Threefoot SA, Srinivasan SR, Berenson GS, Am J Hypertens, 1995;8:657–65.
  12. Ong KL, Cheung BM, Man YB, et al., Hypertension, 2007;49: 69–75.
  13. Su YR, Rutkowski MP, Klanke CA, et al., J Am Soc Nephrol, 1996;7:2543–9.
  14. Turner ST, Schwartz GL, Chapman AB, Boerwinkle E, Hypertension, 2001;37:739–43.
  15. Ergul A, Hypertension, 2000;36:62–7.
  16. Suthanthiran M, Li B, Song JO, et al., Proc Natl Acad Sci USA, 2000;97:3479–84.
  17. Gretler DD, Fumo MT, Nelson KS, Murphy MB, Am J Hypertens, 1994;7:7–14.
  18. Timio M, Venanzi S, Lolli S, et al., Clin Nephrol, 1995;43:382–7.
  19. Taylor AL, Ziesche S, Yancy CW, et al., Circulation, 2007;115: 1747–53.
  20. Taylor AL, Ziesche S, Yancy C, et al., N Engl J Med, 2004;351: 2049–57.
  21. Anand IS, Tam SW, Rector TS, et al., J Am Coll Cardiol, 2007;49: 32–9.
  22. Chobanian AV, Bakris GL, Black HR, et al., JAMA, 2003;289: 2560–72.
  23. Douglas JG, Bakris GL, Epstein M, et al., Arch Intern Med, 2003;163:525–41.
  24. National Collaborating Centre for Chronic Conditions, Hypertension: management of hypertension in adults in primary care: partial update, Royal College of Physicians, 2006.
  25. Appel LJ, Moore TJ, Obarzanek E, et al., N Engl J Med, 1997;336: 1117–24.
  26. Appel LJ, Sacks FM, Carey VJ, et al., JAMA, 2005;294:2455–64.
  27. Appel LJ, Champagne CM, Harsha DW, et al., JAMA, 2003;289: 2083–93.
  28. Miller ER, 3rd, Erlinger TP, Young DR, et al., Hypertension, 2002;40:612–18.
  29. The ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group, JAMA, 2002;288:2981–97.
  30. Wright JT Jr, Bakris G, Greene T, et al., JAMA, 2002;288: 2421–31.
  31. Pepine CJ, Handberg EM, Cooper-DeHoff RM, et al., JAMA, 2003;290:2805–16.
  32. Dahlof B, Devereux RB, Kjeldsen SE, et al., Lancet, 2002;359: 995–1003.
  33. VA Cooperative Group, JAMA, 1982;248:2004–11.
  34. VA Cooperative Group, JAMA, 1982;248:1996–2003.
  35. Materson BJ, Reda DJ, Cushman WC, Am J Hypertens, 1995;8:189–92.
  36. The Beta-Blocker Evaluation of Survival Trial Investigators, N Engl J Med, 2001;344:1659–67.
  37. Exner DV, Dries DL, Domanski MJ, Cohn JN, N Engl J Med, 2001;344:1351–7.
  38. Julius S, Alderman MH, Beevers G, et al., J Am Coll Cardiol, 2004;43:1047–55.